This paper was aimed to investigate the effect of gastrodin( GAS) on hippocampal neurogenesis after cerebral was chemic and to explore its mechanism of action related to NO. The cerebral ischemia model of C57 BL/6 mice was established by bilateral common carotid artery occlusion. The pathological changes in hippocampal CA1 region and the cognitive function of mice were assessed by HE staining and Morris water maze test,respectively. The count of Brd U/Neu N positive cells in dentate gyrus was detected by immunofluorescence assay. The NOS activity and the NO content were determined by colorimetric and nitrate reduction methods,respectively.The level of c GMP was measured by ELISA kit,and the PKG protein expression was tested by Western blot. On postoperative day 8,the hippocampal CA1 pyramidal neurons of mice showed irregular structure,with obvious nuclear pyknosis,loose cell arrangement and obvious decrease in the number of neurons. On postoperative day 29,the spatial learning ability and memory were decreased. These results indicated cerebral ischemia in mice. Meanwhile,the Brd U/Neu N positive cells were increased significantly in ischemic mice,indicating that neurogenesis occurred in hippocampus after cerebral ischemia. Treatment with different doses of gastrodin( 50 and 100 mg·kg-1) significantly ameliorated the pathological damages in the CA1 region,improved the ability of learning and memory,and promoted hippocampal neurogenesis. At the same time,both the NOS activity and the NO concentration were decreased in model group,but the c GMP level was increased,and the PKG protein expression was up-regulated. Gastrodin administration activated the NOS activity,promoted NO production,further increased c GMP level and up-regulated PKG protein expression. These results suggested that gastrodin can promote hippocampal neurogenesis after cerebral ischemia and improve cognitive function in mice,which may be related to the activation of NO-cGMP-PKG signaling pathway.

中文翻译：

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天麻素通过NO-cGMP-PKG信号通路改善脑缺血小鼠海马神经发生的作用。

本文旨在探讨天麻素（GAS）对脑缺血后海马神经发生的影响，并探讨其与NO相关的作用机理。通过双侧颈总动脉闭塞建立C57 BL / 6小鼠的脑缺血模型。HE染色和Morris水迷宫试验分别评估海马CA1区的病理变化和小鼠的认知功能。通过免疫荧光法检测齿状回中Brd U / Neu N阳性细胞的数量。用比色法和硝酸盐还原法分别测定NOS活性和NO含量。ELISA试剂盒测定c GMP水平，Western blot检测PKG蛋白表达。术后第8天，小鼠海马CA1锥体神经元结构不规则，核固缩明显，细胞排列疏松，神经元数目明显减少。术后第29天，空间学习能力和记忆力下降。这些结果表明小鼠脑缺血。同时，缺血小鼠的Brd U / Neu N阳性细胞显着增加，表明脑缺血后海马发生神经发生。不同剂量天麻素（50和100 mg·kg-1）治疗可明显减轻CA1区域的病理损伤，提高学习记忆能力，促进海马神经发生。同时，模型组NOS活性和NO浓度均降低，但c GMP水平升高，PKG蛋白表达上调。天麻素管理激活了NOS活性，促进NO生成，进一步提高c GMP水平和上调PKG蛋白表达。这些结果提示天麻素可以促进脑缺血后海马神经发生，改善小鼠的认知功能，这可能与NO-cGMP-PKG信号通路的激活有关。