Aim: Neuropathy is one of the potentially serious late complications of diabetes that occurs in certain tissues as a consequence of long-term hyperglycemia. Oxidative stress has been implicated to play an important role in the pathogenesis of diabetic neuropathy. In the present study, we have investigated the effect of silymarin, as a potent free radical scavenger in streptozotocin (STZ)-induced diabetic neuropathy in rats.
Material and methods: The rats were randomly divided into six experimental groups; i.e. control, vehicle-treated control, silymarin-treated control, diabetic, vehicle-treated diabetic and silymarin-treated diabetic. Diabetes was induced by a single intraperitoneal injection of streptozotocin (60 mg/kg) dissolved in cold 0.9% saline immediately before use.
Results: After 8 weeks of diabetes induction by STZ, rats showed significant deficit in motor nerve conduction velocity (MNCV) and mechanical, chemical and thermal hyperalgesia, indicating development of diabetic neuropathy. Antioxidant enzyme superoxide dismutase level was reduced and malondialdehyde (MDA) level was significantly increased in diabetic rats as compared to control rats. This indicated the involvement of oxidative stress in diabetic neuropathy. The pre-treatment of diabetic rats, 1 h before diabetic induction (200 mg/kg, i.p.) for 8 weeks post-treatment (100 mg/kg, i.p., daily) with silymarin significantly ameliorated the alteration in MNCV, hyperalgesia, MDA levels and antioxidant enzyme in diabetic rats.
Conclusion: Results of the present study suggest the potential of silymarin in treatment of diabetic neuropathy.
25 - 29 Apr 2009
European Society of Endocrinology