Hariprasad MG, Rema Razdan, Yasha TC and Tripathy Amrutanand S
Objectives: The treatment options for diabetic peripheral neuropathy (DPN) currently include anti-depressants, anti-convulsants and opioid analgesics. These agents are modestly effective for symptomatic relief, but they do not affect the underlying pathology nor do they slow progression of the disease. Therefore, effective treatment for diabetes induced neuropathy would be a major advantage for patients. It is well established. TH plays an important role in regulating the development and regeneration of the nervous system and local administration of triiodothyronine (T3) at the level of transected rat sciatic nerve increased the number and diameter of regenerated axons and SCG10 protein levels about two-fold in the different segments of transected nerve during the regeneration period. Thyroxine(T4) has shown the range of biological actions and is important in both development and maturation. The etiology of diabetic neuropathy revolves around, AGE formation, lipid peroxidation, oxidative stress etc. All these have been reported to stimulate inflammatory processes, which lead to DPN. Progression in DPN can cause functional and behavioral deficits. Therefore, the present study was undertaken to evaluate the protective effect of thyroxine in diabetes induced peripheral neuropathy in rats. Methods: Experimental diabetes in rats was induced by single intraperitoneal (i.p.) injection of Streptozotocin(SIGMA-ALDRICH, USA) at a dose of 55 mg/kg i.p. freshly dissolved in 100 mM sodium citrate buffer, pH 4.5. The degree of protection was determined by measuring behavioural parameters like motor in-coordination, thermal and cold hyperalgesia, grip strength, electrophysiological properties of sciatic nerve like nerve conduction velocity, and histopathological studies. Results: DPN was evidenced in diabetic control rats and ameliorated with administration of Thyroxine (T4) (1mg/kg, s.c.) thrice a week for 5 weeks by augmenting all the above parameters. Conclusions: T4 exhibited neuroprotective activity, which would be attributed to its activity as neurotrophic effect.