Jain Vivek, Pareek Ashutosh, Bhardwaj Yashumati Ratan, Singh Nirmal
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala-147002, Punjab, India.
BMC Complement Altern Med. 2013 Oct 21;13:274. doi: 10.1186/1472-6882-13-274.
Injury to a nerve is the most common reason of acquired peripheral neuropathy. Therefore, searching for effective substance to recover of nerve after injury is need of present era. The current study investigates the protective potential of Standardized Fruit Extract of Punica granatum L (PFE) [Ellagic acid (41.6%), Punicalagins (10%), Granatin (5.1%)] in Tibial & Sural Nerve Transection (TST) induced neuropathic pain in rats.
TST was performed by sectioning tibial and sural nerve portions of the sciatic nerve and leaving the common peroneal nerve intact. Acetone drop, pin-prick, hot plate, paint brush & Walking Track tests were performed to assess cold allodynia; mechanical heat, hyperalgesia and dynamic mechanical allodynia & tibial functional index respectively. The levels of TNF-α, TBARS, GSH and Nitrite were measured in the sciatic nerve as an index of inflammation & oxidative stress.
TST led to significant development of cold allodynia; mechanical and heat hyperalgesia; dynamic mechanical allodynia; functional deficit in walking along with rise in the levels of TBARS, TNF-α, GSH and Nitrite. Administrations of PFE (100 & 300 mg/kg oral), significantly attenuate TST induced behavioral & biochemical changes. Pretreatments of BADGE (120 mg/kg IP) a PPAR-γ antagonist and nitric oxide precursor L-arginine (100 mg/kg IP) abolished the protective effect of PFE. Whereas, pretreatment of L-NAME (5 mg/kg IP) a NOS inhibitor significantly potentiated PFE's protective effect of PFE.
PFE shown to have attenuating effect in TST induced neuropathic pain which may be attributed to potential PPAR-gamma agonistic activity, nitric oxide inhibitory, anti-inflammatory and anti oxidative actions.
神经损伤是后天性周围神经病变最常见的原因。因此，寻找损伤后促进神经恢复的有效物质是当今时代的需求。本研究调查了标准化石榴果实提取物（PFE）[鞣花酸（41.6%）、石榴皮鞣素（10%）、石榴素（5.1%）]对大鼠胫神经和腓肠神经横断（TST）诱导的神经性疼痛的保护潜力。
通过切断坐骨神经的胫神经和腓肠神经部分，同时保留腓总神经完整来进行TST。分别进行丙酮滴注、针刺、热板、毛刷和行走轨迹测试，以评估冷觉异常性疼痛、机械性热痛觉过敏、动态机械性异常性疼痛和胫神经功能指数。测量坐骨神经中TNF-α、TBARS、GSH和亚硝酸盐的水平，作为炎症和氧化应激的指标。
TST导致冷觉异常性疼痛、机械性和热痛觉过敏、动态机械性异常性疼痛显著发展，行走功能障碍，同时TBARS、TNF-α、GSH和亚硝酸盐水平升高。给予PFE（100和300mg/kg口服）可显著减轻TST诱导的行为和生化变化。PPAR-γ拮抗剂BADGE（120mg/kg腹腔注射）和一氧化氮前体L-精氨酸（100mg/kg腹腔注射）预处理可消除PFE的保护作用。而NOS抑制剂L-NAME（5mg/kg腹腔注射）预处理可显著增强PFE的保护作用。
PFE对TST诱导的神经性疼痛具有减轻作用，这可能归因于潜在的PPAR-γ激动活性、一氧化氮抑制、抗炎和抗氧化作用。
