Publications by authors named "Hamed Haghi-Aminjan"

30 Publications

  • Page 1 of 1

An updated review of various medicinal applications of p-coumaric acid: From antioxidative and anti-inflammatory properties to effects on cell cycle and proliferation.

Mini Rev Med Chem 2021 Jan 14. Epub 2021 Jan 14.

Gastroenterohepatology Research Center, Shiraz University of Medical Sciences, Shiraz. Iran.

P-Coumaric acid (p-CA) is a hydroxycinnamic acid, an organic compound that is a hydroxyl derivative of cinnamic acid. P-CA is the most abundant isomer of the three in nature and can be found in a wide variety of edible plants such as fungi, peanuts, navy beans, tomatoes, carrots, basil, and garlic. Recently, the therapeutic properties of p-CA have received a great deal of attention from the scientific society. Here, we described the medicinal effects of p-CA on various pathological conditions. This review was performed via evaluating PubMed reported studies from January 2010 to January 2020 also reference lists were checked to find additional studies. All intermediation or complementarity of animal models, case-control and cohort studies, in-vitro studies, and controlled trials (CTs) on p-CA were acceptable, although, plant extract studies without indication of main active substances were excluded due to the considerable diversities and heterogeneities. According to recent evidence regarding the beneficial effects of p-CA, numerous diseases such as nephropathies, cardiovascular diseases, neuro-inflammatory diseases, liver diseases, cancers, and some metabolic disorders could potentially control by this natural herb. Interestingly, autophagy is a novel molecular mechanism involved in the crosstalk between classic effects of p-CA and introduces alternative therapeutic pathways for this compound. Much work remains in clarifying the main therapeutic properties among the various p-CA effects; these will be the subject of forthcoming work, which could be resulting in presenting the further mechanism of action.
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http://dx.doi.org/10.2174/1389557521666210114163024DOI Listing
January 2021

Synergic effects of nanoparticles-mediated hyperthermia in radiotherapy/chemotherapy of cancer.

Life Sci 2021 Mar 12;269:119020. Epub 2021 Jan 12.

Medical Technology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran; Radiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Sciences, Kermanshah, Iran. Electronic address:

The conventional cancer treatment modalities such as radiotherapy and chemotherapy suffer from several limitations; hence, their efficiency needs to be improved with other complementary modalities. Hyperthermia, as an adjuvant therapeutic modality for cancer, can result in a synergistic effect on radiotherapy (radiosensitizer) and chemotherapy (chemosensitizer). Conventional hyperthermia methods affect both tumoral and healthy tissues and have low specificity. In addition, a temperature gradient generates in the tissues situated along the path of the heat source, which is a more serious for deep-seated tumors. Nanoparticles (NPs)-induced hyperthermia can resolve these drawbacks through localization around/within tumoral tissue and generating local hyperthermia. Although there are several review articles dealing with NPs-induced hyperthermia, lack of a paper discussing the combination of NPs-induced hyperthermia with the conventional chemotherapy or radiotherapy is tangible. Accordingly, the main focus of the current paper is to summarize the principles of NPs-induced hyperthermia and more importantly its synergic effects on the conventional chemotherapy or radiotherapy. The heat-producing nanostructures such as gold NPs, iron oxide NPs, and carbon NPs, as well as the non-heat-producing nanostructures, such as lipid-based, polymeric, and silica-based NPs, as the carrier for heat-producing NPs, are discussed and their pros and cons highlighted.
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http://dx.doi.org/10.1016/j.lfs.2021.119020DOI Listing
March 2021

Short-term Effects of Metformin on Cardiac and Peripheral Blood Cells Following Cecal Ligation and Puncture-induced Sepsis.

Drug Res (Stuttg) 2020 Dec 21. Epub 2020 Dec 21.

Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran.

Aim Of The Study: Sepsis has well-documented inflammatory effects on cardiovascular and blood cells. This study is designed to investigate potential anti-inflammatory effects of metformin on cardiac and blood cells 12 and 24 h following cecal ligation and puncture (CLP)-induced sepsis.

Methods: For the purpose of this study, 36 male Wistar rats were divided into six groups: two groups underwent CLP, two groups underwent CLP and received metformin, and two groups only received sham operations. 12 h later, 18 rats (half of rats in each of the three aforementioned groups) were sacrificed and cardiac and blood cells were harvested. Subsequently, 12 h later, the rest of the rats were euthanatized. In all harvested blood and cardiac cells, oxidative stress indicators, antioxidant properties, count of blood cells, neutrophil infiltration, percentage of weight loss and pathological assessment were conducted.

Results: In our experiment, metformin elevated antioxidant levels, improved function of blood cells and percentage of weight loss. Moreover, in the groups which received metformin, oxidative stress and neutrophil infiltration markers were decreased significantly. Moreover, pathological investigations of cardiac cell injury were reduced in the metformin group.

Conclusions: Our findings suggest that in CLP induced sepsis model, metformin can improve the function of blood and cardiac cells through alleviating inflammation, improvement of anti-inflammation properties, and enhancement of blood profile, and all these effects are more pronounced after 24 h in comparison with 12 h after induction of sepsis.
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http://dx.doi.org/10.1055/a-1322-7478DOI Listing
December 2020

Therapeutic Effects of Gallic Acid in Regulating Senescence and Diabetes; an In Vitro Study.

Molecules 2020 Dec 11;25(24). Epub 2020 Dec 11.

Toxicology and Diseases Group, Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, 1417613151 Tehran, Iran.

Gallic acid (GA), a plant-derived ubiquitous secondary polyphenol metabolite, can be a useful dietary supplement. This in vitro study's primary purpose was to assess the anti-aging properties of GA using rat embryonic fibroblast (REF) cells, antidiabetic effects via pancreatic islet cells, and finally, elucidating the molecular mechanisms of this natural compound. REF and islet cells were isolated from fetuses and pancreas of rats, respectively. Then, several senescence-associated molecular and biochemical parameters, along with antidiabetic markers, were investigated. GA caused a significant decrease in the β-galactosidase activity and reduced inflammatory cytokines and oxidative stress markers in REF cells. GA reduced the G0/G1 phase in senescent REF cells that led cells to G2/M. Besides, GA improved the function of the β cells. Flow cytometry and spectrophotometric analysis showed that it reduces apoptosis via inhibiting caspase-9 activity. Taken together, based on the present findings, this polyphenol metabolite at low doses regulates different pathways of senescence and diabetes through its antioxidative stress potential and modulation of mitochondrial complexes activities.
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http://dx.doi.org/10.3390/molecules25245875DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7763304PMC
December 2020

The role of taurine on chemotherapy-induced cardiotoxicity: A systematic review of non-clinical study.

Life Sci 2021 Jan 1;265:118813. Epub 2020 Dec 1.

Department of Toxicology and Pharmacology, School of Pharmacy, and Toxicology and Diseases Group, Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Aims: Although chemotherapeutic agents have highly beneficial effects against cancer, they disturb the body's normal homeostasis. One of the critical side effects of chemotherapeutic agents is their deleterious effect on the cardiac system, which causes limitations of their clinical usage. Taurine constitutes more than 50% of the amino acids in the heart. The use of taurine might prevent chemotherapy-induced cardiotoxicity. This systematic study aims to evaluate the protective role of taurine against cardiotoxicity induced by chemotherapy.

Methods: A systematic search was performed in databases up to November 2020, and the review is designed on PRISMA guidelines. The search keywords were selected based on our study target and were searched in the title and abstract. After the consecutive screening, out of a whole of 94 articles, 8 articles were included according to our inclusion and exclusion criteria.

Key Findings: According to the study results, chemotherapy decreases body and heart weight and increases mortality. Also, it induces some biochemical and histological changes compared to the control group. By co-administration of taurine with chemotherapy, alterations returned near to the average level. These protective effects of taurine are mediated through anti-oxidant, anti-inflammatory, and anti-apoptotic properties.

Significance: Based on evaluated non-clinical studies, taurine ameliorates chemotherapy-induced cardiotoxicity, but its possible interaction with the efficacy of anti-cancer medicines that mostly act through induction of oxidants remains to be elucidated in the future. This needs conducting well-designed studies to assess the effectiveness and safety of this combination simultaneously.
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http://dx.doi.org/10.1016/j.lfs.2020.118813DOI Listing
January 2021

Resveratrol as an Enhancer of Apoptosis in Cancer: A Mechanistic Review.

Anticancer Agents Med Chem 2020 Oct 20. Epub 2020 Oct 20.

Department of Medical Physics and Radiology, Faculty of Paramedical Sciences, Kashan University of Medical Sciences, Kashan. Iran.

Resistance of cancer cells to therapy is a challenge for achieving an appropriate therapeutic outcome. Cancer (stem) cells possess several mechanisms for increasing their survival following exposure to toxic agents such as chemotherapy drugs, radiation as well as immunotherapy. Evidences show that apoptosis plays a key role in response of cancer (stem) cells and their multi drug resistance. Modulation of both intrinsic and extrinsic pathways of apoptosis can increase efficiency of tumor response and amplify the therapeutic effect of radiotherapy, chemotherapy, targeted therapy and also immunotherapy. To date, several agents as adjuvant have been proposed to overcome resistance of cancer cells to apoptosis. Natural products are interesting because of low toxicity on normal tissues. Resveratrol is a natural herbal agent that has shown interesting anti-cancer properties. It has been shown to kill cancer cells selectively, while protecting normal cells. Resveratrol can augment reduction/oxidation (redox) reactions, thus increases the production of ceramide and the expression of apoptosis receptors such as Fas ligand (FasL). Resveratrol also triggers some pathways which induce mitochondrial pathway of apoptosis. On the other hand, resveratrol has an inhibitory effect on anti-apoptotic mediators such as nuclear factor κ B (NFκB), cyclooxygenase-2 (COX-2), phosphatidylinositol 3-kinase (PI3K) and mTOR. In this review, we explain the modulatory effects of resveratrol on apoptosis, which can augment the therapeutic efficiency of anti-cancer drugs or radiotherapy.
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http://dx.doi.org/10.2174/1871520620666201020160348DOI Listing
October 2020

Metformin Attenuates Brain Injury by Inhibiting Inflammation and Regulating Tight Junction Proteins in Septic Rats.

Cell J 2020 Jul 18;22(Suppl 1):29-37. Epub 2020 Jul 18.

Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran. Electronic Address:

Objective: Metformin has a potent inhibitory activity against inflammation and oxidative stress, which inevitably occur in sepsis-associated encephalopathy (SAE). The precise mechanisms underlying neuroprotective effects of metformin in SAE, are still unclear. In the present work, the protective effect of metformin on SAE using cecal ligation and puncture (CLP) model of sepsis, was assessed.

Materials And Methods: In this experimental study, CLP procedure was performed in Wistar rats and 50 mg/kg metformin was administered immediately. Specific markers of sepsis severity, inflammation, blood brain barrier (BBB) dysfunction, and brain injury, were investigated. Specific assay kits and real-time polymerase chain reaction (RT-PCR) were used. Histopathological assessment was also carried out.

Results: Treatment with metformin decreased murine sepsis score (MSS), lactate, platelet lymphocyte ratio (PLR), and high mobility group box (HMGB1) levels. The expression levels of claudin 3 () and claudin 5 () were increased following treatment with metformin. Metformin decreased the expression of S100b, neuron specific enolase (), and glial fibrillary acidic protein ().

Conclusion: Our study suggests that metformin may inhibit inflammation and increase tight junction protein expressions which may improve BBB function and attenuate CLP-induced brain injury. Hence, the potential beneficial effects of metformin in sepsis, should be considered in future.
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http://dx.doi.org/10.22074/cellj.2020.7046DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7481907PMC
July 2020

The role of curcumin/curcuminoids during gastric cancer chemotherapy: A systematic review of non-clinical study.

Life Sci 2020 Sep 4;257:118051. Epub 2020 Jul 4.

Pharmaceutical Sciences Research Center, Ardabil University of Medical Sciences, Ardabil, Iran. Electronic address:

Aims: Chemotherapy is an effective therapeutic modality which is commonly used for battling various cancers. However, several side effects induced by chemotherapeutic drugs would limit their clinical use. The present systematic review aims to evaluate the role of curcumin/curcuminoids co-administration during gastric cancer chemotherapy.

Methods: This systematic review was done according to PRISMA guidelines and a full systematic search in the electronic databases up to May 2020 using search terms in the titles and abstracts for the identification of relevant literature. 279 articles were found in electronic databases and 175 articles screened by title and abstract. Finally, 13 articles were included in this systematic review according to our inclusion and exclusion criteria.

Key Findings: The findings indicated that gastric cancer chemotherapy induces cytotoxicity effects in various ways including a decrease of cell viability, colony formation, metastasis, tumor growth, and weight, as well as elevation of apoptosis pathway, oxidative stress pathway compared to the control group. Co-administration of curcumin/curcuminoids with chemotherapy synergistically increased the effects of anti-cancer chemotherapy compared to the group solo treated with chemotherapeutic agents. Also, in chemoresistance gastric cancer cells, co-administration of curcumin reduced chemoresistance mainly through the reduction of NF-κB activation and elevation of apoptosis.

Significance: According to the findings, the use of curcumin/curcuminoids during gastric cancer chemotherapy has chemosensitizing effects, and also it can reduce chemoresistance in gastric cancer.
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http://dx.doi.org/10.1016/j.lfs.2020.118051DOI Listing
September 2020

Cannabinoids as anti-ROS in aged pancreatic islet cells.

Life Sci 2020 Sep 15;256:117969. Epub 2020 Jun 15.

Toxicology and Diseases Group, Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences (TUMS), Tehran, Iran. Electronic address:

Aims: Cannabinoids are the chemical compounds with a high affinity for cannabinoid receptors affecting the central nervous system through the release of neurotransmitters. However, the current knowledge related to the role of such compounds in the regulation of cellular aging is limited. This study aimed to investigate the effect of cannabidiol and tetrahydrocannabinol on the function of aged pancreatic islets.

Main Methods: The expression of p53, p38, p21, p16, and Glut2 genes and β-galactosidase activity were measured as hallmarks of cell aging applying real-time PCR, ELISA, and immunocytochemistry techniques. Pdx1 protein expression, insulin release, and oxidative stress markers were compared between young and aged rat pancreatic islet cells.

Key Findings: Upon the treatment of aged pancreatic islets cells with cannabidiol and tetrahydrocannabinol, the expression of p53, p38, p21 and the activity of β-galactosidase were reduced. Cannabidiol and tetrahydrocannabinol increase insulin release, Pdx1, Glut2, and thiol molecules expression, while the oxidative stress parameters were decreased. The enhanced expression of Pdx1 and insulin release in aged pancreatic islet cells reflects the extension of cell healthy aging due to the significant reduction of ROS.

Significance: This study provides evidence for the involvement of cannabidiol and tetrahydrocannabinol in the oxidation process of cellular aging.
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http://dx.doi.org/10.1016/j.lfs.2020.117969DOI Listing
September 2020

Development of a Novel Anti-Obesity Compound with Inhibiting Properties on the Lipid Accumulation in 3T3-L1 Adipocytes

Iran Biomed J 2020 05 30;24(3):155-63. Epub 2019 Nov 30.

Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.

Background: Obesity as a developing global challenge can be characterized by increase in adipocyte number and size arising from adipogenesis. Control of adipogenesis, as a potential strategy, can prevent and manage obesity. So far, the effectiveness of herbal medicine and active ingredients therapies for obesity and metabolic syndrome treatment has been investigated. In this study, a novel combination of berberine, catechin, and capsaicin was developed, and their effect on 3T3-L1 adipocytes was investigated.

Mthods: The effect of active ingredient on the cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Adipocytes were treated with various concentrations of berberine (3 and 6.25 μM), catechin (6.25 and 12.5 μM), and capsaicin (6.25 and 12.5 μM) alone and in combination.

Results: All active ingredients did not affect the cell viability by MTT assay at different concentrations. The dual and triple combinations of three active ingredients showed excellent potential as anti-obese without any toxicity. The inhibitory effect of berberine, catechin, and capsaicin on the differentiation of 3T3-L1 preadipocytes was found to be dose-dependent. These results indicate that catechin in both doses may have a stronger effect than the two other active ingredients on the intracellular lipid accumulation. Also, the triple combination of the aforementioned ingredients showed better responses than their dual combination.

Conclusion: This work is the first report to simultaneously investigate these three active ingredients in a single, dual, and triple formats. The berberine, catechin, and capsaicin co-treatment inhibits the adipogenesis during the differentiation process. This compound can be a prospective therapy for obesity and relevant diseases such as dyslipidemia.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7275626PMC
May 2020

The role of melatonin on doxorubicin-induced cardiotoxicity: A systematic review.

Life Sci 2020 Jan 13;241:117173. Epub 2019 Dec 13.

Pharmaceutical Sciences Research Center, Ardabil University of Medical Sciences, Ardabil, Iran. Electronic address:

Purpose: Doxorubicin, as an effective chemotherapeutic drug, is commonly used for combating various solid and hematological tumors. However, doxorubicin-induced cardiotoxicity is considered as a serious adverse effect, and it limits the clinical use of this chemotherapeutic drug. The use of melatonin can lead to a decrease in the cardiotoxic effect induced by doxorubicin. The aim of this review was to evaluate the potential role of melatonin in the prevention of doxorubicin-induced cardiotoxicity.

Methods: This review was conducted by a full systematic search strategy based on PRISMA guidelines for the identification of relevant literature in the electronic databases of PubMed, Web of Science, Embase, and Scopus up to January 2019 using search terms in the titles and abstracts. 286 articles were screened in accordance with our inclusion and exclusion criteria. Finally, 28 articles were selected in this systematic review.

Results: The findings demonstrated that doxorubicin-treated groups had increased mortality, decreased body weight and heart weight, and increased ascites compared to the control groups; the co-administration of melatonin revealed an opposite pattern compared to the doxorubicin-treated groups. Also, this chemotherapeutic agent can lead to biochemical and histopathological changes; as for most of the cases, these alterations were reversed near to normal levels (control groups) by melatonin co-administration. Melatonin exerts these protection effects through mechanisms of anti-oxidant, anti-apoptosis, anti-inflammatory, and mitochondrial function.

Conclusion: The results of this systematic review indicated that co-administration of melatonin ameliorates the doxorubicin-induced cardiotoxicity.
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http://dx.doi.org/10.1016/j.lfs.2019.117173DOI Listing
January 2020

Effect of the herbal medicines in obesity and metabolic syndrome: A systematic review and meta-analysis of clinical trials.

Phytother Res 2020 Mar 2;34(3):526-545. Epub 2019 Dec 2.

Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.

Obesity is a medical situation in which excess body fat has gathered because of imbalance between energy intake and energy expenditure. In spite of the fact that the variety of studies are available for obesity treatment and management, its "globesity" still remains a big challenge all over the world. The current systematic review and meta-analysis aimed to evaluate the efficacy, safety, and mechanisms of effective herbal medicines in the management and treatment of obesity and metabolic syndrome in human. We systematically searched all relevant clinical trials via Web of Science, Scopus, PubMed, and the Cochrane database to assess the effects of raw or refined products derived from plants or parts of plants on obesity and metabolic syndrome in overweight and obesity adult subjects. All studies conducted by the end of May 2019 were considered in the systematic review. Data were extracted independently by two experts. The quality assessment was assessed using Consolidated Standards of Reporting Trials checklist. The main outcomes were anthropometric indices and metabolic syndrome components. Pooled effect of herbal medicines on obesity and metabolic syndrome were presented as standardized mean difference (SMD) and 95% confidence interval (CI). A total of 279 relevant clinical trials were included. Herbals containing green tea, Phaseolus vulgaris, Garcinia cambogia, Nigella sativa, puerh tea, Irvingia gabonensis, and Caralluma fimbriata and their active ingredients were found to be effective in the management of obesity and metabolic syndrome. In addition, C. fimbriata, flaxseed, spinach, and fenugreek were able to reduce appetite. Meta-analysis showed that intake of green tea resulted in a significant improvement in weight ([SMD]: -0.75 [-1.18, -0.319]), body mass index ([SMD]: -1.2 [-1.82, -0.57]), waist circumference ([SMD]: -1.71 [-2.66, -0.77]), hip circumference ([SMD]: -0.42 [-1.02, -0.19]), and total cholesterol, ([SMD]: -0.43 [-0.77, -0.09]). In addition, the intake of P. vulgaris and N. sativa resulted in a significant improvement in weight ([SMD]: -0.88, 95 % CI: [-1.13, -0.63]) and triglyceride ([SMD]: -1.67, 95 % CI: [-2.54, -0.79]), respectively. High quality trials are still needed to firmly establish the clinical efficacy of the plants in obesity and metabolic syndrome.
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http://dx.doi.org/10.1002/ptr.6547DOI Listing
March 2020

The Protective Mechanism of Cannabidiol in Cardiac Injury: A Systematic Review of Non-Clinical Studies.

Curr Pharm Des 2019 ;25(22):2499-2507

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.

Background: Cardiac disease is accounted as the leading cause of worldwide morbidity and mortality. The disease is characterized by the overproduction of reactive oxygen and/or nitrogen species (ROS/RNS), and induction of oxidative stress. Cannabidiol (CBD) is a non-psychoactive ingredient of marijuana that has been reported to be safe and well tolerated in patients. Due to its pleiotropic effect, CBD has been shown to exert cytoprotective effects. This study intended to clarify the mechanisms and the potential role of CBD regarding cardiac injuries treatment.

Methods: A systematic literature search was conducted, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, in the electronic databases including PubMed, Web of Science, Scopus, and Embase up to June 2019 using predefined search terms in the titles and abstracts. Accordingly, a set of pre-specified inclusion and exclusion criteria were considered and 8 articles were ultimately included in this study.

Results: Our findings demonstrate that CBD has multi-functional protective assets to improve cardiac injuries; preliminary through scavenging of free radicals, and reduction of oxidative stress, apoptosis, and inflammation.

Conclusion: CBD can protect against cardiac injuries, mainly through its antioxidative and antiapoptotic effects on the basis of non-clinical studies. The cardioprotective effects of the CBD need to be further studied in welldesigned clinical trials.
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http://dx.doi.org/10.2174/2210327909666190710103103DOI Listing
April 2020

Targeting of oxidative stress and inflammation through ROS/NF-kappaB pathway in phosphine-induced hepatotoxicity mitigation.

Life Sci 2019 Sep 26;232:116607. Epub 2019 Jun 26.

Department of Pharmacology and Toxicology, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Electronic address:

Aims: Poisoning with aluminium phosphide (AlP) commonly has a high rate of mortality and morbidities. Phosphine gas is the main cause of AlP poisoning that has deleterious effect on multi-organs especially heart, kidney, and liver. Furthermore, several studies reported that resveratrol has cytoprotective effects through its pleiotropic property. The purpose of this study was to estimate the dose-dependent role of resveratrol on phosphine induced acute hepatic toxicity in rat model.

Main Methods: The rats have been exposed to LD of AlP (12 mg/kg) by gavage, and resveratrol doses (20, 40, and 80 mg/kg) were injected 30 min after intoxication. After 24 h, the serum and liver tissue were collected for present study.

Key Findings: The results indicated that phosphine causes an alteration in oxidative stress markers including elevation of ROS, and GSH level, MPO activity, reduction in SOD, catalase and G6PD activity as well as reduction in SOD1 and catalase expression. Furthermore, phosphine significantly induced phosphorylation of IkappaB, NF-kappaB and up-regulation of TNF-α, IL-1β, IL-6, and ICAM-1 expression. Also, phosphine induces markedly reduced hepatocytes lives cell and elevated apoptosis and necrosis. Co-treatment of resveratrol in a dose-dependent manner reversed aforementioned alterations. All in all, histological analysis indicated a deleterious effect of phosphine on the liver, which is mitigated by resveratrol administration.

Significance: The results of the present study suggest targeting ROS/NF-kappaB signalling pathway by resveratrol may have a significant effect on the improvement of hepatic injury induced by phosphine. It also may be a possible candidate for the treatment of phosphine-poisoning.
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http://dx.doi.org/10.1016/j.lfs.2019.116607DOI Listing
September 2019

Thyroid function following breast cancer chemotherapy: A systematic review.

J Cell Biochem 2019 08 25;120(8):12101-12107. Epub 2019 Apr 25.

Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

Background: Chemotherapy, as a systemic therapy, is one of the most effective modalities for cancer treatment. However, the use of chemotherapeutic drugs in patients with breast cancer can lead to thyroid dysfunction. This systematic review summarizes the available data on thyroid function following breast cancer chemotherapy.

Methods: To illuminate the thyroid toxicities induced by different chemotherapy regimens in patients with breast cancer, a systematic search was done in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline in Scopus, Embase, PubMed and Web of Science electronic databases up to December 2018. On the basis of a set of prespecified inclusion and exclusion criteria, eight eligible articles providing data on thyroid function following chemotherapy in patients with breast cancer were included in the study.

Results: According to the obtained results, it was found that for most cases, the levels of triiodothyronine (T3), free T3 (FT3), thyroxin (T4) and free T4 (FT4) hormones decrease following breast cancer chemotherapy regimens used in these eligible studies. However, alteration of thyroid-stimulating hormone (TSH) level after breast cancer chemotherapy was not clear.

Conclusion: The findings showed that thyroid function and TSH hormone level can change in patients with breast cancer receiving different chemotherapy regimens.
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http://dx.doi.org/10.1002/jcb.28771DOI Listing
August 2019

Effects of French maritime pine bark extract (Oligopin®) supplementation on bone remodeling markers in postmenopausal osteopenic women: A randomized clinical trial.

Phytother Res 2019 Apr 24;33(4):1233-1240. Epub 2019 Mar 24.

Department of Clinical Nutrition, School of Nutritional Sciences and Dietetics, International Campus, Tehran University of Medical Sciences, Tehran, Iran.

French maritime pine bark extract (FMPBE; Oligopin®), a dietary supplement, is rich in procyanidin. The objective of this study was to determine the effects of FMPBE on bone remodeling in postmenopausal osteopenic women. This randomized, double-blinded, placebo-controlled clinical trial was conducted on 40 postmenopausal osteopenic women. Individuals were randomly assigned to either FMPBE (250 mg/day, n = 21) or placebo (250-mg starch/day, n = 19) for 12 weeks. Biochemical indices, including bone remodeling marker, were assessed before and after the intervention. After the 12-week intervention, that is, FMPBE supplementation, a significant increase in bone alkaline phosphatase (BAP), procollagen type 1 amino-terminal propeptide (P1NP) levels and a significant decrease in C-terminal telopeptide of type I collagen (CTx1) were observed. Compared with the control group, FMPBE supplementation resulted in a significant increase in P1NP (0.015), BAP levels (0.001), and BAP/CTx1 ratio (p = 0.001) and a significant decrease in CTx1 levels (0.006). FMPBE supplementation for 12 weeks in postmenopausal osteopenic women produced favorable effects on bone markers. Meanwhile, further research is needed to determine whether FMPBE supplements can be used as a preventive strategy for bone loss in postmenopausal osteopenic women.
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http://dx.doi.org/10.1002/ptr.6320DOI Listing
April 2019

A systematic review of radiation-induced testicular toxicities following radiotherapy for prostate cancer.

J Cell Physiol 2019 Feb 10. Epub 2019 Feb 10.

Neurogenic Inflammation Research Center, Mashhad University of Medical Science, Mashhad, Iran.

Background: Prostate cancer is the second most common malignancy in men in the world, and radiotherapy is used as a standard treatment modality for this cancer. Although this treatment modality effectively kills prostate cancerous cells, it unavoidably irradiates the organs/tissues that are away from the treatment site. In this regard, radiation-induced testicular toxicities following prostate radiotherapy can affect sexual function, reproduction, and quality of life in cancer survivors. This review summarizes the available data on testicular exposure to radiation during prostate radiotherapy and the consequences on testicular function.

Methods: To illuminate the radiation-induced testicular toxicities following prostate radiotherapy, a systematic search was conducted based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline in PubMed, Web of Science, Scopus, Embase, and clinical trials electronic databases up to September 2018. According to a set of prespecified inclusion and exclusion criteria, 31 eligible articles providing data on testicular function following radiotherapy in patients with prostate cancer were included in the study.

Results: According to the different radiotherapeutic techniques used for prostate cancer treatment, the total tumor dose and scattered testicular dose values were ranging from 36.25 to 78.00 Gy and 0.06 to 6.48 Gy, respectively. Luteinizing hormone and follicle-stimulating hormone levels after prostate radiotherapy were significantly higher in comparison with the pretreatment levels. Around 60% of the studies showed that testosterone levels after prostate radiotherapy were significantly lower than the pretreatment levels. Furthermore, erectile dysfunction (ED), as an adverse side effect resulting from prostate radiotherapy, was reported and this complication is significantly correlated with lower satisfaction with sexual life. Testicular atrophy following prostate radiotherapy has also been observed and its frequency in patients with prior prostate radiotherapy is 2.5 times more than that in the patients without prior radiotherapy.

Conclusion: The data revealed that the scattered dose to testicular tissues during prostate radiotherapy can lead to testicular atrophy, variation of the male sex hormones, and quality of sexual life.
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http://dx.doi.org/10.1002/jcp.28283DOI Listing
February 2019

Manipulation of molecular pathways and senescence hallmarks by natural compounds in fibroblast cells.

J Cell Biochem 2019 04 26;120(4):6209-6222. Epub 2018 Nov 26.

Medicinal Plants Research Center, Institute of Medicinal Plants, ACECR, Karaj, Iran.

Aging contributes to an increased risk of developing a number of neurodegenerative and chronic disorders, predominantly related to oxidative stress (OS) and defects in the antioxidant balance. This study focused on the antisenescence effect of four plant species (Falcaria vulgaris, Ixiolirion tataricum, Ajuga chamaecistus, and Scabiosa flavida) on H O -induced premature senescence in rat NIH3T3 fibroblasts, which were found to be rich in effective phytochemicals with traditional ethnobotanical backgrounds. Plant materials were collected, identified, and extracted. To determine the viability of NIH3T3 cells, an MTT assay was conducted. The levels of OS markers and the senescence-associated ß-galactosidase (SA-ß-GAL) activity were analyzed by the Elisa reader. The cell cycle pattern was evaluated by flow cytometry. The expression of senescence-related inflammatory cytokines and the molecules involved in aging signaling pathways were investigated using the real-time reverse transcription polymerase chain reaction (RT-PCR). H O treatment decreased cell viability and increased lipid peroxidation (LPO) and the reactive oxygen species (ROS) in NIH3T3s. However, S. flavida exhibited low cytotoxicity, reduced OS and SA-ß-GAL activities in NIH3T3 cells compared with the H O -treated group. I. tataricum was the second best plant, although it was more toxic to NIHT3T cells. S. flavida decreased G0/G1 arrest and facilitated the G2/M transition of NIH3T3s, also downregulated the expression of p38, p53, p16, and the related inflammatory mediators. S. flavida potentially modulated senescence-associated hallmarks in fibroblasts exposed to H O , thus it may inhibit the aging process via controlling the OS. Therefore it is a promising candidate for future antiaging explorations.
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http://dx.doi.org/10.1002/jcb.27909DOI Listing
April 2019

The role of minocycline in alleviating aluminum phosphide-induced cardiac hemodynamic and renal toxicity.

Environ Toxicol Pharmacol 2018 Dec 2;64:26-40. Epub 2018 Oct 2.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Diseases Group, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Poisoning with aluminum phosphide (AlP) has been attributed to the high rate of mortality among many Asian countries. It affects several organs, mainly heart and kidney. Numerous literature demonstrated the valuable effect of minocycline in mitigating pathological symptoms of heart and kidney disease. The aim of the present study was to evaluate the probable protective effect of minocycline on cardiac hemodynamic parameters abnormalities and renal toxicity induced by AlP-poisoning in the rat model. AlP was administered by gavage at 12 mg/kg body weight followed by injection of minocycline for two interval times of 12 and 24 h, at 40, 80, 120 mg/kg body weight. Electrocardiographic (ECG) parameters were monitored, 30 min after AlP gavage for 6 h using an electronic cardiovascular monitoring device. Kidney tissue and serum were collected for the study of histology, mitochondrial complexes I, II, IV, lactate dehydrogenase (LDH) and myeloperoxidase (MPO) activity, ADP/ATP ratio, mitochondrial cytochrome c release, apoptosis, lactate, BUN, and Cr levels. The results demonstrated that AlP induces ECG abnormalities, and failure of heart rate and blood pressure, which improved significantly by minocycline. Minocycline treatment significantly improved complexes I, IV, MPO and LDH activities, and also reduced the ADP/ATP ratio, lactate level, release of cytochrome c, and apoptosis in the kidney following AlP-poisoning. Also, the histological results showed an improvement of kidney injury in minocycline treated groups. In conclusion, the findings of this study showed that minocycline could improve cardiac hemodynamic abnormalities and kidney injury following AlP-poisoning, suggesting minocycline might be a possible candidate for the treatment of AlP-poisoning.
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http://dx.doi.org/10.1016/j.etap.2018.09.008DOI Listing
December 2018

Pulmonoprotective Action of Zataria multiflora Ethanolic Extract on Cyclophosphamide-Induced Oxidative Lung Toxicity in Mice.

Chin J Integr Med 2020 Oct 22;26(10):754-761. Epub 2018 Sep 22.

Department of Pathology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, 48471-91971, Iran.

Objective: To evaluate the protective effect of Zataria multiflora extract, an antioxidative medicinal plant, against cyclophosphamide (CP)-induced oxidative lung damage in mice.

Methods: Mice were intraperitoneally pre-treated with various doses of Zataria multiflora extract (50, 100, 200, and 400 mg/kg) once daily for 7 consecutive days. Animals were then injected with a single 200 mg/kg intraperitoneal dose of CP 1 h after the last administration of O. vulgare. Twenty-four hours later, mice were euthanized, the lungs were immediately removed, and biochemical and histological studies were conducted.

Results: A single dose of CP markedly altered the levels of several biomarkers associated with oxidative stress in lung homogenates. Pretreatment with Zataria multiflora significantly inhibited the elevation of lipid peroxidation level and the depletion in glutathione content, and superoxide dismutase and catalase activities induced by CP in lung. In addition, Zataria multiflora effectively alleviated CP-induced histopathological abnormality and pulmonary damages in mice lung tissues.

Conclusions: The results reveal that Zataria multiflora protects lung tissues from CP-induced toxicity and suggest a role for oxidative stress in the pathogenesis of lung toxicity produced by CP in mice. Because Zataria multiflora has been extensively used as an additive agent and is regarded as safe, it may be used concomitantly as a good supplement for reducing organ toxicity in patients undergoing chemotherapy, besides their consolidated ethnopharmacological uses.
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http://dx.doi.org/10.1007/s11655-018-2984-4DOI Listing
October 2020

Expression of MT1 receptor in patients with gastric adenocarcinoma and its relationship with clinicopathological features.

Neuro Endocrinol Lett 2018 05;39(2):111-118

Pharmaceutical Sciences Research Centre, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Gastric cancer accounts 8% of the total cancer cases leading to 10% of total cancer deaths worldwide. The indoleamine N-acetyl-5-methoxytryptamine, better known as melatonin, is the principal hormone produced by the pineal gland. Recently, it has been well documented some anti-cancer roles of melatonin in some malignancies as breast and colon cancer; as well as some its protective roles in the GI tract that have been known as free radical scavenger, antimitogenic and apoptotic properties. According to the anti-cancer effects of melatonin, wide distribution of this neurohormone in GI tract and some proposed physiologic and pharmacologic roles for this neurohormone and following our previous study which has shown expression of MT2 receptor in gastric adenocarcinoma, this study initially scheduled to determine the expression of melatonin receptor MT1 in tissue samples of adenocarcinoma cancer patients. A total of 10 gastric adenocarcinoma patients and 10 normal individuals were examined for MT1 gene expression by real-time PCR. Additionally, for screening of different alleles of MT1 in our samples, the SSCP-PCR procedure was developed. Our results have shown interestingly high expression for MT1 receptor in cancer and marginal cancer groups comparing with normal group. Our findings also have shown that a remarkable association between MT1 receptor mRNA levels and grade in individuals over age 50. PCR-SSCP analysis results showed a variation between individuals which may be effective on their gene expression patterns. According to our knowledge, for the first time this study evaluated the expression of MT1 receptor gene in gastric adenocarcinoma tissues which consistent with our previous study but with some difference in comparisons between kind of tissue expression and difference in polymorphisms. Moreover, these results show the defending role of melatonin in the GI system.
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May 2018

The protective role of melatonin in chemotherapy-induced nephrotoxicity: a systematic review of non-clinical studies.

Expert Opin Drug Metab Toxicol 2018 09;14(9):937-950

a Department of Toxicology and Pharmacology, Faculty of Pharmacy , Tehran University of Medical Sciences , Tehran , Iran.

BSTRACT Introduction: The aim of this study was to investigate the potential role of melatonin in the prevention of chemotherapy-induced nephrotoxicity at the preclinical level. Areas to be covered: To illuminate the possible role of melatonin in preventing chemotherapy-related nephrotoxicity, Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline was followed. A comprehensive search strategy was developed to include PubMed, Web of Science, Scopus, and Embase electronic databases from their inception to May 2018. Based on a set of prespecified inclusion and exclusion criteria, 21 non-clinical articles were ultimately included in the study. Expert opinion: Our findings clearly demonstrate that melatonin has a protective role in the prevention of chemotherapy-induced nephrotoxicity which may be caused by different chemotherapy agents such as cyclophosphamide, cisplatin, doxorubicin, methotrexate, oxaliplatin, etoposide, and daunorubicin. On the basis of current review of non-clinical studies, this protective effect of melatonin is attributed to different mechanisms such as reduction of oxidative stress, apoptosis, and inflammation. The findings presented in this review are based on non-clinical studies and thus conducting appropriate clinical trials to evaluate the real effectiveness of the concurrent use of chemotherapy agents with melatonin in the cancer patients is necessary.
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http://dx.doi.org/10.1080/17425255.2018.1513492DOI Listing
September 2018

Regulation of tumor angiogenesis by microRNAs: State of the art.

J Cell Physiol 2019 02 2;234(2):1099-1110. Epub 2018 Aug 2.

Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

MicroRNAs (miRNAs, miRs) are small (21-25 nucleotides) endogenous and noncoding RNAs involved in many cellular processes such as apoptosis, development, proliferation, and differentiation via binding to the 3'-untranslated region of the target mRNA and inhibiting its translation. Angiogenesis is a hallmark of cancer, which provides oxygen and nutrition for tumor growth while removing deposits and wastes from the tumor microenvironment. There are many angiogenesis stimulators, among which vascular endothelial growth factor (VEGF) is the most well known. VEGF has three tyrosine kinase receptors, which, following VEGF binding, initiate proliferation, invasion, migration, and angiogenesis of endothelial cells in the tumor environment. One of the tumor microenvironment conditions that induce angiogenesis through increasing VEGF and its receptors expression is hypoxia. Several miRNAs have been identified that affect different targets in the tumor angiogenesis pathway. Most of these miRNAs affect VEGF and its tyrosine kinase receptors expression downstream of the hypoxia-inducible Factor 1 (HIF-1). This review focuses on tumor angiogenesis regulation by miRNAs and the mechanism underlying this regulation.
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http://dx.doi.org/10.1002/jcp.27051DOI Listing
February 2019

Regulation of aging and oxidative stress pathways in aged pancreatic islets using alpha-lipoic acid.

Mol Cell Biochem 2018 Dec 25;449(1-2):267-276. Epub 2018 Apr 25.

The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran.

Oxidative stress has been involved in the aging process and the pathogenesis of type-2 diabetes, which is a serious health problem worldwide. This study investigates the anti-aging, anti-apoptotic, and antioxidant properties of alpha-lipoic acid (ALA), aiming to improve aged rat pancreatic cells. In this regard, half maximal effective concentration (EC) of ALA based on the survival of aged pancreatic islet cells was determined as 100 µM. Following this, p38 and p53 genes expression as key factors in aging, oxidative stress biomarkers, insulin secretion, and Pdx1 protein expression were evaluated using real-time PCR, ELISA reader, and fluorescence microscope. It was revealed that ALA reduces and controls the effects of aging on beta cells mainly by suppressing p38 and p53 at the gene level (P < 0.001 and P < 0.01), respectively, reducing reactive oxygen species (P < 0.001) and enhancing levels of thiols (P < 0.05) compared with the aged islets. Furthermore, both qualitative and quantitative investigations of insulin secretion have shown that ALA can improve aged cells' function and increase insulin secretion specially in the stimulating concentration of glucose. Also, the expression of Pdx1 was considerably increased by ALA in comparison to the aged pancreatic islets (P < 0.001). As far as the authors of the present study are concerned, this is the first study, which evaluated aging associated with p38 and p53 pathways, oxidative stress parameters, and the expression of insulin in beta cells of an aged rat and reaffirmed the fact that ALA has a significant antioxidant role in reducing the aging process.
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http://dx.doi.org/10.1007/s11010-018-3363-3DOI Listing
December 2018

A glance at the therapeutic potential of irisin against diseases involving inflammation, oxidative stress, and apoptosis: An introductory review.

Pharmacol Res 2018 03 3;129:44-55. Epub 2018 Feb 3.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Diseases Group, Pharmaceutical Sciences Research Centre, Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Irisin is a hormone-like molecule mainly released by skeletal muscles in response to exercise. Irisin induces browning of the white adipose tissue and has been shown to regulate glucose and lipid homeostasis. Keeping its energy expenditure and metabolic properties in view, numerous studies have focused on its therapeutic potential for the treatment of metabolic disorders like obesity and type 2 diabetes. Recently, the anti-inflammatory, anti-apoptotic and anti-oxidative properties of irisin have received a great deal of attention of the scientific society. These pathogenic processes are often associated with initiation, progression, and prognosis of numerous diseases like myocardial infarction, kidney diseases, cancer, lung injury, inflammatory bowel diseases, atherosclerosis, liver diseases, obesity and type 2 diabetes. In the current review, we present evidence regarding the anti-inflammatory, anti-apoptotic and anti-oxidative potential of irisin pertaining to various pathological conditions. Here, we explore multiple molecular pathways targeted by irisin therapy. Given the promising effects of irisin, many diseases with evident oxidative stress, inflammation and apoptosis can be targeted by irisin.
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http://dx.doi.org/10.1016/j.phrs.2018.01.012DOI Listing
March 2018

The role of melatonin on chemotherapy-induced reproductive toxicity.

J Pharm Pharmacol 2018 Mar 23;70(3):291-306. Epub 2017 Nov 23.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.

Objectives: Reproductive malfunctions after chemotherapy still are a reason of reducing fertility and need specialized intensive care. The aim of this review was to investigate the effect of melatonin on the reproductive system under threatening with chemotherapeutic drugs.

Methods: To find the role of melatonin in the reproductive system during chemotherapy, a full systematic literature search was carried out based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines in the electronic databases up to 17 April 2017 using search terms in the titles and abstracts. A total of 380 articles are screened according to our inclusion and exclusion criteria. Finally, 18 articles were included in this study.

Key Findings: It has been cleared that melatonin has bilateral effects on reproductive cells. Melatonin protects normal cells via mechanisms, including decrease in oxidative stress, apoptosis, inflammation and modulating mitochondrial function, and sexual hormones. Furthermore, melatonin with antiproliferative properties and direct effects on its receptors improves reproductive injury and function during chemotherapy. On the other hand, melatonin sensitizes the effects of chemotherapeutic drugs and enhances chemotherapy-induced toxicity in cancerous cells through increasing apoptosis, oxidative stress and mitochondrial malfunction.

Conclusions: The study provides evidence of the bilateral role of melatonin in the reproductive system during chemotherapy.
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http://dx.doi.org/10.1111/jphp.12855DOI Listing
March 2018

Melatonin as an angiogenesis inhibitor to combat cancer: Mechanistic evidence.

Toxicol Appl Pharmacol 2017 11 30;335:56-63. Epub 2017 Sep 30.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Diseases Group, Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Melatonin, a pineal indolamine, participates in different body functions and is shown to possess diverse biological activities such as anti-tumor action. Angiogenesis inhibition is one of the mechanisms by which melatonin exerts its oncostatic effects. Increased angiogenesis is a major feature of tumor progression, thus angiogenesis inhibition is a critical step in cancer therapy. Melatonin employs a variety of mechanisms to target nutrients and oxygen supply to cancer cells. At the transcriptional level, hypoxia induced factor-1α (HIF-1α) and the genes under its control, such as vascular endothelial growth factor (VEGF) are the main targets of melatonin for inhibition of angiogenesis. Melatonin prevents translocation of HIF-1α into the nucleus thereby hindering VEGF expression and also prevents the formation of HIF-1α, phospho-STAT3 and CBP/p300 complex which is involved in the expression of angiogenesis-related genes. Angiostatic properties of melatonin could be also due to its ability to inhibit VEGFR2's activation and expression. Other angiostatic mechanisms of melatonin include the inhibition of endothelial cell migration, invasion, and tube formation. In the present study, we have reviewed the molecular anti-angiogenesis pathways mediated by melatonin and the responsible mechanisms in various types of cancers both in vitro and in vivo.
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http://dx.doi.org/10.1016/j.taap.2017.09.022DOI Listing
November 2017

On the mechanisms of melatonin in protection of aluminum phosphide cardiotoxicity.

Arch Toxicol 2017 Sep 27;91(9):3109-3120. Epub 2017 May 27.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.

Aluminum phosphide (AlP), one of the most commonly used pesticides worldwide, has been the leading cause of self-poisoning mortalities among many Asian countries. The heart is the main organ affected in AlP poisoning. Melatonin has been previously shown to be beneficial in reversing toxic changes in the heart. The present study reveals evidence on the probable protective effects of melatonin on AlP-induced cardiotoxicity in rats. The study groups included a control (almond oil only), ethanol 5% (solvent), sole melatonin (50 mg/kg), AlP (16.7 mg/kg), and 4 AlP + melatonin groups which received 20, 30, 40 and 50 mg/kg of melatonin by intraperitoneal injections following AlP treatment. An electronic cardiovascular monitoring device was used to record the electrocardiographic (ECG) parameters. Heart tissues were studied in terms of oxidative stress biomarkers, mitochondrial complexes activities, ADP/ATP ratio and apoptosis. Abnormal ECG records as well as declined heart rate and blood pressure were found to be related to AlP administration. Based on the results, melatonin was highly effective in controlling AlP-induced changes in the study groups. Significant improvements were observed in the activities of mitochondrial complexes, oxidative stress biomarkers, the activities of caspases 3 and 9, and ADP/ATP ratio following treatment with melatonin at doses of 40 and 50 mg/kg. Our results indicate that melatonin can counteract the AlP-induced oxidative damage in the heart. This is mainly done by maintaining the normal balance of intracellular ATP as well as the prevention of oxidative damage. Further research is warranted to evaluate the possibility of using melatonin as an antidote in AlP poisoning.
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http://dx.doi.org/10.1007/s00204-017-1998-6DOI Listing
September 2017

A systematic review on potential mechanisms of minocycline in kidney diseases.

Pharmacol Rep 2017 Aug 8;69(4):602-609. Epub 2017 Feb 8.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Diseases Group, Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Kidney diseases need specialized health care and still are a reason of death. There is a large body of evidence that indicates minocycline possesses some cytoprotective effects beside of antibacterial properties. In this review, we aimed to explain cytoprotective mechanisms and kidney protection of minocycline. In order to find the effects of minocycline on kidney diseases a systematic literature search was performed, according to the guidelines proposed at the PRISMA statement in the electronic databases, including: PubMed, Scopus, and Web of Science up to August 2016, using the term 'minocycline' combined either by 'kidney' or 'renal' and published in English language. The following criteria were included: (1) studies that used minocycline in renal diseases; (2) full-text articles; (3) English language; (4) no limitation in publications with in-vivo or in-vitro and human or animal subjects. Our search provided a total of 1056 articles which 1045 of them were discarded due to not meeting the inclusion criteria. It has been clear that several factors, including apoptosis, oxidative stress, mitochondrial dysfunction and inflammation have pivotal roles in the development and progression of kidney diseases. Minocycline protective properties are via several ways, including anti-apoptotic, free radical scavenging, anti-inflammatory, effect on mitochondrial functions and inhibition of matrix metalloproteinase. This systematic review confirmed that minocycline could have significant effects on treatment of renal malfunctions. However, regarding any possible adverse effects of antibiotics, it appears that more investigation is still needed in this context.
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http://dx.doi.org/10.1016/j.pharep.2017.02.001DOI Listing
August 2017

An ethanol extract of Origanum vulgare attenuates cyclophosphamide-induced pulmonary injury and oxidative lung damage in mice.

Pharm Biol 2014 Oct 19;52(10):1229-36. Epub 2014 Mar 19.

Pharmaceutical Sciences Research Center, Faculty of Pharmacy .

Context: Injury to normal tissues is the major limiting side effect of using cyclophosphamide (CP), an antineoplastic alkylating compound.

Objective: This study was undertaken to evaluate the protective effect of an extract of Origanum vulgare L. (Lamiaceae), an antioxidative medicinal plant, against CP-induced oxidative lung damage in mice.

Materials And Methods: Mice were pre-treated with various doses of O. vulgare extract (50, 100, 200, and 400 mg/kg) for 7 consecutive days followed by an injection with CP (200 mg/kg b.w.) One hour after the injection of O. vulgare on the last day, mice were injected with CP; 24 h later, they were euthanized, their lungs were immediately removed, and biochemical and histological studies were conducted.

Results: A single dose of CP markedly altered the levels of several biomarkers associated with oxidative stress in lung homogenates. Pretreatment with O. vulgare significantly reduced the levels of lipid peroxidation and attenuated the alterations in glutathione content and superoxide dismutase activity induced by CP in lung tissue. In addition, O. vulgare effectively alleviated CP-induced histopathological changes in lung tissue.

Conclusions: Our results revealed that O. vulgare protects lung tissues from CP-induced pulmonary damage and suggest a role for oxidative stress in the pathogenesis of lung disease produced by CP. Because O. vulgare has been extensively used as an additive agent and is regarded as safe, it may be used concomitantly as a supplement for reducing lung damage in patients undergoing chemotherapy.
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http://dx.doi.org/10.3109/13880209.2013.879908DOI Listing
October 2014