Abstract
Aim of the present study is to investigate the effect of silymarin (SM), a potent antioxidant and anti-inflammatory compound on experimentally-induced Diabetic Neuropathy (DN) in male Wistar rats. Diabetes was induced by single streptozotocin (STZ) injection in rats. Pain-related behavior tests were performed including tail flick, paw-pressure analgesia and Rota-rod performance. Silymarin treatment was started after 21st day of diabetes induction and continued for 6 consecutive weeks. In serum fasting glucose, insulin, tumor necrosis factor-&alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1&beta (IL-1&beta) levels were estimated and in sciatic nerve, thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), Superoxide Dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST), glutathione-reductase (GR) and glutathione peroxidase (GSH-Px) activities were measured. Diabetic rats developed neuropathy which was apparent from decreased tail-flick latency and paw-withdrawal latency.This was escorted by decreased motor coordination as assessed by performance on Rota-rod treadmill. Treatment with SM ameliorated the hyperalgesia, analgesia and improved motor coordination. STZ significantly increased TBARS and decreased GSH levels in sciatic nerve where silymarin treatment significantly protected those changes. Enzymatic activities such as SOD, CAT, GST, GSH-Px and GR were significantly inhibited in sciatic nerve of diabetic rats. The SM treatment significantly ameliorated decrease in antioxidant defense. Our results clearly demonstrate protective effect of SM is mediated through attenuation of oxidative stress and suggest therapeutic potential of SM in attenuation of diabetic neuropathy.
Highlights
Neuropathic pain is a form of chronic pain induced by damage or abnormal function of central or peripheral nervous system (Abdi et al, 2004; Woolf, 2004)
Diabetic neuropathy is associated with metabolic syndromes like diabetes mellitus
The pathophysiological mechanisms of Diabetic Neuropathy (DN) include a complex network of unified vascular (Cameron and Cotter, 1999); metabolic (Stevens et al, 2000) and neurotrophic (Calcutt, 2004) defects, which end with electrophysiological discrepancies, abnormal sensory perception and progressive damage and loss of unmyelinated and myelinated nerve fibers (Sima et al, 2000)
Summary
Neuropathic pain is a form of chronic pain induced by damage or abnormal function of central or peripheral nervous system (Abdi et al, 2004; Woolf, 2004). Experimental design: Normal healthy rats were divided in five groups (six rats in each group): lipid peroxidation (Velussi et al, 1997), inhibit lowdensity lipoprotein oxidation (Sobolová et al, 2006) and scavenge Reactive Oxygen Species (ROS) (Dehmlow et al, 1996) It can increase antioxidative enzyme levelsand limit lipid peroxidation (Soto et al, 2003) and enhance Superoxide Dismutase (SOD) activity (Baluchnejadmojarad et al, 2010). Mechanical hyperalgesia (Randall and Selitto we designed this study to investigate the potent effects method): Mean right and left paw pressure thresholds of silymarin supplementation on diabetic-induced were determined using the paw pressure analgesia changes inpro-inflammatory cytokines, and oxidative meter Pressure increased at a linear rate of 10 mm Hg with a cut-off at 500 mm Hg to avoid tissue
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
