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      Curcumin inhibits apoptosis by modulating Bax/Bcl-2 expression and alleviates oxidative stress in testes of streptozotocin-induced diabetic rats

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          Abstract

          Scope

          The present study was designed to examine the damage caused by high-fat diet and streptozotocin-induced diabetes on the testis of rats and the effects of curcumin against oxidative stress and apoptosis from high-fat diet and diabetes.

          Methods

          Diabetes was induced by intraperitoneal injection of streptozotocin (30 mg/kg in 0.1 M sodium citrate buffer, pH 4.5) in obese rats. The rats in the obese and diabetic groups were treated with a daily dose of curcumin by intragastric intubation (100 mg/kg body weight) for 8 weeks. Testis tissue sections were stained with hematoxylin–eosin, and apoptosis was identified in situ by using terminal deoxynucleotidyl transferase dUTP nick end labeling.

          Results

          Curcumin treatment improved the histological appearance of the testis and significantly reduced the apoptosis level in the testicular cells of the obese and the diabetic rats. The expression of proliferating cell nuclear antigen (PCNA) was restored in the testis tissues of diabetic rats at the end of curcumin treatment. Molecular analysis demonstrated that curcumin treatment significantly and simultaneously decreased Bax and increased Bcl-2 expressions, therefore elevating the ratio of Bcl-2/Bax. Furthermore, curcumin treatment significantly decreased malondialdehyde (MDA) and increased superoxide dismutase (SOD) levels in testis tissue samples of the diabetic rats.

          Conclusion

          Curcumin treatment preserved the morphology of testes; restored the expression of PCNA, MDA, and SOD; and inhibited testicular cell death in diabetic rats. The capability of curcumin in inhibiting oxidative stress and modulating the Bax/Bcl-2-mediated cell death pathway reveals its potential as a therapeutic agent against diabetes.

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          Most cited references 18

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          A simple method for clinical assay of superoxide dismutase.

          This assay for superoxide dismutase (SOD, EC 1.15.1.1) activity involves inhibition of nitroblue tetrazolium reduction, with xanthine-xanthine oxidase used as a superoxide generator. By using a reaction terminator, we can determine 40 samples within 55 min. One unit of activity of pure bovine liver Cu,ZnSOD and chicken liver MnSOD was expressed by 30 ng and 500 ng of protein, respectively. The mean concentrations of Cu,ZnSOD as measured by this method in blood from normal adults were 242 (SEM 4) mg/L in erythrocytes, 548 (SEM 20) micrograms/L in serum, and 173 (SEM 11) micrograms/L in plasma. The Cu,ZnSOD concentrations in serum and plasma of patients with cancer of the large intestine tended to be less and greater than these values, respectively, but not statistically significantly so.
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            Malondialdehyde determination as index of lipid peroxidation.

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              Melatonin mitigates mitochondrial malfunction.

              Melatonin, or N-acetyl-5-methoxytryptamine, is a compound derived from tryptophan that is found in all organisms from unicells to vertebrates. This indoleamine may act as a protective agent in disease conditions such as Parkinson's, Alzheimer's, aging, sepsis and other disorders including ischemia/reperfusion. In addition, melatonin has been proposed as a drug for the treatment of cancer. These disorders have in common a dysfunction of the apoptotic program. Thus, while defects which reduce apoptotic processes can exaggerate cancer, neurodegenerative disorders and ischemic conditions are made worse by enhanced apoptosis. The mechanism by which melatonin controls cell death is not entirely known. Recently, mitochondria, which are implicated in the intrinsic pathway of apoptosis, have been identified as a target for melatonin actions. It is known that melatonin scavenges oxygen and nitrogen-based reactants generated in mitochondria. This limits the loss of the intramitochondrial glutathione and lowers mitochondrial protein damage, improving electron transport chain (ETC) activity and reducing mtDNA damage. Melatonin also increases the activity of the complex I and complex IV of the ETC, thereby improving mitochondrial respiration and increasing ATP synthesis under normal and stressful conditions. These effects reflect the ability of melatonin to reduce the harmful reduction in the mitochondrial membrane potential that may trigger mitochondrial transition pore (MTP) opening and the apoptotic cascade. In addition, a reported direct action of melatonin in the control of currents through the MTP opens a new perspective in the understanding of the regulation of apoptotic cell death by the indoleamine.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2017
                28 August 2017
                : 13
                : 1099-1105
                Affiliations
                [1 ]Department of Pathology, Zhejiang Provincial Hospital of TCM, Hangzhou
                [2 ]Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People’s Republic of China
                Author notes
                Correspondence: Guorong Chen, Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, 2 Fuxue Alley, Ouhai, Wenzhou 325000, People’s Republic of China, Email guorongchen123@ 123456163.com
                Article
                tcrm-13-1099
                10.2147/TCRM.S141738
                5584885
                © 2017 Zhao et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Medicine

                apoptosis, curcumin, diabetes, oxidative stress, testis

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