Antioxidant Activity of Lipoic Acid on Cyclosporine A-Induced Physiological Changes to the Kidneys in Male Albino Rats
- Authors
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Nura I. Al-Zail
Zoology Department, Faculty of Science, Omar Al-Mukhtar University, LibyaAuthor
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- Keywords:
- Lipoic acid, cyclosporine A, oxidative stress, renal toxicity
- Abstract
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Cyclosporine A (CsA) is the most widely used immunosuppressive drug for preventing graft rejection and autoimmune disease. However, the therapeutic treatment induces several side effects such as nephrotoxicity, cardiotoxicity and hepatotoxicity. This study aimed to assess the protective role of lipoic acid (LA) on kidney toxicity of male albino rats induced by cyclosporine (CsA). Forty adult male rats were allocated into four groups: Group (I) served as a control group. Group (II); received treatments orally with CsA (25 mg/kg b.w.), daily for 3 weeks. Group III: (Recovery CsA group): treated orally with CsA (25 mg/kg b.w.), daily for 3 weeks, then recovered for another 3 weeks. Group IV (LA and CsA group): received LA (100 mg/kg b. w.) orally 1 h before treatment by CsA (25 mg/kg b. w.) daily for 3 weeks. The results indicated that treatment of CsA caused a significant elevation in the concentrations of serum urea, creatinine, and uric acid which indicate injury to the kidney function. Renal malondialdehyde (MDA) concentration was markedly increased reflecting increased lipid peroxidation, whereas, reduced glutathione (GSH) and superoxide dismutase (SOD) were significantly decreased. On the other hand, LA plus CsA dose-dependently inhibited activities of serum urea, creatinine, and uric acid. The administration of LA plus CsA exhibited significant reduction in lipid peroxidation while GSH content and SOD activity were enhanced significantly which reflect an improvement in renal toxicity. In conclusion, the results indicated a negative role of CsA on kidney function and oxidative stress in induction toxicity, suggested Thus, Lipoic acid play a positive role on toxicity of kidney induced by cyclosporine A.
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- 2017-06-30
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- Vol. 32 No. 1 (2017)
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