Attenuation of experimentally induced diabetic neuropathy in association with reduced oxidative-nitrosative stress by chronic administration of.docVIP

Advances in Bioscience and Biotechnology, 2013, 4, 356-363 ABB /10.4236/abb.2013.43047 Published Online March 2013 (/journal/abb/) Attenuation of experimentally induced diabetic neuropathy in association with reduced oxidative-nitrosative stress by chronic administration of Momordica charantia Zafar Ahmad Malik , Nahida Tabassum , Pyare Lal Sharma 1* 2 1 1 2 Department of Pharmacology, ISF College of Pharmacy, Moga, India Department of Pharmaceutical Sciences, Univeristy of Kashmir, Srinagar, India zafar18@, n.tabassum.uk@, plsharma.isf@ Email: * Received 6 January 2013; revised 16 February 2013; accepted 28 February 2013 ABSTRACT lem affecting more than half of all diabetic patients and is a leading cause of nontraumatic amputations and auto- nomic failure [1,2]. Diabetes induced neuropathic pain is much more difficult to treat than nociceptive pain [3]. Various classes of drugs such as nonsteroidal anti-in- flammatory drugs, antidepressants and anticonvulsants have partial utility because of their limited effectiveness and severe potential toxicity [4]. Opoids are effective antinociceptive drugs; however, their antinonciceptive activity decreases in diabetes associated neuropathic pain [5]. The development of safe and effective drugs for pre- vention and treatment of diabetes-associated neuropathy is, therefore, highly warranted. The pathogenesis of diabetic neuropathy still remains unclear although a number of mechanisms have been implicated which include increased aldose reductase (AR) activity, nonenzymatic glycation, activation of protein kinase C, and impaired neurotrophic support. These mechanisms contribute to increased production of reac- tive oxygen species (ROS) and nitrogen species (RNS), insufficient up-regulation or down-regulation of antioxi- dative defense system [6-8].