[提取物名称]提取物通过改变PI3K/Akt信号通路对异氟烷诱导的神经元损伤的保护作用 。 需注意，原文中“Extract of ”处提取物名称缺失。
Protective Effect of Extract of on Isoflurane Induced Neuronal Injury By Altering PI3K/Akt Pathway.
作者信息
Zhao Guoqing, Li Kai, Chen Junyang, Li Longyun
机构信息
Department of anesthesiology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China, 130033.
出版信息
Transl Neurosci. 2018 Dec 31;9:183-189. doi: 10.1515/tnsci-2018-0027. eCollection 2018.
BACKGROUND
Present investigation evaluates the neuroprotective effect of on isoflurane induced neuronal injury rat model.
METHODOLOGY
Neuronal injury was induced by exposing the pups (P7) isoflurane (0.75%) in oxygen (30%) for the period of 6 hr and rats were treated with at a dose of . At the end of protocol neurological score was estimated and serum concentration of inflammatory cytokines was estimated. Isolated brains tissue was prepared to perform immunohistochemical analysis, TUNEL assay and western blot assay.
RESULTS
Result of the study reveals that treatment with BS significantly (p<0.01) reduces the neurological score compared to negative control group. Level of inflammatory cytokines in the serum and the expression of p-Akt, Bcl-xL and Bad protein were significantly attenuated in BS treated group. Moreover the cleaved caspase-3 and TUNEL positive cell was significantly (p<0.01) reduced in BS treated group compared to negative control group of rats.
CONCLUSION
Present study concludes that ethanolic extract of protects the neuronal injury by reducing apoptosis in isoflurane induced neuronal injury rats.
背景
本研究评估了[具体物质]对异氟烷诱导的神经元损伤大鼠模型的神经保护作用。
方法
通过将幼崽（P7）暴露于含30%氧气的0.75%异氟烷中6小时来诱导神经元损伤，并用[具体剂量]的[具体物质]对大鼠进行治疗。在实验方案结束时，评估神经学评分并测定血清中炎性细胞因子的浓度。制备分离的脑组织以进行免疫组织化学分析、TUNEL检测和蛋白质印迹分析。
结果
研究结果表明，与阴性对照组相比，用[具体物质]治疗显著（p<0.01）降低了神经学评分。在[具体物质]治疗组中，血清中炎性细胞因子水平以及p-Akt、Bcl-xL和Bad蛋白的表达均显著降低。此外，与大鼠阴性对照组相比，[具体物质]治疗组中裂解的caspase-3和TUNEL阳性细胞显著（p<0.01）减少。
结论
本研究得出结论，[具体物质]的乙醇提取物通过减少异氟烷诱导的神经元损伤大鼠的细胞凋亡来保护神经元损伤。
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