| RESEARCH ARTICLE |
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| Year : 2014 | Volume
: 46
| Issue : 2 | Page : 161-165 |
Mechanism of testicular protection of carvedilol in streptozotocin-induced diabetic rats
Maggie M Ramzy1, Azza A. K El-Sheikh2, Maha Y Kamel2, Soha A Abdelwahab3, Mohamed A Morsy2
1 Department Biochemistry, Faculty of Medicine, Minia University, Minia, Egypt
2 Department Pharmacology, Faculty of Medicine, Minia University, Minia, Egypt
3 Department Histology, Faculty of Medicine, Minia University, Minia, Egypt
Correspondence Address:
Mohamed A Morsy
Department Pharmacology, Faculty of Medicine, Minia University, Minia
Egypt
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.129307
Aims: Male sub-fertility and infertility are major complications of diabetes mellitus. The non-selective β-blocker carvedilol has been reported to have favorable effects on some of the diabetic complications based on its antioxidant and anti-apoptotic effects. This study aims to evaluate the possible testicular protective effect of carvedilol in streptozotocin (STZ)-induced diabetic rat model and its possible mechanisms.
Materials and Methods: Diabetes was induced by a single i.p. dose of 65 mg/kg of STZ. In parallel groups of diabetic rats, carvedilol in low and high doses (1 and 10 mg/kg/day orally) were administered for 4 weeks. Oxidative stress markers as reduced glutathione (GSH) and the product of lipid peroxidation; malondialdehyde (MDA) were evaluated in testicular homogenate. The level of expression of the apoptotic marker; caspase 3, was assessed using western blot, followed by densitometric analysis.
Results: Induction of diabetes caused distortion of histological normal testicular structure, with decrease (P < 0.05) in GSH and increase (P < 0.05) in MDA, as well as induction of caspase 3 expression. Carvedilol in low or high doses reverted diabetes-induced histological damage, restored antioxidant activity and ameliorated caspase 3 expression.
Conclusion: Carvedilol confers testicular protection against diabetes-induced damage through antioxidant and anti-apoptotic mechanisms.
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