Thiagarajan Venkata Rathina Kumar, Shanmugam Palanichamy, Krishnan Uma Maheswari, Muthuraman Arunachalam, Singh Nirmal
School of Chemical and Biotechnology, Sastra University, Thanjavur, Tamilnadu, India.
Toxicol Ind Health. 2013 Feb;29(1):3-13. doi: 10.1177/0748233711432573. Epub 2012 Jan 27.
Neuropathic pain is a chronic neurodegenerative disease. It is well characterized by spontaneous pain, hyperalgesia, hypothesia, dysesthesia and allodynia. The present study was designed to investigate the antinociceptive potential of Butea monosperma on vincristine-induced painful neuropathy in rats. Vincristine was administered for induction of neuropathic pain in experimental animals. Hot plate, acetone drop, paw pressure, Von Frey hair and tail immersion tests were performed to assess the degree of thermal hyperalgesia, cold chemical allodynia, mechanical hyperalgesia and allodynia in the hind paw and tail thermal hyperalgesia, respectively, as an index of peripheral and central pain sensation. Tissue thiobarbituric acid reactive substances (TBARSs), reduced glutathione (GSH) and total calcium levels were estimated to assess the biochemical changes in the sciatic nerve tissue. Microscopically, histopathological changes were also observed in the sciatic nerve tissue. Ethanolic extract of B. monosperma leaves and pregabalin were administered for 14 consecutive days. Vincristine administration resulted in significant reduction in behavioural (i.e. hyperalgesia and allodynic pain sensation) changes along with a rise in the levels of TBARS, total calcium and decrease in GSH levels when compared with the normal control group. Moreover, significant histological changes were also observed. Pretreatment with B. monosperma significantly attenuated vincristine-induced development of painful behavioural, biochemical and histological changes in a dose-dependent manner, which is similar to that of pregabalin-pretreated group. B. monosperma ameliorated vincristine-induced painful neuropathy. It may be due to its potential of antioxidative, neuroprotective and calcium channel inactivation.
神经性疼痛是一种慢性神经退行性疾病。其特征表现为自发痛、痛觉过敏、感觉减退、感觉异常和痛觉超敏。本研究旨在探讨单籽紫铆对长春新碱诱导的大鼠疼痛性神经病变的抗伤害感受潜力。给实验动物注射长春新碱以诱导神经性疼痛。分别进行热板试验、丙酮滴注试验、 paw压力试验、von Frey毛发试验和尾浸试验，以评估后爪的热痛觉过敏程度、冷化学性痛觉超敏、机械性痛觉过敏和痛觉超敏以及尾部热痛觉过敏程度，作为外周和中枢疼痛感觉的指标。测定组织硫代巴比妥酸反应物质（TBARS）、还原型谷胱甘肽（GSH）和总钙水平，以评估坐骨神经组织的生化变化。在显微镜下，也观察到了坐骨神经组织的组织病理学变化。连续14天给予单籽紫铆叶乙醇提取物和普瑞巴林。与正常对照组相比，注射长春新碱导致行为学变化（即痛觉过敏和痛觉超敏性疼痛感觉）显著降低，同时TBARS水平、总钙水平升高，GSH水平降低。此外，还观察到了显著的组织学变化。单籽紫铆预处理以剂量依赖的方式显著减轻长春新碱诱导的疼痛行为、生化和组织学变化的发展，这与普瑞巴林预处理组相似。单籽紫铆改善了长春新碱诱导的疼痛性神经病变。这可能归因于其抗氧化、神经保护和钙通道失活的潜力。
