Defence Institute of Physiology and Allied Sciences, DRDO, At/Po: Timarpur, Lucknow Road, Delhi-110054, India.
J Ethnopharmacol. 2013 Jan 30;145(2):431-41. doi: 10.1016/j.jep.2012.10.063. Epub 2012 Dec 2.
Withania somnifera (WS) root extract has been used traditionally in ayurvedic system of medicine as a memory enhancer and anti-stress agent.
To evaluate the neuroprotective and prophylactic potential of WS root extract in ameliorating hypobaric hypoxia (HH) induced memory impairment and to explore the underlying molecular mechanism.
WS root extract was administered to male Sprague Dawley rats during a period of 21 days pre-exposure and 07 days exposure to a simulated altitude of 25,000 ft. Spatial memory was assessed by Morris Water Maze. Neurodegeneration, corticosterone, acetylcholine (Ach) levels, acetylcholine esterase (AchE) activity, oxidative stress markers and nitric oxide (NO) concentration were assessed in the hippocampus. Synaptic and apoptotic markers were also investigated by immunoblotting. To study the role of NO in regulating corticosterone mediated signaling, the neuronal nitric oxide synthase (n-NOS) inhibitor, L-Nitro-arginine methyl ester (L-Name) and NO agonist sodium nitroprusside (SNP) were administered from 3rd to 7th day of hypoxic exposure.
Administration of WS root extract prevented HH induced memory impairment and neurodegeneration along with decreased NO, corticosterone, oxidative stress and AchE activity in hippocampal region. Inhibition of NO synthesis by administration of L-Name reduced corticosterone levels in hippocampus during hypoxic exposure while co-administration of corticosterone increased neurodegeneration. Administration of sodium nitroprusside (SNP) along with WS root extract supplementation during hypoxic exposure increased corticosterone levels and increased the number of pyknotic cells.
WS root extract ameliorated HH induced memory impairment and neurodegeneration in hippocampus through NO mediated modulation of corticosterone levels.
睡茄（WS）根提取物在印度阿育吠陀医学体系中传统上被用作增强记忆力和抗应激剂。
评估 WS 根提取物在改善低压缺氧（HH）引起的记忆障碍方面的神经保护和预防潜力，并探索其潜在的分子机制。
在暴露于模拟海拔 25000 英尺的环境前 21 天和暴露期间，给予雄性 Sprague Dawley 大鼠 WS 根提取物。通过 Morris 水迷宫评估空间记忆。评估海马中的神经退行性变、皮质酮、乙酰胆碱 (Ach) 水平、乙酰胆碱酯酶 (AchE) 活性、氧化应激标志物和一氧化氮 (NO) 浓度。还通过免疫印迹研究突触和凋亡标志物。为了研究 NO 在调节皮质酮介导的信号中的作用，给予神经元型一氧化氮合酶 (n-NOS) 抑制剂 L-硝基精氨酸甲酯 (L-Name) 和 NO 激动剂硝普钠 (SNP)，从缺氧暴露的第 3 天到第 7 天。
WS 根提取物的给药可预防 HH 引起的记忆障碍和神经退行性变，同时降低海马区的 NO、皮质酮、氧化应激和 AchE 活性。给予 L-Name 抑制 NO 合成可降低缺氧暴露期间海马中的皮质酮水平，而同时给予皮质酮可增加神经退行性变。在缺氧暴露期间给予硝普钠 (SNP) 并同时给予 WS 根提取物补充可增加皮质酮水平并增加固缩细胞的数量。
WS 根提取物通过 NO 介导的皮质酮水平调节改善了 HH 引起的海马记忆障碍和神经退行性变。
