Kumar Anil, Rinwa Puneet, Dhar Hitesh
Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, 160014, India,
Inflammopharmacology. 2014 Jun;22(3):155-67. doi: 10.1007/s10787-013-0187-3. Epub 2013 Sep 20.
Traumatic brain injury produces several neuropathological alterations, some of them are analogous to patients suffering from memory disorders. Role of neuroinflammation and oxidative stress has been suggested in the pathophysiology of brain injury-induced cognitive dysfunction. Therefore, the present study was designed to explore the possible role of ginseng and its interaction with minocycline (microglial inhibitor) against experimental brain trauma-induced behavioral, biochemical and molecular alterations. Wistar rats were exposed to brain traumatic injury using weight-drop method. Following injury and a post-injury rehabilitation period of 2 weeks, animals were administered vehicle/drugs for another 2 weeks. Brain injury caused significant memory impairment in Morris water maze task as evident from increase in escape latency and total distance travelled to reach the hidden platform. This was followed by a significant decrease in time spent in target quadrant and frequency of appearance in target quadrant. Further, there was a significant increase in oxidative stress markers, neuroinflammation (TNF-α and IL-6) and acetylcholinesterase levels in both cortex and hippocampal regions of traumatized rat brain. Ginseng (100 and 200 mg/kg) and minocycline (50 mg/kg) treatment for 2 weeks significantly attenuated all these behavioral, biochemical and molecular alterations. Further, combination of sub-effective doses of ginseng (50 and 100 mg/kg) and minocycline (25 mg/kg) potentiated their protective effects which was significant as compared to their effects alone. The results of the present study suggest that the therapeutic effects of ginseng might involve inhibition of microglial pathway against head trauma-induced cognitive impairment and neuroinflammation in rats.
创伤性脑损伤会产生多种神经病理学改变，其中一些与患有记忆障碍的患者相似。神经炎症和氧化应激在脑损伤诱导的认知功能障碍的病理生理学中发挥了作用。因此，本研究旨在探讨人参及其与米诺环素（小胶质细胞抑制剂）的相互作用对实验性脑创伤诱导的行为、生化和分子改变的可能作用。采用重物落体法使Wistar大鼠遭受脑创伤。损伤后及2周的损伤后康复期后，动物再接受2周的赋形剂/药物处理。脑损伤在莫里斯水迷宫任务中导致显著的记忆障碍，逃避潜伏期延长和到达隐藏平台所行进的总距离增加即可证明。随后，在目标象限停留的时间和在目标象限出现的频率显著降低。此外，创伤大鼠脑的皮质和海马区域中氧化应激标志物、神经炎症（TNF-α和IL-6）以及乙酰胆碱酯酶水平均显著升高。人参（100和200 mg/kg）和米诺环素（50 mg/kg）处理2周显著减轻了所有这些行为、生化和分子改变。此外，人参（50和100 mg/kg）和米诺环素（25 mg/kg）的亚有效剂量联合使用增强了它们的保护作用，与单独使用时的效果相比具有显著性。本研究结果表明，人参的治疗作用可能涉及抑制小胶质细胞途径，以对抗大鼠头部创伤诱导的认知障碍和神经炎症。
