Liu Ping, Wang Li-Ye, Wang Yu-Qing, Wang Rong-Liang, Li Fang-Fang, Zhang Sijia, Tao Zhen, Zhao Hai-Ping, Han Zi-Ping, Chen Zhi-Gang, Luo Yu-Min
Institute of Cerebrovascular Diseases Research and Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, 10053, P. R. China.
Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, 10078, P. R. China.
J Integr Neurosci. 2020 Mar 30;19(1):21-29. doi: 10.31083/j.jin.2020.01.1213.
The neuroprotective role of in a model of chronic cerebral hypoperfusion with cognitive decline was focused on neural plasticity and microglia/macrophage polarization. Chronic cerebral hypoperfusion was induced by bilateral common carotid artery ligation. shortened escape latency and added the number of platform crossings of rats, up-regulated the expression of synaptophysin in the gray matter and increased myelin basic protein expression in the white matter. Further mechanistic experiments were conducted to examine microglia activation and M1/M2 polarization. It was shown that reduced the activation of microglia revealed by decreased expression of ionized calcium-binding adapter molecule-1, inhibited M1 polarization of microglia and improved microglial M2 polarization shown by down-regulated the expression of inducible nitric oxide synthase and Fc fragment of IgG receptor IIIa and up-regulated the expression of arginase-1. In conclusion, the Chinese herb can improve cognitive function following chronic cerebral hypoperfusion by down-regulating the activation of microglia, inhibiting microglial M1 polarization, and improving neural plasticity.
[文中未提及具体物质名称，暂用“该物质”指代]在伴有认知功能下降的慢性脑灌注不足模型中的神经保护作用集中在神经可塑性和小胶质细胞/巨噬细胞极化方面。双侧颈总动脉结扎诱导慢性脑灌注不足。该物质缩短了大鼠的逃避潜伏期并增加了平台穿越次数，上调了灰质中突触素的表达，并增加了白质中髓鞘碱性蛋白的表达。进行了进一步的机制实验以检测小胶质细胞的激活和M1/M2极化。结果表明，该物质通过降低离子钙结合衔接分子-1的表达所显示的小胶质细胞激活，抑制小胶质细胞的M1极化，并通过下调诱导型一氧化氮合酶和IgG受体IIIa的Fc片段的表达以及上调精氨酸酶-1的表达来改善小胶质细胞的M2极化。总之，该中药可以通过下调小胶质细胞的激活、抑制小胶质细胞的M1极化和改善神经可塑性来改善慢性脑灌注不足后的认知功能。
