Archana and Annapurna, IJPSR, 2016; Vol. 7(11): 4494-4500. E-ISSN: 0975-8232; P-ISSN: 2320-5148 International Journal of Pharmaceutical Sciences and Research 4494 IJPSR (2016), Vol. 7, Issue 11 (Research Article) Received on 27 May, 2016; received in revised form, 12 July, 2016; accepted, 27 July, 2016; published 01 November, 2016 NEUROPROTECTIVE AND ANTIOXIDANT ROLE OF PREGABALIN IN STREPTOZOTOCIN INDUCED NEUROTOXICITY Archana Jorige *1 and Akula Annapurna 2 RBVRR Women’s College of Pharmacy (Affiliated to Osmania University) 1 , Barktpura, Hyderabad- 500039, Telangana, India. University College of Pharmaceutical Sciences, Andhra University 2 , Visakhapatnam-530003, Andhrapradesh, India ABSTRACT: Streptozotocin (STZ) induced neurotoxicity causes development of diabetic neuropathy in rodent models and oxidative stress is the main culprit in development of diabetic neuropathy. In the present study we aimed to evaluate the neuroprotective and antioxidant role of Pregabalin in STZ induced neurotoxicity. After 8 weeks, STZ induced diabetic rats showed sciatic nerve damage which was evident from hyperalgesia, allodynia, motor deficits and Transmission Electron Microscopic studies of sciatic nerves. Pregabalin treatment at a daily dose of 15 mg/kg for 7 weeks ameliorated hyperalgesia, allodynia, motor deficits and prevented the structural abnormalities in sciatic nerves of diabetic rats. STZ neurotoxicity reduced antioxidant enzyme levels in sciatic nerves. Pregabalin treatment significantly ameliorated the decrease in antioxidant defence in diabetic rats. These results demonstrated neuroprotective effect of Pregabalin, which is mediated through attenuation of oxidative stress. The antioxidant mediated neuroprotective role along with its analgesic activity can prove it as a better option in prevention and treatment of Diabetic neuropathy. INTRODUCTION: Streptozotocin is a diabetogenic DNA alkylating or methylating agent which is normally used as an experimental model of type 1 diabetes in rodents. It contains a glucose molecule (in deoxy form) that is linked to a highly reactive methyl nitrosourea moiety that is thought to exert STZ’s cytotoxic effects, while the glucose moiety directs the chemical to the pancreatic β cells.STZ recognizes the GLUT2 receptor that is abundant on β cell plasma membranes. QUICK RESPONSE CODE DOI: 10.13040/IJPSR.0975-8232.7(11).4494-00 Article can be accessed online on: www.ijpsr.com DOI link: http://dx.doi.org/10.13040/IJPSR.0975-8232.7 (11).4494-00 Therefore, pancreatic β cell is a specific target of STZ 1 . Chronic hyperglycemia and the corresponding glucotoxicity are the main pathogenic mechanisms of diabetes and its complications. Glucose toxicity derives from the interplay of several metabolic reactions. Induction of oxidative stress is critical; both in terms of its effect on cellular function per se and in terms of the generation of more reactive molecules from glucose. These molecules then combine with cellular and extracellular macromolecules, altering their functional properties and causing downstream adverse effects on cell function. Subsequent changes in cellular phenotype give rise to diminished neurotrophic support, disturbed Keywords: Neurotoxicity, Sciatic nerves, Hyperalgesia, Allodynia, Oxidative stress, Diabetic Neuropathy Correspondence to Author: Dr. Archana Jorige Associate professor RBVRR Women’s College of Pharmacy, Barkatpura, Hyderabad - 50039, Telangana, India. Email: archana_jarc@yahoo.com