Publications by authors named "Esrafil Mansouri"

47 Publications

Pretreatment with Gallic Acid Mitigates Cyclophosphamide Induced Inflammation and Oxidative Stress in Mice.

Curr Mol Pharmacol 2021 May 31. Epub 2021 May 31.

Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Cyclophosphamide (CP) as an alkylating compound has been widely applied to treat cancer and autoimmune diseases. CP is observed to be nephrotoxic in humans and animals because it produces reactive oxygen species. Gallic acid (GA), a polyhydroxy phenolic compound, is reported to exhibit antioxidant and anti-inflammatory effects.

Objective: The current research aimed at evaluating the GA effect on CP-related renal toxicity.

Methods: In total, 35 male mice were assigned to 5 groups. Group1: receiving normal saline, group 2: CP group, receiving one CP injection (200 mg/kg; i.p.) on day 6. Groups 3 and 4: GA+CP, GA (10 and 30 mg/kg; p.o.; respectively) received through six consecutive days plus CP on the 6th day 2 hr after the last dose of GA, group 5: received GA (30 mg/kg; p.o.) for six consecutive days. Then on day 7, blood samples were collected for determining creatinine (Cr), serum kidney injury molecule-1 (KIM-1), blood urea nitrogen (BUN), and neutrophil gelatinase-associated lipocalin (NGAL) concentrations. Malondialdehyde (MDA), nitric oxide (NO) concentration, catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx) activities, and IL-1β, TNF-α levels were assessed in renal tissue.

Results: CP administration significantly increases KIM-1, NGAL, Cr, BUN, MDA, NO, IL-1β, and TNF-α level. It also decreases GSH concentration, SOD, GPx, and CAT function. Pretreatment with GA prevented these changes. Histopathological assessments approved the GA protective effect.

Conclusion: Our results showed that GA is possibly effective as a protective agent in cyclophosphamide-associated toxicities.
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http://dx.doi.org/10.2174/1874467214666210531162741DOI Listing
May 2021

Therapeutic effects of Wharton's jelly-derived Mesenchymal Stromal Cells on behaviors, EEG changes and NGF-1 in rat model of the Parkinson's disease.

J Chem Neuroanat 2021 04 15;113:101921. Epub 2021 Feb 15.

Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Physiology, Medicine Faculty, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Human Wharton's jelly-derived Mesenchymal Stromal Cells (hWJ-MSCs) have shown beneficial effects in improving the dopaminergic cells in the Parkinson's disease (PD). In the present study, the effects of hWJ-MSCs on hyperalgesia, anxiety deficiency and Pallidal local electroencephalogram (EEG) impairment, alone and combined with L-dopa, were examined in a rat model of PD. Adult male Wistar rats were divided into five groups: 1) sham, 2) PD, 3) PD + C (Cell therapy), 4) PD + C+D (Drug), and 5) PD + D. PD was induced by injection of 6-OHDA (16 μg/2 μl into medial forebrain bundle (MFB)). PD + C group received hWJ-MSCs (1 × 10 cells, intravenous (i.v.)) twice post PD induction. PD + C+D groups received hWJ-MSCs combined with L-Dopa/Carbidopa, (10/30 mg/kg, intraperitoneally (i.p.)). PD + D group received L-Dopa/Carbidopa alone. Four months later, analgesia, anxiety-like behaviors, were evaluated and Pallidal local EEG was recorded. Level of insulin-like growth factor 1 (IGF-1) was measured in the striatum and dopaminergic neurons were counted in substantia nigra (SNc). According to data, MFB-lesioned rats showed hyperalgesia in tail flick, anxiety-like symptoms in cognitive tests, impairment of electrical power of pallidal local EEG as field potential, count of dopaminergic neurons in SNc and level of IGF-1 in striatum. These complications restored significantly by MSCs treatment (p < 0.001). Our findings confirm that chronic treatment with hWJ-MSC, alone and in combination with L-Dopa, improved nociception and cognitive deficit in PD rats which may be the result of increasing IGF-1 and protect the viability of dopaminergic neurons.
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http://dx.doi.org/10.1016/j.jchemneu.2021.101921DOI Listing
April 2021

Transplanted Wharton's jelly mesenchymal stem cells improve memory and brain hippocampal electrophysiology in rat model of Parkinson's disease.

J Chem Neuroanat 2020 12 28;110:101865. Epub 2020 Sep 28.

Persian Gulf Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Anatomical Sciences, Cellular & Molecular Research Center, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Background: Experimental findings have shown that stem cell transplantation is a therapeutic procedure for Parkinson's disease (PD). In this study, effects of human Wharton's jelly-derived mesenchymal stem cells (hWJ-MSCs), alone and combined with l-dopa, were examined for repairing memory impairment in a rat model of PD.

Methods: Fifty adult male Wistar rats were randomly divided into five groups: 1) sham, 2) PD, 3) PD + C, 4) PD + C+D, and 5) PD + D. PD was induced by 6-OHDA injection (16 μg/2 μl) into medial forebrain bundle (MFB) and was confirmed 14 days later by contralateral rotation using apomorphine injection. The rats received hWJ-MSCs (1 × 10 cells, i.v.) twice on the 14th and 28th days post PD induction. Treated PD rats received hWJ-MSCs alone or combined with l-Dopa and Carbidopa (10/30 mg/kg, i.p.). Four months later, memory, hippocampal long-term potentiation (hLTP), histological changes, and the levels of BDNF and NGF in striatum were evaluated.

Results: PD caused both cell loss with small dark stained nuclei in granular zone as well as significant decrement of BDNF and NGF (P < 0.001) in striatum. These pathological alterations were associated with memory and hLTP deficits (P < 0.001 respectively). Treating PD rats with hWJ-MSCs, alone (P < 0.05 and P < 0.001) and combined with l-Dopa (P < 0.001), significantly restored the levels of both of the neurotrophins followed by improving cognition and hLTP (P < 0.001).

Conclusion: Current findings showed that chronic treatment of PD rats with hWJ-MSCs, alone and in combination with l-Dopa, could restore memory and hLTP by reconstructing dopaminergic neurons and elevating the BDNF and NGF factors.
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http://dx.doi.org/10.1016/j.jchemneu.2020.101865DOI Listing
December 2020

Protective effects of Vitex pseudo-negundo leaves on diabetic-induced nephropathy in rats.

J Basic Clin Physiol Pharmacol 2020 Aug 10. Epub 2020 Aug 10.

Department of Internal Medicine, Faculty of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran.

Objectives The belief of therapeutic effects of herbal remedies in diseases such as diabetes is rooted in medical history. The present study evaluated protective efficacy of the hydroalcoholic extract of Vitex pseudo-negundo leaves (VLHE) on the renal disorders in streptozotocin-induced diabetic rats. Methods Fifty Wistar male rats were recruited and divided into five groups of 10, including healthy controls and diabetic controls: three diabetic groups of which first group was treated with glibenclamide, and two groups treated with 250 and 500 mg/kg of VLHE, respectively, for six weeks. Renal biochemical tests and tissue histopathological evaluation were performed and the antioxidant status was examined. Results There were significant decreases in superoxide dismutase and glutathione peroxidase activities and increases in malondialdehyde levels in renal tissue of diabetic groups compared with healthy controls. In the VLHE-treated rats, fasting blood sugar, blood urea nitrogen and creatinine were declined, serum albumin elevated, kidney weight lowered, lipid peroxidation and reinforcement of the activities of antioxidant enzymes decreased compared with healthy groups. Histological assessments revealed that the vacuolar degeneration of tubules and shrinkage of glomeruli in VLHE-treated rats was decreased compared with diabetic rats. Conclusions The study suggested that administrating of VLHE in nephropathic rats ameliorated the disease by reduction of oxidative stress and increase in renal antioxidant enzyme activities.
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http://dx.doi.org/10.1515/jbcpp-2019-0308DOI Listing
August 2020

The effect of glycyrrhizin acid on and expression in hepatotoxicity induced by Titanium dioxide nanoparticles in rats.

Gastroenterol Hepatol Bed Bench 2020 ;13(2):168-176

Cell & Molecular Research Center, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Aim: This research studied the effects of glycyrrhizic acid (GA) on apoptosis induced with by titanium dioxide (NTiO2) in the liver of rats.

Background: It is widely accepted that the contamination resulting from nanoparticles (NPs) is an emerging dangerous issue. Metal oxide nanoparticles have high environmental stability and cause toxicity in the food chain. Thus, the present study investigated the anti-apoptotic effects of glycyrrhizic acid (GA) on the hepatotoxicity generated by titanium dioxide (NTiO2) NPs in the liver tissue.

Methods: Thirty-two male Wistar rats were randomly divided into four groups. NTiO2-treated rats were given 300 mg / kg of NTiO2 solution via gavage for 14 days; GA-treated were administered 100 mg/kg GA for 14 days; protection group was pre-treated with GA before NTiO2 administration for 7 days. Then, apoptotic index was evaluated through immunolocalization of Bax and Bcl-2 and TUNEL assay.

Results: we found that HSCORE of Bax expression and apoptotic index experienced a significant increase with NTiO2 (P <0.001), while Bcl-2 expression significantly diminished in NTiO2-treated rats (P <0.001). The results revealed that the increased Bax expression and apoptotic index were reversed by GA and enhanced the activities of Bcl2.

Conclusion: The results revealed that GA effectively attenuated apoptosis against NTiO2 in rats.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7149808PMC
January 2020

P-Coumaric Acid Mitigates Doxorubicin-Induced Nephrotoxicity Through Suppression of Oxidative Stress, Inflammation and Apoptosis.

Arch Med Res 2020 01 18;51(1):32-40. Epub 2020 Feb 18.

Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Background And Aims: P-Coumaric acid (PCA) is one the compound that has free radical scavenging effects. This study investigates the protective effect of PCA on tissue damage in DOX-induced nephrotoxicity.

Methods: Thirty two Wistar rats were divided into control, PCA, DOX (15 mg/kg, i.p.) and DOX plus PCA (100 mg/kg, orally) groups. DOX-induced nephrotoxicity was indicated by marked increase in blood urea nitrogen (BUN) and serum creatinine (Cr) compared to controls. DOX group also showed elevations in lipid peroxidation and reductions in enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). Expression of renal inflammatory cytokines including tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) and apoptosis were also elevated in the DOX group.

Results: PCA significantly reversed, nephrotoxicity induced by DOX via lowering BUN, serum Cr and improving histopathological scores as compared to the DOX group. PCA also decreased lipid peroxidation, increased activities of GPx, SOD and CAT, to levels relatively comparable to control. Significant reductions in expression of TNF-α, IL-1β and apoptosis were also observed following Co-administration of PCA relative to the DOX group.

Conclusions: Results describe a protective effect of PCA against DOX-induced nephrotoxicity. This effect is likely facilitated through inhibition of oxidative stress, inflammation and apoptosis.
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http://dx.doi.org/10.1016/j.arcmed.2019.12.004DOI Listing
January 2020

Protective effect of alpha-lipoic acid on di-(2-ethylhexyl) phthalate-induced testicular toxicity in mice.

Environ Sci Pollut Res Int 2020 Apr 7;27(12):13670-13678. Epub 2020 Feb 7.

Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Phthalates are synthetic chemicals, widely used as plasticizers due to their flexibility in plastics. Human populations may be exposed to phthalates through direct contact or environmental contamination. Most studies have focused on the effects of phthalates on the reproductive tract and have classified these compounds as endocrine disruptors. In this study, we aimed to investigate the possible oxidative damage induced by di-(2-ethylhexyl) phthalate (DEHP) in the mouse testis and to evaluate the regulatory effects of alpha-lipoic acid (LA). For this purpose, forty male mice were divided into four experimental groups. Group I received normal saline (2 mL/kg; p.o.) and corn oil (5 mL/kg; p.o.) as the control group, group II received DEHP (2 g/kg; p.o.), group III received DEHP and LA (20 mg/kg; p.o.), and group IV was treated with LA alone; treatments continued for 2 weeks. The glutathione level (GSH), as well as glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities, was determined in mice. In addition, serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, interleukin-1β (IL-1β), and tumor necrosis factor-alpha (TNF-α) were measured. Nitric oxide (NO) level, malondialdehyde (MDA) level, sperm characteristics, and histological changes of the testes were also evaluated. The results showed that 2 g/kg of DEHP could significantly decrease the sperm motility. Based on our findings, DEHP significantly reduced the production and count of sperms; these toxic effects were associated with alterations in the serum hormone levels. In the DEHP group, a significant reduction was reported in the serum testosterone, FSH, and LH levels. LA improved DEHP-induced changes in hormonal levels and sperm index. According to our findings, treatment with DEHP triggered histopathological changes and oxidative stress, which were normalized by LA pretreatment. In conclusion, DEHP disrupts the testicular function in rats, at least partly through induction of oxidative stress. On the other hand, LA exhibits potential protective effects on testicular toxicity induced by DEHP.
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http://dx.doi.org/10.1007/s11356-020-07817-1DOI Listing
April 2020

Assessment of the effect of sodium hydrogen sulfide (hydrogen sulfide donor) on cisplatin-induced testicular toxicity in rats.

Environ Sci Pollut Res Int 2020 Mar 3;27(8):8119-8128. Epub 2020 Jan 3.

Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Cisplatin (CIS) is an antineoplastic drug able to produce free radicals that are capable to induce various side effects in different tissues. Hydrogen sulfide (HS) has notable antioxidant, anti-apoptotic, and anti-inflammatory effects in different systems but its role in male reproductive system is not fully understood. In the present research, the effect of sodium hydrosulfide (NaHS) on cisplatin-induced testicular toxicity in male rats was studied. Thirty-two Sprague-Dawley rats were equally divided into 4 groups. The control group was treated with normal saline by intraperitoneal injection. The NaHS group received NaHS (200 μg/kg/day) intraperitoneally for 15 days. The CIS group received single dose of cisplatin (5 mg/kg) intraperitoneally, while the combination of CIS and NaHS was given to the CIS+ NaHS group. At the end of the study, body and testicular weights, plasma testosterone level, histological and morphometrical alterations, inflammation via IL-1β protein, lipid peroxidation, and activity of antioxidant enzymes (including glutathione peroxidase, superoxide dismutase, and catalase) of testicular tissue were evaluated. CIS injection revealed a significant decrease (p < 0.01) in body and testis weights, plasma testosterone concentration, diameter of seminiferous tubules, germinal epithelium thickness, the number of Sertoli cells, spermatogonia and spermatocyte, Johnsen's testicular score, and testicular antioxidant enzymes, whereas it caused a significant increase (p < 0.01) in lumen diameter of the seminiferous tubules, level of lipid peroxidation, and IL-1β protein expression when compared with the control group. NaHS administration to CIS-treated rats provided marked improvement (p < 0.05) in all biochemical, histological, and morphometrical changes induced by CIS. The beneficial effects of NaHS were mediated, at least partly, by its antioxidant and anti-inflammatory properties.
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http://dx.doi.org/10.1007/s11356-019-07266-5DOI Listing
March 2020

Antioxidant effect of p-coumaric acid on interleukin 1-β and tumor necrosis factor-α in rats with renal ischemic reperfusion.

Nefrologia (Engl Ed) 2020 May - Jun;40(3):311-319. Epub 2019 Dec 28.

Cellular and Molecular Research Center, Department of Anatomical Sciences, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Background And Aims: Renal ischemia-reperfusion occurs in some clinical conditions such as kidney surgery that can leads to acute renal failure. The aim of this study was to investigate the effect of p-coumaric acid (CA) on ischemia reperfusion (I/R) injury.

Methods: Thirty rats were randomly divided into five groups; control, CA (100mg/kg), I/R, propylene glycol (10%)+I/R and CA+I/R, (n=6 each). CA and propylene glycol were administered orally for 2 weeks. Then, the rats were subjected to bilateral renal ischemia for 45min and followed by reperfusion for 24h. All rats were killed and kidney function tests, tissue malondialdehyde and activity of antioxidant enzymes were determined. Histopathological evaluations were also performed. In addition, renal expression of the tumor necrosis factor-α and interleukin-1β were determined using enzyme-linked immunosorbent assay and immunohistochemistry.

Results: CA significantly improved the Cr and BUN levels in CA+I/R group compared to I/R group (p<0.005 and p<0.001, respectively). Reduction of tissue superoxide dismutase, glutathione peroxidase and catalase, were significantly improved by CA (p<0.01, p<0.01 and p<0.05). Treatment with CA also resulted in significant reduction in tissue MDA (p<0.05), TNF-α (p<0.001) and interleukin-1β expression (p<0.001) that were increased by renal I/R. Also, the rats treated with CA had nearly normal structure of the kidney.

Conclusions: The present findings suggest that, CA protects the kidneys against I/R injury via its antioxidant and anti-inflammatory effects.
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http://dx.doi.org/10.1016/j.nefro.2019.10.003DOI Listing
June 2021

Analgesic Effect of Intrathecal Melissa officinalis in the Rat Model of Hot-Water and Formalin-Induced Pain.

J Acupunct Meridian Stud 2020 Feb 16;13(1):19-24. Epub 2019 Nov 16.

Zoonoses Research Center, Jahrom University of Medical Sciences, Jahrom, Iran.

Melissa officinalis (MO) is one of the oldest herbal medicines commonly used in traditional medicine, which some studies have investigated for its analgesic effect. This study is an attempt to investigate the effects of intrathecal administration of Melissa officinalis on the pain induced by heat and formalin. In this experimental study, 70 male Wistar rats with an average weight of 270-320 g were randomly divided into five groups: control; sham that received 25 μl of saline through the spinal catheter; and three experimental groups that received 5, 10 or 20 mg/kg M. officinalis via the spinal catheter respectively. Five days after catheterization of the spinal cord from the lumbar region under anesthesia, the effects of Intrathecal administration of M. officinalis on heat- and formalin-induced pain were evaluated. Data were analyzed by using one-way ANOVA. Intrathecal injection of M. officinalis blocked heat-induced pain compared to sham group (p = 0.001). Maximum analgesia was observed 30 min after the injection. Furthermore, intrathecal administration of MO alleviated both acute (p = 0.007) and chronic (p = 0.001) phases of formalin-induced pain. Motor block was not observed in any of the above mentioned groups. The results showed that intrathecal administration of MO could significantly improve hot-water and formalin-induced pain in male Wistar rats.
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http://dx.doi.org/10.1016/j.jams.2019.11.001DOI Listing
February 2020

Diosmin ameliorative effects on oxidative stress and fibrosis in paraquat-induced lung injury in mice.

Environ Sci Pollut Res Int 2019 Dec 15;26(36):36468-36477. Epub 2019 Nov 15.

Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Paraquat (PQ) induces pulmonary fibrosis, a progressive lung disorder resulting in severe respiratory failure and death. Increased oxidative stress, inflammatory reactions, and multiple fibrotic lesions are major features of PQ-induced lung injury. Diosmin (Dio) is a safe drug that is available for clinical use for vascular disorders. Dio exhibits antioxidant, anti-inflammatory, and antifibrotic activities. Accordingly, the aim of this study was to evaluate the protective effect of diosmin on PQ-induced lung injury in mice and the underlying mechanisms involved. Lung injury was induced by PQ (30 mg/kg, intraperitoneally) in NMRI albino mice and Dio (50 and 100 mg/kg, gavage) was administrated 3 days before PQ and continued for 10 or 24 days. After euthanizing the mice, the biochemical and histopathological markers of lung tissue were determined. PQ significantly increased oxidative stress, inflammatory, and fibrotic markers. PQ increased the level of malonedaldehyde (MDA) and hydroxyproline (HYP) and decreased the level of glutathione (GSH) and catalase activity in the lung. Dio (50 and 100 mg/kg) significantly increased GSH levels and catalase activity and decreased HYP content and MDA levels. In addition, Dio reduced histopathological injuries in hematoxylin and eosin-stained and Masson's trichrome-stained sections. These findings suggest that Dio has protective effects against PQ-induced lung injury, which may be due to its antioxidant, anti-inflammatory, and antifibrotic effects.
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http://dx.doi.org/10.1007/s11356-019-06572-2DOI Listing
December 2019

KRAS mutation and abnormal expression of Cripto-1 as two potential candidate biomarkers for detection of colorectal cancer development.

J Cell Biochem 2020 04 6;121(4):2901-2908. Epub 2019 Nov 6.

Colorectal Cancer Research Center, Department of Biochemistry, Shiraz University of Medical Sciences, Shiraz, Iran.

Colorectal cancer (CRC), regardless of standard procedures of treatment and screening, is still considered one of the deadliest cancers in the Western world, and in economically developed Asian countries, especially Iran. The current study was undertaken to investigate whether changes in the level of Cripto-1 (CR-1) expression and KRAS mutations have a cumulative effect on the onset and progression of CRC. Fifty colorectal tissue samples, including 35 colorectal carcinomas with matching adjacent mucosa, and 15 colorectal adenomas, were chosen for analysis. Twenty-five CRC biopsies and 15 adenoma were analyzed for KRAS mutations by DNA sequencing (Sanger sequencing), and all 50 patients (35 CRCs and 15 adenomas) were evaluated by immunohistochemistry for the CR-1 protein expression. The inducible somatic KRAS mutation (G12D) was observed in nine (36%) of CRC patients, and in two (13.3%) of adenoma patients. The CR-1 expression level in both adenomas (P < .05) and carcinomas (P < .001), were significantly different, compared with the matching adjacent mucosa. The intensity of CR-1 staining in adenomas was less than the intensity of staining, detected in the CRCs (P < .001). The G12D KRAS mutation and CR-1 abnormalities are significantly associated as two signature biomarkers with potential clinical characteristics for the detection of CRC development.
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http://dx.doi.org/10.1002/jcb.29526DOI Listing
April 2020

Evaluation of the Protective Effects of Doxycycline on Acetaminophen-Induced Hepatotoxicity in Mice.

Iran J Pharm Res 2019 ;18(2):704-712

Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Acetaminophen (APAP) toxicity threatens human health due to increased mortality associated with its overdose. Doxycycline (DC) because of its properties such as antioxidant and anti-inflammatory can be a good therapeutic strategy to treat the acute toxicity induced by APAP. Male mice were divided into six groups in two periods of 3 h and 24 h as normal saline, APAP 400 mg/kg, DC 100 mg/kg and groups treated by 25, 50 and 100 mg/kg DC just before APAP, respectively. At the end of the 3 h and 24 h periods, the hepatic index, biochemical parameters including serum aspartate transaminase (AST) and alanine transaminase (ALT) activity and hepatic catalase activity, glutathione (GSH) and malondialdehyde (MDA) levels in liver and histopathological changes were evaluated. The results indicated that DC had no apparent effect on the hepatic index but significantly normalized the level of biochemical parameters and reduced APAP induced liver damage. Overall, it could be concluded that DC can inhibit or resolve harmful effects of APAP through antioxidant and anti-inflammatory properties. However, more studies are needed to understand exact mechanism of DC and its application for clinical use.
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http://dx.doi.org/10.22037/ijpr.2019.1100669DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6706732PMC
January 2019

Luteolin confers renoprotection against ischemia-reperfusion injury via involving Nrf2 pathway and regulating miR320.

Mol Biol Rep 2019 Aug 14;46(4):4039-4047. Epub 2019 May 14.

Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, 61335, Iran.

This work aims to evaluate the renoprotective effect of luteolin on expression of Nrf2 and miR320 in ischemia-reperfusion (I/R) injury in rats. Thirty rats were randomly divided into five groups; control, Luteolin (50 mg/kg), ischemia-reperfusion (I/R), DMSO (0/1%) + I/R and Luteolin+I/R, (n = 6 each). Administration of luteolin and DMSO was carried out by gavage for 3 days before renal I/R. Then, the rats were subjected to bilateral renal ischemia for 45 min and followed by reperfusion for 2 h. All rats were killed and the renal function, histological changes, oxidative stress degree, in all of groups were evaluated. In addition, the effects of luteolin on renal expression of Nrf2 and miR320 were examined by immunohistochemistry and real time- PCR. Luteolin significantly improved the creatinine (Cr) and blood urea nitrogen (BUN) levels in Luteolin + I/R group compared to I/R group (p < 0.001 and p < 0.001 respectively). Reduction of enzymatic activity of superoxide dismutase, glutathione peroxidase and catalase in I/R and DMSO + I/R groups, was significantly improved by Luteolin (p < 0.05) in Luteolin + I/R group. Pre-treatment with luteolin also resulted in significant reduction in tissue MDA level (p < 0.001), Nrf2 (p < 0.001) and miR320 expression (P < 0.05) that were increased by renal I/R. Also, the rats pretreated with luteolin had nearly normal structure of the kidney. These results indicate that luteolin protects the kidney against I/R injury via reducing oxidative stress, increasing antioxidant enzymes and reducing expression of Nrf2 and miR320.
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http://dx.doi.org/10.1007/s11033-019-04853-0DOI Listing
August 2019

Effects of Quercetin-Loaded Nanoparticles on MCF-7 Human Breast Cancer Cells.

Medicina (Kaunas) 2019 Apr 22;55(4). Epub 2019 Apr 22.

Cancer Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background and objectives: Previous studies have shown anti-tumor activity of quercetin (QT). However, the low bioavailability of QT has restricted its use. This study aimed to assess the toxic effect of QT encapsulated in solid lipid nanoparticles (QT-SLNs) on the growth of MCF-7 human breast cancer cells. Materials and Methods: MCF-7 and MCF-10A (non-tumorigenic cell line) cell lines treated with 25 µmol/mL of QT or QT-SLNs for 48 h. Cell viability, colony formation, oxidative stress, and apoptosis were evaluated to determine the toxic effects of the QT-SLNs. The QT-SLNs with appropriate characteristics (particle size of 85.5 nm, a zeta potential of -22.5 and encapsulation efficiency of 97.6%) were prepared. The QT-SLNs showed sustained QT release until 48 h. Cytotoxicity assessments indicated that QT-SLNs inhibited MCF-7 cells growth with a low IC (50% inhibitory concentration) value, compared to the free QT. QT-SLNs induced a significant decrease in the viability and proliferation of MCF-7 cells, compared to the free QT. QT-SLN significantly increased reactive oxygen species (ROS) level and MDA contents and significantly decreased antioxidant enzyme activity in the MCF-7 cells. Following QT-SLNs treatment, the expression of the protein significantly decreased, whereas Bx expression showed a significant increase in comparison with free QT-treated cells. Furthermore, The QT-SLNs significantly increased apoptotic and necrotic indexes in MCF-7 cells. Viability, proliferation, oxidative stress and apoptosis of MCF-10A cells were not affected by QT or QT-SLNs. According to the results of this study, SLN significantly enhanced the toxic effect of QT against human breast cancer cells.
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http://dx.doi.org/10.3390/medicina55040114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6524048PMC
April 2019

Epicatechin protective effects on bleomycin-induced pulmonary oxidative stress and fibrosis in mice.

Biomed Pharmacother 2019 Jun 20;114:108776. Epub 2019 Mar 20.

Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Toxicology, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Lung fibrosis is a chronic and intermittent pulmonary disease, caused by damage to the lung parenchyma due to inflammation and fibrosis. Epicatechin (Epi) as a flavonoid has antioxidant and anti-inflammatory properties. This study was conducted to evaluate the effect of Epi on oxidative stress, inflammation and pulmonary fibrosis induced by bleomycin (BLM) in mice. Accordingly, animals were randomly assigned into two groups of 7 and 14 days to evaluate the role of Epi in the early oxidative and late fibrotic phases of BLM-induced pulmonary injury, respectively. Each group was divided into six subgroups include control, Epi 100 mg/kg, BLM, and BLM groups pretreated with 25, 50 and 100 mg/kg Epi, respectively, from three days before until 7 or 14 days after BLM. Lung tissue oxidative stress markers including the activity of superoxide dismutase, glutathione peroxidase, catalase and the levels of malondialdehyde and glutathione were determined. Furthermore, alveolitis and inflammation were evaluated by Szapiel grading scores. In addition, fibrotic markers including lung hydroxyproline content, level of transforming growth factor beta and Ashcroft fibrotic grading of lung fibrosis were examined. Epi exerted protective effects against BLM-induced pulmonary injury in a dose-dependent manner in two early and late phases of lung injury. Oxidative stress markers persisted until the late fibrotic phase, as pro-fibrotic events were present in the early oxidative phase of BLM-induced injury. Finally, it is concluded that Epi can protect the lung against BLM-induced pulmonary oxidative stress, inflammation and fibrosis.
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http://dx.doi.org/10.1016/j.biopha.2019.108776DOI Listing
June 2019

Effects of Pravastatin in Adriamycin-Induced Nephropathy in Rats.

Iran J Pharm Res 2018 ;17(4):1413-1419

Cellular and Molecular Research Center, Sabzevar University of Medical Sciences, Sabzevar, Iran.

The aim of this study is to evaluate the effects of pravastatin on Adriamycin (ADR)-induced nephropathy and the mechanisms involved. Forty rats were divided into the following 4 groups: control, ADR (15 mg.kg, IP), ADR plus pravastatin (20 mg.kg which was started 5 days prior to ADR injection), and ADR plus pravastatin (20 mg.kg which was started 5 days after ADR injection). On day 20 after ADR injection, the animals were sacrificed. The results showed that administration of pravastatin decreased the levels of 24-h urinary protein (24-h UP), blood urea nitrogen (BUN), and creatinine ( < 0.05) which had increased after the injection of ADR; in addition, pravastatin reversed structural changes seen in ADR group. Furthermore, pravastatin elevated mRNA and protein expression of nephrin ( < 0.05) which had been reduced in ADR group. We conclude that pravastatin protects and treats renal injury induced by ADR.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6269566PMC
January 2018

Pravastatin attenuates testicular damage induced by doxorubicin - a stereological and histopatological study.

J Basic Clin Physiol Pharmacol 2018 Dec;30(1):103-109

Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background The aim of this study is to investigate the effects of pravastatin (PS) against doxorubicin (DOX)-induced testicular toxicity. Methods A total of 24 healthy male Sprague-Dawley rats were equally divided into four groups. Group I received normal saline, Group II received PS (20 mg/kg b.w.) by gavage, Group III was treated with DOX alone (15 mg/kg b.w., i.p.) and Group IV received the combination of DOX and PS. Results After 8 weeks, the results displayed that DOX caused a decrease in testicular volume and index, epididymal sperm count, seminiferous tubule diameter and germinal epithelium. DOX also reduced the number of spermatogonia, spermatoctyes and Sertoli cells as well as increased the lumen diameter of seminiferous tubules (p<0.05) and the incidence of histopathological changes of the testis. Moreover, elevated malondialdehyde (MDA) levels and declined glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were observed (p<0.05). On the contrary, PS treatment significantly ameliorated nearly all of these abnormalities (p<0.05). Conclusions PS protects against DOX-induced testicular toxicity in rats, which is likely via the inhibition of oxidative stress and the increase of antioxidant enzyme activity.
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http://dx.doi.org/10.1515/jbcpp-2018-0073DOI Listing
December 2018

Ameliorative effect of gallic acid on sodium arsenite-induced spleno-, cardio- and hemato-toxicity in rats.

Life Sci 2019 Jan 22;217:91-100. Epub 2018 Nov 22.

Shoushtar University of Medical Sciences, Shoushtar, Iran. Electronic address:

Aim: Arsenic is an important toxic chemical affecting millions of people around the world. Exposure to inorganic arsenic results in various health problems including skin lesions, hypertension, hematological disturbance, cardiovascular disease, spleen enlargement and cancer. Gallic acid (GA) is an important phenolic compound possessing various pharmacological properties including anti-inflammatory, antioxidant and free radical scavenging activities. The present study investigated effects of GA against sodium arsenite (SA)-induced spleno-, cardio- and hemato-toxicity.

Main Methods: Thirty-five adult male Wistar rats were randomly divided into five groups; group I received normal saline (2 ml/kg/day, p.o.) for 21 days, group II received SA (10 mg/kg/day, p.o.) for 14 days, group III and IV were treated with GA (10 and 30 mg/kg/day, respectively) for 7 days prior to receive SA and treatment was continued up to 21 days in parallel with SA administration, group V received GA (30 mg/kg/day, p.o.) for 21 days. The level of MDA, NO and glutathione (GSH) and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase were measured in heart and spleen tissues. Creatine kinase-MB (CK-MB) activity and hematological and histopathological parameters were also assessed.

Key Findings: GA significantly decreased SA-induced elevation of MDA and NO levels and reduction of GSH level and GPx and SOD activity in heart and spleen tissues. Furthermore, GA improved SA-induced alteration in hematological and histopathological parameters and reduced SA-induced elevation of serum CK-MB activity.

Significance: Our results suggest that GA inhibits SA-induced spleno-, cardio- and hemato-toxicity through reducing oxidative stress.
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http://dx.doi.org/10.1016/j.lfs.2018.11.050DOI Listing
January 2019

The protective effect of betulinic acid on microvascular responsivity and protein expression in alzheimer disease induced by cerebral micro-injection of beta-amyloid and streptozotocin.

Microcirculation 2018 11 8;25(8):e12503. Epub 2018 Oct 8.

Department of Physiology, Faculty of Medicine, Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Objective: Alzheimer's disease (AD) is mainly caused by accumulation of β-amyloid (Aβ) in vessels or parenchyma of the brain. Accordingly, natural compounds such as betulinic acid (BA) might improve the AD signs by increase in blood flow and through reduction in amyloid plaques.

Methods: Intra-hippocampal injection of BA (0.2 and 0.4 μmol/L /10 μL DMSO /rat) was done at intervals of 180 and 10 min before co-microinjection of 0.1 μmol/L Aβ dissolved in PBS (5 μL/rat, hippocampi) and 1.5 mg/kg Streptozotocin dissolved in aCSF (10 μL/rat, lateral ventricles). Cerebro-vascular responsivity tested by Laser Doppler, BBB leakage, Elisa assays of cytokines (TNF-α and IL-10), and Western blot analysis of proteins (BDNF and AchE) in the hippocampus were assessed 1 month after the injections.

Results: Microvascular reaction and BBB function were significantly impaired in AD rats, which were improved via BA pretreatment. BA could increase BDNF expression and decrease cytokine levels in the hippocampus of AD rats (especially 0.1 μmol/L Aβ: 0.4 μmol/L BA); however, no significant changes were detected in the blotting of AchE among the groups.

Conclusions: Betulinic acid could have a role in AD through protecting microcirculation, alleviating inflammation, and up-regulating BDNF expression which is clearer toward 1:4 molar ratios of Aβ to BA.
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http://dx.doi.org/10.1111/micc.12503DOI Listing
November 2018

Protective Effect of Gemfibrozil on Hepatotoxicity Induced by Acetaminophen in Mice: the Importance of Oxidative Stress Suppression.

Adv Pharm Bull 2018 Jun 19;8(2):331-339. Epub 2018 Jun 19.

Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Gemfibrozil (GEM) apart from agonist activity at peroxisome proliferator-activated receptor-alpha (PPAR-α) has antioxidant and anti-inflammatory properties. Accordingly, the present study was designed to investigate the protective effect of GEM on acute liver toxicity induced by acetaminophen (APAP) in mice. In this study, mice divided in seven groups include, control group, APAP group, GEM group, three APAP groups pretreated with GEM at the doses of 25, 50 and 100 mg/kg respectively and APAP group pretreated with N-Acetyl cysteine. GEM, NAC or vehicle were administered for 10 days. In last day, GEM and NAC were gavaged 1 h before and 1 h after APAP injection. Twenty four hours after APAP, mice were sacrificed. Serum parameters include alanine aminotransferase (ALT), aspartate aminotransferase (AST) and liver tissue markers including catalase enzyme activity, reactive oxygen species (ROS), malondialdehyde and reduced glutathione (GSH) levels determined and histopathological parameters measured. GEM led to significant decrease in serum ALT and AST activities and increase in catalase activity and hepatic GSH level and reduces malondialdehyde and ROS levels in the liver tissue. In confirmation, histopathological findings revealed that GEM decrease degeneration, vacuolation and necrosis of hepatocytes and infiltration of inflammatory cells. Present data demonstrated that GEM has antioxidant properties and can protect the liver from APAP toxicity, just in the same pathway that toxicity occurs by toxic ROS and that GEM may be an alternative therapeutic agent to NAC in APAP toxicity.
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http://dx.doi.org/10.15171/apb.2018.038DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046434PMC
June 2018

The Effect of Zinc Sulfate on miR-122, miR-34a, Atioxidants, Biochemical and Histopathological Parameters Following Hepatic Ischemia/Reperfusion Injury in Rats.

Biol Trace Elem Res 2019 Apr 16;188(2):434-440. Epub 2018 Jul 16.

Cellular and Molecular Research Center, Department of Anatomic Sciences, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Liver ischemia-reperfusion (IR) injury is a situation which occurs in various conditions such as pringle maneuver and liver transplantation. The regulatory effect of zinc sulfate (ZnSO4) is an important trace element on several liver disorders well known, but its effects on microRNA (miR-122 and miR-34a) have not been evaluated. The goal of this study was to identify the protective effects of ZnSO4 on IR-induced liver injury, in particular, microRNA in rats. Thirty-two male Wistar rats were randomly assigned into four groups (eight each group): sham, IR, ZnSO4 pretreatment, and ZnSO4 + IR groups. In sham and ZnSO4 pretreatment groups, animals received normal saline (N/S, 2 ml/kg) and ZnSO4 (5 mg/kg) for 7 consecutive days intraperitoneally (ip), then only laparotomy was performed. In IR and ZnSO4 + IR groups, N/S and ZnSO4, respectively, were given with the same dose, time, and route, before induction of ischemia for 45 min followed by reperfusion for 60 min. Blood sample was taken for biochemical and microRNAs analysis. Tissue specimens also were obtained for the measurements of antioxidant activities and histopathological evaluations. Our results showed that ZnSO4 pretreatment ameliorated histopathological changes decreased the increased serum levels of liver enzymes, miR-122 and miR-34a, and enhanced the decreased activity of antioxidant enzymes following hepatic IR injury. The present study indicated that ZnSO4 had potential hepatoprotective action against IR-induced injury. Therefore, it has been suggested that it can be administered as an anti-miR before elective hepatic surgeries for prevention of this complication.
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http://dx.doi.org/10.1007/s12011-018-1425-8DOI Listing
April 2019

Ellagic acid mitigates sodium arsenite-induced renal and hepatic toxicity in male Wistar rats.

Pharmacol Rep 2018 Aug 5;70(4):712-719. Epub 2018 Feb 5.

Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Background: The aim of this study was to investigate the effect of ellagic acid (EA) on arsenic-induced renal and hepatic toxicity in rats.

Methods: A total number of 35 male Wistar rats were randomly divided into five experimental groups. Group 1 received normal saline (po). Group 2 received sodium arsenite (SA, 10mg/kg, po) for 21days. Group 3 received EA (30mg/kg, po) for 14days. Groups 4 and 5 received SA 7days prior to EA (10 and 30mg/kg respectively) treatment and continued up to 21days simultaneous with SA administration. Various biochemical, histological and molecular biomarkers were measured in kidney and liver.

Results: Treatment with EA (more potently at dose of 30mg/kg) restored the SA-induced alterations in serum creatinine (Cr) and blood urine nitrogen (BUN) levels as well as the changes in aspartate aminotransferase (AST), alkaline phosphatase (ALP) and alanine aminotransferase (ALT) concentrations (all p<0.001). Elevated levels of malondialdehyde (MDA) and nitric oxide (NO) in renal and hepatic tissue was reduced by EA treatment (all p<0.001). Treatment with EA enhanced the glutathione (GSH) content in liver (p<0.001) and up-regulated renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) mRNA expression (all p<0.001). The SA-induced histopathological alterations in kidney and liver were reduced by EA treatment.

Conclusion: In conclusion, the presence of EA with SA alleviated its toxic effects and EA treatment might be an effective strategy for the management of arsenic-induced renal and hepatic damage.
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http://dx.doi.org/10.1016/j.pharep.2018.02.007DOI Listing
August 2018

Lycopene abrogates di-(2-ethylhexyl) phthalate induced testicular injury by modulating oxidative, endocrine and inflammatory changes in mice.

Life Sci 2018 Aug 7;207:265-271. Epub 2018 Jun 7.

Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran; Department of Physiology and Pharmacology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Electronic address:

Di (2-ethylhexyl) phthalate (DEHP) is one of the environmental pollutants that causes testicular damage. Lycopene (LYCO), the main active carotenoid in red fruits and vegetables, has well-known antiinflammatory and antioxidant activities. The present study aimed to investigate the effects of LYCO on DEHP-induced testicular injury in male mice. DEHP (2 g/kg, p.o.) was given for two weeks to mice. LYCO was given at 4 mg/kg, p.o., for two weeks, starting the same day of DEHP insult. Serum testosterone, luteinizing hormone and follicle stimulating hormone and testicular total antioxidant status, malondialdehyde, nitric oxide, glutathione, superoxide dismutase, glutathione peroxidase, catalase, tumor necrosis factor-α, interleukin-1β were measured. Also, testicular histopathological examination and sperm analysis were evaluated. Results showed that administration of LYCO significantly attenuated the DEHP-induced gonadotoxicity. Also, the gonadoprotective effects of LYCO were confirmed by the histopathological examination of the testes. Our results suggested that LYCO has produced attenuation of inflammatory, oxidative stress and hormonal parameters against DEHP-induced gonadotoxicity.
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http://dx.doi.org/10.1016/j.lfs.2018.06.009DOI Listing
August 2018

Ellagic acid: A promising protective remedy against testicular toxicity induced by arsenic.

Biomed Pharmacother 2018 Jul 7;103:1464-1472. Epub 2018 May 7.

Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Chronic exposure to arsenic, an inducer of oxidative stress, is one of the major causes of male infertility. Therefore, the present study investigated the protective role of Ellagic acid (EA), as a natural antioxidant, against testicular toxicity evoked by arsenic. Thirty-five male Wistar rats were divided into 5 treatment groups. Group 1 served as control, group 2 were orally exposed to sodium arsenite (SA, 10 mg/kg; 21 days), groups 3 and 4 were initially exposed to SA for 7 days and then were treated with both EA (10 and 30 mg/kg) and SA up to 21 days, and group 5 was treated with EA for 14 days. After this period, biochemical and histopathological parameters were evaluated in serum samples and testicular tissue. SA markedly reduced levels of serum testosterone, total antioxidant capacity, reduced glutathione as well as the activity of antioxidant enzymes. Furthermore, SA enhanced levels of malondialdehyde, tumor necrosis factor-α, interleukin-1β and nitric oxide in testes. Treatment with EA was found to reduce testicular arsenic accumulation and oxidative stress parameters. In addition, EA improved the serum testosterone level, testicular antioxidant markers and histological parameters after exposure to SA. EA may emerge as a promising therapeutic option to protect testes from arsenic-induced toxicity through reducing oxidative stress and inflammatory responses.
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http://dx.doi.org/10.1016/j.biopha.2018.04.194DOI Listing
July 2018

Sodium hydrogen sulfide (NaHS) ameliorates alterations caused by cisplatin in filtration slit diaphragm and podocyte cytoskeletal in rat kidney.

J Nephropathol 2017 Jul 6;6(3):150-156. Epub 2017 Feb 6.

Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Hydrogen sulfide (H2S) has been shown to have a protective role in various kidney disorders.

Objectives: This study investigated the molecular mechanism of NaHS (a H2S donor) in treating on the renal damage induced by cisplatin (CP).

Materials And Methods: Thirty-two male rats were randomly divided into 4 groups: Normal control group (group A)' NaHS group (group B) which received 200 µg/kg/d (intraperitoneal injection; i.p.) for 15 days' CP group (group C) which rats were injected with CP (5 mg/kg, single dose, i.p.), and CP + NaHS group (group D) (5 mg/kg and 200 µg/kg, respectively, i.p.). Samples of urine and serum, tissue of kidney were collected for analysis after treatments for 15 days. Morphological changes were elevated under light microscope' protein expression of desmin and nephrin were determined by immunohistochemistry and western blotting and also malondialdehyde (MDA) level was determined by spectrophotometer.

Results: Compared to the CP group, NaHS treatment mitigated histological damages, decreased 24-hour urine protein excretion, serum urea and creatinine as well as MDA level. NaHS treatment increased protein levels of nephrin. Moreover, NaHS treatment decreased protein levels of desmin.

Conclusions: NaHS can ameliorate CP -induced renal damage in rats which is associated with the increase in nephrin protein expression, and the decrease in MDA level and desmin protein expression.
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http://dx.doi.org/10.15171/jnp.2017.26DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5607976PMC
July 2017

The possible neuroprotective effect of ellagic acid on sodium arsenate-induced neurotoxicity in rats.

Life Sci 2018 Apr 15;198:38-45. Epub 2018 Feb 15.

Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran. Electronic address:

Objective: Arsenic is a well-known environmental contaminant, causing toxicity in different organs. The aim of this study was to investigate the possible neuroprotective effect of ellagic acid (EA) on arsenic-induced neurotoxicity in rats.

Design: Animals were divided into five groups. The first group received normal saline (2 mL/kg) for 21 days as control group. Group 2 was orally treated with sodium arsenite (SA, 10 mg/kg) for 21 days. Groups 3 and 4 were orally treated with SA (10 mg/kg) for 7 days prior to EA (10 and 30 mg/kg respectively) treatment and continued up to 21 days simultaneously with SA administration. Group 5 was orally treated with EA (30 mg/kg) for 14 days. Passive avoidance test and rotarod test were done to evaluate the behavioral changes following SA and/or EA treatment. Different biochemical, histological and molecular biomarkers were assessed in the brain tissue.

Results: Our data showed that SA significantly elevated brain tissue arsenic levels and malondialdehyde, nitric oxide, protein carbonylation, tumor necrosis factor-alpha, and interlukein-1β production. A decrease in the total antioxidant capacity, reduced glutathione content and glutathione peroxidase activity occurred in the brain of rats exposed to SA. SA-treated rats showed a significant impairment in long-term-memory, motor coordination and equilibrium. These results were supported by histopathological observations of the brain. Results revealed that administration of EA (30 mg/kg) reversed all neural markers alternation and ameliorated behavioral and histopathological changes induced by SA.

Conclusion: EA can effectively protect brain tissue against SA-induced neurotoxicity via its antioxidant and anti-inflammatory effects.
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http://dx.doi.org/10.1016/j.lfs.2018.02.022DOI Listing
April 2018

Protective Effect of Ellagic Acid Against Sodium Arsenite-Induced Cardio- and Hematotoxicity in Rats.

Cardiovasc Toxicol 2018 08;18(4):337-345

Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.

Ellagic acid (EA) is a phenolic constituent in certain fruits and nuts with wide range of biological activities, including potent antioxidant, antidiabetic, anti-inflammatory, anticancer and antimutagen properties. The aim of this study was to evaluate the effect of EA on sodium arsenic (SA)-induced cardio- and hematotoxicity in rats. Animals were divided into five groups. The first group was used as control. Group 2 was orally treated with sodium arsenite (SA, 10 mg/kg) for 21 days. Group 3 was orally treated with EA (30 mg/kg) for 14 days. Groups 4 and 5 were orally treated with SA for 7 days prior to EA (10 and 30 mg/kg, respectively) treatment and continued up to 21 days simultaneous with SA administration. Various biochemical, histological and molecular biomarkers were assessed in blood and heart. The results indicate that SA-intoxicated rats display significantly higher levels of plasma cardiac markers (AST, CK-MB, LDH and cTnI) than normal control animals. Moreover, an increase in MDA and NO with depletion of GSH and activities of CAT, SOD and GPx occurred in the heart of rats treated with SA. Furthermore, SA-treated rats showed significantly lower WBC, RBC, HGB, HCT and PLT and significantly higher MCV and MCH. Administration of EA (30 mg/kg) resulted in a significant reversal of hematological and cardiac markers in arsenic-intoxicated rats. These biochemical disturbances were supported by histopathological observations of the heart. In conclusion, the results of this study suggest that EA treatment exerts a significant protective effect on SA-induced cardio- and hematotoxicity.
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http://dx.doi.org/10.1007/s12012-018-9446-2DOI Listing
August 2018

Renoprotective effect of crocin following liver ischemia/ reperfusion injury in Wistar rats.

Iran J Basic Med Sci 2017 Oct;20(10):1172-1177

Virology department, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Objectives: The objectives of the current study were to evaluate the effects of hepatic ischemia/reperfusion (IR) injury on the activity of antioxidant enzymes, biochemical factors, and histopathological changes in rat kidney, and to investigate the effect of crocin on IR-related changes.

Materials And Methods: Thirty-two male Wistar rats were randomly allocated into four groups (n=8). They were sham-operated, IR, crocin pre-treatment, and crocin pretreatment+IR groups. Sham-operated and Crocin pre-treatment groups received normal saline (N/S, 2 ml/day) and crocin (200 mg/kg) for seven consecutive days intraperitoneally (IP), respectively, then rats underwent laparotomy, only. IR and crocin pretreatment+IR groups received N/S and crocin with the same dose, time, and route, respectively, then rats underwent partial (70%) ischemia for 45 min that was followed by reperfusion for 60 min. At the end of the experiment, kidney specimens were taken for histopathological and antioxidant evaluations and also blood samples were obtained for biochemical analysis.

Results: The results of the present study showed that crocin pre-treatment significantly increased the activity of antioxidants, decreased the serum levels of liver enzymes and blood urea nitrogen following IR-induced hepatic injury. Crocin also ameliorated kidney's histopathological disturbance beyond IR-induced hepatic injury.

Conclusion: Crocin as an antioxidant agent protected renal insult following liver IR injury by increasing the activity of antioxidant enzymes, reducing serum levels of liver enzymes, and improving histopathological changes.
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http://dx.doi.org/10.22038/IJBMS.2017.9450DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5673703PMC
October 2017

Investigation of the role of alginate containing high guluronic acid on osteogenic differentiation capacity of human umbilical cord Wharton's jelly mesenchymal stem cells.

J Microencapsul 2017 Dec 7;34(8):732-743. Epub 2017 Nov 7.

c Department of Statistics and Epidemiology , Faculty of Public Health, Ahvaz Jundishapur University of Medical Sciences (AJUMS) , Ahvaz , Iran.

Background And Aim: Cell encapsulation using biodegradable material has promising results for tissue engineering. Since pressure is an effective factor on stem cell behaviour and various concentrations of alginate create different pressures on the cells, therefore our goal was to evaluate the mechanical effect of 1/2% (w/v) and 1/8% (w/v) alginate containing high guluronic acid on viability and osteogenic capacity of HUCWJ cells.

Methods: Cell viability was evaluated by MTT assay after 1, 7 and 14 days. Alkaline phosphatase activity was evaluated by alkaline phosphatase assay kit after 14 and 21 days. Alizarin red S staining was performed for calcium deposition among histological section.

Results: MTT assay showed significant difference in the mean of viability rates between groups in day 14 (p < 0.05). Alizarin red S staining was higher in the group 1.8%. In addition, there was statistically significant higher ALP activity in the group 1.8% compared to the group 1.2%.
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http://dx.doi.org/10.1080/02652048.2017.1393115DOI Listing
December 2017
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