Publications by authors named "Mahdi Ghatrehsamani"

19 Publications

  • Page 1 of 1

Ghrelin induces autophagy and CXCR4 expression via the SIRT1/AMPK axis in lymphoblastic leukemia cell lines.

Cell Signal 2020 02 3;66:109492. Epub 2019 Dec 3.

Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran. Electronic address:

T cell acute lymphoblastic leukemia (T-ALL) is one of the most frequent malignancies in children, and the CXCR4 receptor plays an important role in the metastasis of this malignancy. Ghrelin is a hormone with various functions including stimulation of the release of growth hormone and autophagy in cancer cells. Moreover, SIRT1 and AMPK (AMP-activated protein kinase) stimulate expression of proteins involved in autophagy. On the other hand, autophagic cell death can be an alternative target for cancer therapy, in the absence of apoptosis. The relationship between ghrelin and the SIRT1/AMPK axis and the resulting effects on autophagy, apoptosis, proliferation, and expression of CXCR4 and the ghrelin receptor (GHS-R1a), in Jurkat and Molt-4 human lymphoblastic cell lines was not previously clear. Here we demonstrate that SIRT1 expression is upregulated during the induction of autophagy by ghrelin, an effect that is inhibited by inactivation of SIRT1/AMPK axis. In addition, ghrelin can affect CXCR4 and GHS-R1a expression. In conclusion, this work reveals that ghrelin induces autophagy, invasion, and downregulation of ghrelin receptor expression via the SIRT1/AMPK axis in lymphoblastic cell lines. However, in these cell lines ghrelin-induced autophagy does not lead to cell death due to weak induction of apoptosis.
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http://dx.doi.org/10.1016/j.cellsig.2019.109492DOI Listing
February 2020

The beneficial role of SIRT1 activator on chemo- and radiosensitization of breast cancer cells in response to IL-6.

Mol Biol Rep 2020 Jan 28;47(1):129-139. Epub 2019 Nov 28.

Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, PO Box: 88155-571, Shahrekord, Iran.

Tumor environmental cytokines, such as IL-6, has a major role in the outcome of radiation and chemotherapy. In this study, we hypothesized that IL-6 mediates its effects via SIRT1 as a protein deacetylase and activator of phosphatidylinositol-3 kinase pathways. In the present study, we evaluated the effects of the novel dual inhibitor of phosphatidylinositol-3 kinase/mammalian target of rapamycin, NVP-BEZ235, and SIRT1 inhibitor and activator plus radiotherapy in breast cancer cells treated with IL-6. Here, IL-6 untreated/pretreated human breast cancer cells were cultured with single or combination of NVP-BEZ235 and/or SIRT1 activator (SRT1720)/inhibitor (EX-527) under radiotherapy condition. After all treatments, the MTT assay and flow cytometry assay were used to explore cell viability and the ability of our treatments in altering cancer stem cells (CSCs) population or cellular death (apoptosis + necrosis) induction. Simultaneous exposure to NVP-BEZ235 and SRT1720 sensitized breast cancer cells to radiotherapy but elevated CSCs. Treatment with IL-6 for 2 weeks significantly decreased CSCs population. Activation of SIRT1 via SRT1720 in combination with NVP-BEZ235 significantly decreased breast cancer cells viability in IL-6 pretreatment cultures. Inhibition of SIRT1 via EX-527 diminished the beneficial effects of IL-6 pretreatment. The combination of NVP-BEZ235 and SRT1720 as a SIRT1 activation could effectively decrease breast cancer cells population and augments the efficacy of radiotherapy.
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http://dx.doi.org/10.1007/s11033-019-05114-wDOI Listing
January 2020

Targeting the phosphoinositide 3-kinase/AKT pathways by small molecules and natural compounds as a therapeutic approach for breast cancer cells.

Mol Biol Rep 2019 Oct 16;46(5):4809-4816. Epub 2019 Jul 16.

Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, PO Box 88155-571, Shahrekord, Iran.

The phosphoinositide 3-kinase/AKT/mTOR (PI3K/AkT/mTOR) pathway plays a pivotal role in the uncontrolled growth, migration and development of human breast cancer. The elevated expression of TGF-β1 increases the PI3K/AkT/mTOR activity in human breast cancer tissue and potentially motivates tumor metastasis and resistance to chemotherapy. Here, we investigated whether treatment with PI3K/AkT/mTOR dual inhibitor NVP-BEZ235 alone or in combination with caffeic acid phenyl ester (CAPE) could prevent TGF-β1 effects on breast cancer cells. MCF-7 human breast cancer cells were exposed to TGF-β1 for 14 days and then were treated with/without NVP-BEZ235 and/or CAPE. Cell viability, apoptosis, CXCR4 surface expression and mRNA levels of CXCR4 and TWIST-1 were analyzed in all treated groups. We found that treatment of human breast cancer cells with a combination of NVP-BEZ235 and CAPE increased induction of cellular death. Although flow cytometry analysis demonstrated that NVP-BEZ235 alone treatment reduced CXCR4 expression while increasing CXCR4 mRNA level; when NVP-BEZ235 was combined with CAPE, inhibition of CXCR4 surface expression and enhancement of CXCR4 mRNA expression was diminished. In addition, TWIST-1 mRNA expression was down regulated in samples treated with both NVP-BEZ235 and CAPE. These altogether signified that NVP-BEZ235 in combination with CAPE showed improved therapeutic efficacy in breast cancer cells by decreasing apoptotic resistance and reduction of CXCR4 and TWIST-1 expression at mRNA level could be one of mechanism of action.
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http://dx.doi.org/10.1007/s11033-019-04929-xDOI Listing
October 2019

A review on proteomics analysis to reveal biological pathways and predictive proteins in sulfur mustard exposed patients: roles of inflammation and oxidative stress.

Inhal Toxicol 2019 01 23;31(1):3-11. Epub 2019 Apr 23.

a Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences , Tehran , Iran.

Sulfur mustard (SM) is a mutagenic compound that targets various organs. Although it causes a wide range of abnormalities, cellular and molecular mechanisms of its action are not-well-understood. Oxidation of DNA, proteins, lipids, as well as depletion of cellular nicotinamide adenine dinucleotide (NAD), antioxidants and increase of intracellular calcium are the hypothesized mechanisms of its action at the acute phase of injury. In this review, the proteome analysis of SM toxicity has been considered. We selected articles that considered proteomics analysis of SM toxicity with two-dimensional gel electrophoresis (2DE) followed by mass spectrometry. Our search yielded nine related articles, four original in vitro and five human studies. The results of these studies have revealed a change in expression pattern of various proteins such as haptoglobin, amyloid A1, surfactant proteins, S100 proteins, apolipoprotein, Vit D binding protein, transferrin, alpha 1 antitrypsin, protein disulfide isomerase and antioxidant enzymes in patients who were exposed to SM about 30 years ago. Most of these proteins are up- or down-regulated in response to excessive production of reactive oxygen species (ROS) and oxidative stress (OS). There is a tight link between the expression pattern of these proteins with accumulation of leukocytes, inflammatory conditions, antioxidant depletion, mitochondrial deficiency, as well as increased expression or activity of several proteases such as caspases and matrix metalloproteinases (MMPs). Therefore, excessive production of ROS and OS along with chronic inflammatory may be the long-term toxic effects of SM following acute exposure.
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http://dx.doi.org/10.1080/08958378.2018.1558316DOI Listing
January 2019

Improvement in infected wound healing in type 1 diabetic rat by the synergistic effect of photobiomodulation therapy and conditioned medium.

J Cell Biochem 2019 06 16;120(6):9906-9916. Epub 2018 Dec 16.

Department of Biology and Anatomical Sciences, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.

We investigated the effects of photobiomodulation therapy (PBMT) and conditioned medium (CM) of human bone marrow mesenchymal stem cells (hBM-MSC) individually and/or in combination on the stereological parameters and the expression of basic fibroblast growth factor (bFGF), hypoxia-inducible factor (HIF-1α), and stromal cell-derived factor-1α (SDF-1α) in a wound model infected with methicillin-resistant Staphylococcus aureus (MRSA) in diabetic rats. CM was provided by culturing hBM-MSCs. Type 1 diabetes mellitus (T1DM) was induced in 72 rats, divided into four groups, harboring 18 rats each: group 1 served as a control group, group 2 received PBMT, group 3 received CM, and group 4 received CM + PBMT. On days 4, 7, and 15, six animals from each group were euthanized and the skin samples were separated for stereology examination and gene expression analysis by real-time polymerase chain reaction. In the CM + PBMT, CM, and PBMT groups, significant decreases were induced in the number of neutrophils (1460 ± 93, 1854 ± 138, 1719 ± 248) and macrophages (539 ± 69, 804 ± 63, 912 ± 41), and significant increases in the number of fibroblasts (1073 ± 116, 836 ± 75, 912 ± 41) and angiogenesis (15 230 ± 516, 13 318 ± 1116, 14 041 ± 867), compared with those of the control group (2690 ± 371, 1139 ± 145, 566 ± 90, 12 585 ± 1219). Interestingly, the findings of the stereological examination in the CM + PBMT group were statistically more significant than those in the other groups. In the PBMT group, in most cases, the expression of bFGF, HIF-1α, and SDF-1α, on day 4 (27.7 ± 0.14, 28.8 ± 0.52, 27.5 ± 0.54) and day 7 (26.8 ± 1.4, 29.6 ± 1.4, 28.3 ± 1.2) were more significant than those in the control (day 4, 19.3 ± 0.42, 25.5 ± 0.08, 22.6 ± 0.04; day 7, 22.3 ± 0.22, 28.3 ± 0.59, 24.3 ± 0.19) and other treatment groups. The application of PBMT + CM induced anti-inflammatory and angiogenic activities, and hastened wound healing process in a T1 DM model of MRSA infected wound.
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http://dx.doi.org/10.1002/jcb.28273DOI Listing
June 2019

Cellular and molecular mechanisms of sulfur mustard toxicity on spermatozoa and male fertility.

Toxicol Res (Camb) 2018 Nov 9;7(6):1029-1035. Epub 2018 Jul 9.

Chemical Injuries Research Center , Systems biology and poisonings institute , Baqiyatallah University of Medical Sciences , Tehran , Iran . Email: ; Tel: +21-82482502.

Sulfur mustard (SM) is a toxic compound that can target human spermatozoa. SM induces a wide variety of pathological effects in human reproductive organs, including sexual hormone disturbance, testicular atrophy, impaired spermatogenesis, poor sperm quality, defects in embryo development, childhood physical abnormalities, and severe fertility problems. However, the molecular and cellular mechanisms of SM action on male reproductive health and human sperm function are unclear. Excessive production of reactive oxygen species and the resulting oxidative stress is likely a significant mechanism of SM action, and could be associated with sperm DNA damage, membrane lipid peroxidation, reduced membrane fluidity, mitochondrial deficiency, apoptosis, and poor sperm quality. In this review, we aim to discuss the cellular and molecular mechanisms of SM action on sperm and reproductive health, the significance of OS, and the mechanisms through which SM enhances the infertility rate among SM-exposed individuals.
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http://dx.doi.org/10.1039/c8tx00062jDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6220723PMC
November 2018

Role of oxidative stress and antioxidant therapy in acute and chronic phases of sulfur mustard injuries: a review.

Cutan Ocul Toxicol 2019 Mar 10;38(1):9-17. Epub 2018 Sep 10.

a Chemical Injuries Research Center, Systems biology and poisonings institute, Baqiyatallah University of Medical Sciences , Tehran , Iran.

Sulfur mustard (SM) is a chemical compound that preferentially targets ocular, cutaneous and pulmonary tissues. Although pathologic effect of SM has been extensively considered, molecular and cellular mechanism of its toxicity, especially at the chronic phase of injury is not well-understood. Excessive production of reactive oxygen species (ROS) and oxidative stress (OS) appears to be involved in SM-induced injuries. SM may trigger several molecular and cellular pathways linked to OS and inflammation that can subsequently result in cell death and apoptosis. At the acute phase of injury, SM can enhance ROS production and OS by reducing the activity of antioxidants, depletion of intercellular glutathione (GSH), decreasing the productivity of GSH-dependent antioxidants, mitochondrial deficiency, accumulation of leukocytes and pro-inflammatory cytokines. Overexpression of ROS producing enzymes and down-regulation of antioxidant enzymes are probably the major events by which SM leads to OS at the chronic phase of injury. Therefore, antioxidant therapy with potent antioxidants such as N-acetylcysteine and curcumin may be helpful to mitigate SM-induced OS damages. This review aims to discuss the proposed cellular and molecular mechanisms of acute and delayed SM toxicity, the importance of OS and mechanisms by which SM increases OS either at the acute or chronic phases of injuries along with research on antioxidant therapy as a suitable antidote.
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http://dx.doi.org/10.1080/15569527.2018.1495230DOI Listing
March 2019

Evaluation of the Effects of Photobiomodulation on Partial Osteotomy in Streptozotocin-Induced Diabetes in Rats.

Photomed Laser Surg 2018 Aug 31;36(8):406-414. Epub 2018 May 31.

8 Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences , Tehran, Iran .

Objective: We examined the effects of photobiomodulation (PBM) on stereological parameters, and gene expression of Runt-related transcription factor 2 (RUNX2), osteocalcin, and receptor activator of nuclear factor kappa-B ligand (RANKL) in repairing tissue of tibial bone defect in streptozotocin (STZ)-induced type 1 diabetes mellitus (TIDM) in rats during catabolic response of fracture healing.

Background Data: There were conflicting results regarding the efficacy of PBM on bone healing process in healthy and diabetic animals.

Materials And Methods: Forty-eight rats have been distributed into four groups: group 1 (healthy control, no TIDM and no PBM), group 2 (healthy test, no TIDM and PBM), group 3 (diabetic control, TIDM and no PBM), and group 4 (diabetic test, no TIDM and PBM). TIDM was induced in the groups 3 and 4. A partial bone defect in tibia was made in all groups. The bone defects of groups second and fourth were irradiated by a laser (890 nm, 80 Hz, 1.5 J/cm). Thirty days after the surgery, all bone defects were extracted and were submitted to stereological examination and real-time polymerase chain reaction (RT-PCR).

Results: PBM significantly increased volumes of total callus, total bone, bone marrow, trabecular bone, and cortical bone, and the numbers of osteocytes and osteoblasts of callus in TIDM rats compared to those of callus in diabetic control. In addition, TIDM increased RUNX2, and osteocalcin in callus of tibial bone defect compared to healthy group. PBM significantly decreased osteocalcin gene expression in TIDM rats.

Conclusions: PBM significantly increased many stereological parameters of bone repair in an STZ-induced TIDM during catabolic response of fracture healing. Further RT-PCR test demonstrated that bone repair was modulated in diabetic rats during catabolic response of fracture healing by significant increase in mRNA expression of RUNX2, and osteocalcin compared to healthy control rats. PBM also decreased osteocalcin mRNA expression in TIDM rats.
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http://dx.doi.org/10.1089/pho.2018.4438DOI Listing
August 2018

Alteration in CD8 T cell subsets in enterovirus-infected patients: An alarming factor for type 1 diabetes mellitus.

Kaohsiung J Med Sci 2018 May 20;34(5):274-280. Epub 2018 Jan 20.

Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.

Type 1 diabetes is a multi-factorial disease that can develop due to the combination of genetic and environmental factors. Viruses, particularly enteroviruses, are major environmental candidates in the pathogenesis of type 1 diabetes, even though the mechanisms of pathogenicity of these viruses and their effects on the immune system have not been understood very well yet. Previous studies show that any imbalance in the population of different lymphocyte subsets could develop autoimmune diseases. Our theory is that enteroviral infection causes an impairment in the distribution of lymphocyte subtypes and consequently results in the diabetes onset in some individuals. Therefore, in this project, we evaluated the distribution of T CD8+ lymphocytes and their subsets in type 1 diabetes patients. This study was conducted to investigate the relationship between enteroviral infection and type 1 diabetes mellitus in an Iranian population, and suggestion a predicting approach for susceptible subjects.
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http://dx.doi.org/10.1016/j.kjms.2017.12.010DOI Listing
May 2018

SRT1720, a potential sensitizer for radiotherapy and cytotoxicity effects of NVB-BEZ235 in metastatic breast cancer cells.

Pathol Res Pract 2018 Jun 5;214(6):889-895. Epub 2018 Apr 5.

Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. Electronic address:

Background: Chemo-radio therapy (CRT) resistance is a main barrier in treating the triple negative breast cancer (TNBC). The success of conventional treatment may be ameliorated by elevating the responsiveness of the cancer cells to CRT. NVP-BEZ235 as a PI3K/AKT/mTOR dual inhibitor has been shown promising results in treating breast cancer cells. However, potential radiation-sensitizing effect of NVP-BEZ235 in TNBC remained unclear. In addition, SIRT-1 activation state and environmental cytokine were identified as being responsible for cancer cells responses to CRT. Herein, we investigate the role of interleukin 6 (IL-6) as a tumor environmental cytokine and SIRT1 in the effectiveness of NVP-BEZ235 plus radiotherapy.

Material And Methods: TNBC cells were pre-treated with/without IL-6 and were exposed to single and combination of SRT1720 (SIRT1 activator)/EX-527 (SIRT1 inhibitor) and/or NVP-BEZ235 and/or gamma radiation. The effect of our treatments on cellular growth was determined by MTT and the cellular death and CSCs percentage were determined by Flow cytometry. Senescence detection kit was used to assay the effect of our treatments on cellular senescence induction.

Results: Activation of SIRT1 via SRT1720 increased the efficacy of CRT in TNBC cells, especially when IL-6 exists in tumor microenvironment. Additionally, IL-6 pre-treatment followed by exposure to SRT1720 and NVP-BEZ235 significantly increased sensitivity of the cancer stem cells to radiation (p < 0.05).

Conclusion: Our result shows that combination of NVP-BEZ235 and SRT1720 may effectively improve late stage breast cancer cells therapeutics approach. Activation of SIRT1 and STAT3 in resistance breast cancer cells improves the in-vitro therapeutic efficacy of CRT.
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http://dx.doi.org/10.1016/j.prp.2018.04.001DOI Listing
June 2018

Evaluation of the effects of photobiomodulation on vertebras in two rat models of experimental osteoporosis.

Lasers Med Sci 2017 Sep 19;32(7):1545-1560. Epub 2017 Jul 19.

Cellular and Molecular Biology Research Center, Department of Anatomical Sciences and Biology, School of Medicine, Shahid Beheshti University of Medical Sciences, 19395/4719, Tehran, 1985717443, Iran.

The aim of this study was to evaluate the effects of photobiomodulation (PBM) on cancellous bone in rat models of ovariectomized induced osteoporosis (OVX-D) and glucocorticoid-induced osteoporosis (GIOP). The experiment comprised of nine groups. A group of healthy rats was used for baseline evaluations. The OVX-D rats were further divided into groups as follows: control rats with osteoporosis, OVX-D rats that received alendronate (1 mg/kg 60 days), OVX-D rats treated with pulsed wave laser (890 nm, 80 Hz, 900 s, 0.0061 W/cm, 5.5 J/cm, three times a week, 60 days), and OVX-D rats treated with alendronate + pulsed laser. Dexamethasone was administered to the remaining rats that were split into four groups: control, alendronate-treated rats, laser-treated rats, and GIOP rats treated with alendronate + laser. T12, L1, L2, and L3 vertebrae were subjected to laser. Results of the current study demonstrated that OVX-D and GIOP significantly decreased some stereological parameters, and type 1 collagen gene expression compared to the healthy group. There was a significant increase in osteoclast number in both OVX-D and glucocorticoid administration compared to the healthy group. However, the detrimental effect of the OVX-D procedure on bone was more serious than glucocorticoid administration. Results showed that laser alone had a detrimental effect on trabecular bone volume, and cortical bone volume in groups GIOP and OVX-D compared to those in the healthy group. Alendronate significantly improved total vertebral bone volume, trabecular bone volume, and cortical bone volume, in GIOP and OVX-D groups compared to the laser-treated groups. Furthermore, the alendronate + laser in OVX-D rats and GIOP rats produced significantly increased osteoblast number and type 1 collagen gene expression and caused a significant decrease in osteoclast number compared to the controls.
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http://dx.doi.org/10.1007/s10103-017-2278-7DOI Listing
September 2017

Synergistic antitumor effect of NVP-BEZ235 and CAPE on MDA-MB-231 breast cancer cells.

Biomed Pharmacother 2017 Aug 18;92:39-45. Epub 2017 May 18.

Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. Electronic address:

Triple negative breast cancer (TNBC) is the most lethal and aggressive kind of breast cancer. Studies with TNBC cells suggest that tumor environmental cytokines such as Transforming Growth Factor β1 (TGF-β1) have important roles in tumors fate. In the present study, we aimed to investigate, the effect of phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway dual inhibitor, NVP-BEZ235 and Caffeic acid phenyl ester (CAPE) on TNBC cell line (MDA-MB-231), stimulated with TGF-β1 for 14days in vitro. We found that TGF-β1 as a local tumor environmental cytokine plays important role in the progression and invasiveness of TNBC cells. NVP-BEZ235 inhibited the enhanced cell viability and CXCR4 expression induced by TGF-β1. In addition, the combined treatment of TNBC cell lines with CAPE and NVP-BEZ235 synergistically inhibited cell growth and reduced CXCR4 expression. Also, treatment of MDA-MB-231 cells with CAPE and NVP-BEZ235 led to decreasing the expression levels of p-FOXO3a in a time-dependent manner. Overall, these results suggest that tumor metastasis and progression in TNBC cells can be effectively reduced through the concurrent use of NVP-BEZ235 and CAPE. This could be of particular interest in assessing the effects of this therapy in the reduction of tumor metastasis and progression in other tumor types.
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http://dx.doi.org/10.1016/j.biopha.2017.05.051DOI Listing
August 2017

Evaluation of sHLA-G levels in serum of patients with prostate cancer identify as a potential of tumor marker.

Anat Cell Biol 2017 Mar 29;50(1):69-72. Epub 2017 Mar 29.

Cellular and Molecular Biology Research Centre, Shahrekord University of Medical Sciences, Shahrekord, Iran.

Prostate cancer is the most common cancer type in men and is the second cause of death, due to cancer, in patients over 50, after lung cancer. Prostate specific antigen (PSA) is a widely used tumor marker for prostate cancer. Recently, PSA is discovered in non-prostatic cancer tissues in men and women raising doubts about its specificity for prostatic tissues. PSA exists in low serum level in healthy men and in higher levels in many prostate disorders, including prostatitis and prostate cancer. Thus, a supplementary tumor marker is needed to accurately diagnose the cancer and to observe the patient after treatment. Recently, soluble human leukocyte antigen-G (sHLA-G) has been introduced as a new tumor marker for different cancer types, including colorectal, breast, lung, and ovary. The present descriptive-experimental study was carried out including patients with malignant prostate tumor, patients with benign prostate tumor, and a group of health men as the control group, as judged by an oncologist as well as a pathologist. After sterile blood sampling, sHLA-G was measured by enzyme-linked immunosorbent assay in each group. The data was then analyzed using one-way ANOVA. ≤0.05 was considered as statistically significant. The results showed that the mean of sHLA-G level was high in patients. Also, it was found that there was a significant difference in sHLA serum level between the three groups. The data revealed that sHLA-G can be a novel supplementary tumor marker in addition to PSA to diagnose prostate cancer.
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http://dx.doi.org/10.5115/acb.2017.50.1.69DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386928PMC
March 2017

Evaluation of the effects of pulsed wave LLLT on tibial diaphysis in two rat models of experimental osteoporosis, as examined by stereological and real-time PCR gene expression analyses.

Lasers Med Sci 2016 May 10;31(4):721-32. Epub 2016 Mar 10.

Department of Anatomical Sciences and Biology, School of Medicine, Shahid Beheshti University of Medical Sciences, PO Box: 19395/4719, Tehran, 1985717443, Iran.

Osteoporosis (OP) and osteoporotic fracture are major public health issues for society; the burden for the affected individual is also high. Previous studies have shown that pulsed wave low-level laser therapy (PW LLLT) has osteogenic effects. This study intended to evaluate the impacts of PW LLLT on the cortical bone of osteoporotic rats' tibias in two experimental models, ovariectomized and dexamethasone-treated. We divided the rats into four ovariectomized induced OP (OVX-d) and four dexamethasone-treated (glucocorticoid-induced OP, GIOP) groups. A healthy (H) group of rats was considered for baseline evaluations. At 14 weeks following ovariectomy, we subdivided the OVX-d rats into the following groups: (i) control which had OP, (ii) OVX-d rats treated with alendronate (1 mg/kg), (iii) OVX-d rats treated with LLLT, and (iv) OVX-d rats treated with alendronate and PW LLLT. The remaining rats received dexamethasone over a 5-week period and were also subdivided into four groups: (i) control rats treated with intramuscular (i.m.) injections of distilled water (vehicle), (ii) rats treated with subcutaneous alendronate injections (1 mg/kg), (iii) laser-treated rats, and (iv) rats simultaneously treated with laser and alendronate. The rats received alendronate for 30 days and underwent PW LLLT (890 nm, 80 Hz, 0.972 J/cm(2)) three times per week during 8 weeks. Then, the right tibias were extracted and underwent a stereological analysis of histological parameters and real-time polymerase chain reaction (RT-PCR). A significant increase in cortical bone volume (mm(3)) existed in all study groups compared to the healthy rats. There were significant decreases in trabecular bone volume (mm(3)) in all study groups compared to the group of healthy rats. The control rats with OP and rats from the vehicle group showed significantly increased osteoclast numbers compared to most other groups. Alendronate significantly decreased osteoclast numbers in osteoporotic rats. Concurrent treatments (compounded by PW LLLT and alendronate) produce the same effect on osteoporotic bone.
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http://dx.doi.org/10.1007/s10103-016-1916-9DOI Listing
May 2016

An evaluation of the effect of pulsed wave low-level laser therapy on the biomechanical properties of the vertebral body in two experimental osteoporosis rat models.

Lasers Med Sci 2016 Feb 30;31(2):305-14. Epub 2015 Dec 30.

Cellular and Molecular Biology Research Centre, Shahid Beheshti University of Medical Sciences, Po Box 19395/4719, 1985717443, Tehran, Iran.

Osteoporosis (OP) increases vertebral fragility as a result of the biomechanical effects of diminished bone structure and composition. This study has aimed to assess the effects of pulsed wave low-level laser therapy (PW LLLT) on cancellous bone strength of an ovariectomized (OVX-d) experimental rat model and a glucocorticoid-induced OP (GIOP) experimental rat model. There were four OVX-d groups and four dexamethasone-treated groups. A group of healthy rats was used for baseline evaluations. The OVX-d rats were further subdivided into the following groups: control rats with OP, OVX-d rats that received alendronate, OVX-d rats treated with PW LLLT, and OVX-d rats treated with alendronate and PW LLLT. The remaining rats received dexamethasone and were divided into four groups: control, alendronate-treated rats, laser-treated rats, and laser-treated rats with concomitant administration of alendronate. PW LLLT (890 nm, 80 Hz, 0.972 J/cm(2)) was performed on the spinal processes of the T12, L1, L2, and L3 vertebras. We extracted the L1 vertebrae and submitted them to a mechanical compression test. Biomechanical test findings showed positive effects of the PW LLLT and alendronate administration on increasing bending stiffness and maximum force of the osteoporotic bones compared to the healthy group. However, laser treatment of OVA-d rats significantly increased stress high load compared to OVA-d control rats. PW LLLT preserved the cancellous (trabecular) bone of vertebra against the detrimental effects of OV-induced OP on bone strength in rats compared to control OV rats.
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http://dx.doi.org/10.1007/s10103-015-1842-2DOI Listing
February 2016

2,3,7,8-tetrachlorodibenzo-p-dioxin decrease expression of aryl hydrocarbon receptor in peripheral lymphocyte of β-thalassemia major patients.

Adv Biomed Res 2015 28;4:218. Epub 2015 Sep 28.

Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Background: β-thalassemia major is a hereditary disease with inefficient erythropoiesis. Level of inflammatory cytokine is elevated in these patients. In this study, we investigate the effect of aryl hydrocarbon receptor (AhR) ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on the expression of inflammatory mediators in β-thalassemia major patient's lymphocytes.

Materials And Methods: Peripheral blood mononuclear cells of patients and healthy participants was isolated and cultured in favor of lymphocytes increment. Based on the treatment, we divided the cell into four groups. The orders of group's treatments were no treatment, tumor necrosis factor-α (TNF-α) treatment, TNF-α and TCDD treatment, TCDD treatment in Group 1-4, respectively. After cell culture, we extracted the cells RNA and converted them to cDNA. Real-time polymerase chain reaction was performed to assessment relative expression of caspase-1, NLRP3, and AhR. We compared all patient groups with equal healthy (control) groups.

Results: Results showed that expression of caspase-1 in patients (Groups 1 and 2) was significantly lower than healthy individuals (P < 0.05). Although, no significant difference was found (Groups 1, 2, and control) in AhR gene expression (P > 0.05). Expression of AhR in other groups of patients (3 and 4) was significantly lower than control groups (P < 0.05). Expression of caspase-1 in Group 4 was significantly larger than the control group (P < 0.001).

Conclusions: We show here that chronic inflammation decrease caspase-1 expression and exposure of human lymphocytes to TCDD promote caspase-1 expression. Furthermore, activation of AhR with TCDD decreases AhR expression in lymphocytes of β-thalassemia major disease.
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http://dx.doi.org/10.4103/2277-9175.166165DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4627176PMC
November 2015

Tumor necrosis factor-α inhibits effects of aryl hydrocarbon receptor ligands on cell death in human lymphocytes.

Adv Biomed Res 2015 28;4:216. Epub 2015 Sep 28.

Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Background: Activation of aryl hydrocarbon receptor (AhR) leads to diverse outcome in various kinds of cells. AhR activation may induce apoptosis or prevent of apoptosis and cell death. Recent studies suggest that apoptosis effects of AhR can be modulated by inflammatory cytokine like tumor necrosis factor alpha (TNF-α). In this study, we try to investigate the possible interaction of TNF-α with the 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a ligand of AhR, on peripheral lymphocytes.

Materials And Methods: Human peripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood by discontinuous density gradient centrifugation on ficoll. Isolated PBMCs were divided into four groups: Control group, TNF-α administered group, TCDD administered group, co-administered group with TCDD and TNF-α. Cells were maintained for a week in lymphocyte culture condition. Then, TNF-α was added to group 2 and 4. Finally, apoptosis and necrosis were analyzed in all samples using flowcytometry.

Result: In group 4, the mean percent of necrosis and apoptosis in TCDD treatment groups was significantly larger than other groups; (P < 0.05). Furthermore, there was no significant difference between the mean percent of cell death in TNF-α administered group and TCDD administered group (P > 0.05). However, the mean percent of cell death in co-administered group with TCDD and TNF-α was significantly lower than other groups; (P < 0.05).

Conclusion: TNF-α could significantly inhibit effects of TCDD on lymphocytes apoptosis. Combination effects of TNF-α and TCDD on lymphocyte increase cell survival.
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http://dx.doi.org/10.4103/2277-9175.166163DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4627181PMC
November 2015

Edaravone leads to proteome changes indicative of neuronal cell protection in response to oxidative stress.

Neurochem Int 2015 Nov 29;90:134-41. Epub 2015 Jul 29.

Department of Biological Sciences, St John's University, New York, NY, USA; The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Norway. Electronic address:

Neuronal cell death, in neurodegenerative disorders, is mediated through a spectrum of biological processes. Excessive amounts of free radicals, such as reactive oxygen species (ROS), has detrimental effects on neurons leading to cell damage via peroxidation of unsaturated fatty acids in the cell membrane. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) has been used for neurological recovery in several countries, including Japan and China, and it has been suggested that Edaravone may have cytoprotective effects in neurodegeneration. Edaravone protects nerve cells in the brain by reducing ROS and inhibiting apoptosis. To gain further insight into the cytoprotective effects of Edaravone against oxidative stress condition we have performed comparative two-dimensional gel electrophoresis (2DE)-based proteomic analyses on SH-SY5Y neuroblastoma cells exposed to oxidative stress and in combination with Edaravone. We showed that Edaravone can reverse the cytotoxic effects of H2O2 through its specific mechanism. We observed that oxidative stress changes metabolic pathways and cytoskeletal integrity. Edaravone seems to reverse the H2O2-mediated effects at both the cellular and protein level via induction of Peroxiredoxin-2.
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http://dx.doi.org/10.1016/j.neuint.2015.07.024DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675627PMC
November 2015
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