With multiple targets and low cytotoxicity, natural medicines can be used as potential neuroprotective agents. The increase in oxidative stress levels and inflammatory responses in the brain caused by radiation affects cognitive function and neuronal structure, and ultimately leads to abnormal changes in neurogenesis, differentiation, and apoptosis. Astragaloside Ⅳ (AS-Ⅳ), one of the main active constituents of astragalus, is known for its antioxidant, antihypertensive, antidiabetic, anti-infarction, anti-inflammatory, anti-apoptotic and wound healing, angiogenesis, and other protective effects. In this study, the mechanism of AS-IV against radiation-induced apoptosis of brain cells in vitro and in vivo was explored by radiation modeling, which provided a theoretical basis for the development of anti-radiation Chinese herbal active molecules and brain health products. In order to study the protective mechanism of AS-IV on radiation-induced brain cell apoptosis in mice, the paper constructed a radiation-induced brain cell apoptosis model, using TUNEL staining, flow cytometry, Western blotting to analyze AS-IV resistance mechanism to radiation-induced brain cell apoptosis. The results of TUNEL staining and flow cytometry showed that the apoptosis rate of radiation group was significantly increased. The results of Western blotting indicated that the expression levels of p-JNK, p-p38, p53, Caspase-9 and Caspase-3 protein, and the ratio of Bax to Bcl-2 in radiation group were significantly increased. There was no significant difference in the expression levels of JNK and p38. After AS-IV treatment, the apoptosis was reduced and the expression of apoptosis related proteins was changed. These data suggested that AS-IV can effectively reduce radiation-induced apoptosis of brain cells, and its mechanism may be related to the phosphorylation regulation of JNK-p38.

具有多个靶点和低细胞毒性，天然药物可用作潜在的神经保护剂。辐射引起的脑部氧化应激水平和炎症反应的增加会影响认知功能和神经元结构，并最终导致神经发生，分化和凋亡的异常变化。黄芪甲苷Ⅳ（AS-Ⅳ）是黄芪的主要活性成分之一，以其抗氧化剂，抗高血压药，抗糖尿病药，抗梗塞药，抗炎药，抗凋亡和伤口愈合，血管生成和其他保护作用而著称。在这项研究中，通过辐射建模探索了AS-IV在体外和体内对抗辐射诱导的脑细胞凋亡的机制，这为抗辐射中草药活性分子和脑保健产品的开发提供了理论依据。为了研究AS-IV对辐射诱导的小鼠脑细胞凋亡的保护机制，本文采用TUNEL染色，流式细胞仪，Western blotting等方法建立了AS-IV对小鼠辐射诱导的脑细胞凋亡的保护机制。辐射诱导的脑细胞凋亡。TUNEL染色和流式细胞仪检测结果表明，放射组细胞凋亡率明显增加。Western blotting结果显示，放射组p-JNK，p-p38，p53，Caspase-9和Caspase-3蛋白的表达水平明显升高，Bax与Bcl-2的比例明显升高。JNK和p38的表达水平没有显着差异。AS-IV处理后，凋亡减少，凋亡相关蛋白的表达发生变化。这些数据表明，AS-IV可以有效减少辐射诱导的脑细胞凋亡，其机制可能与JNK-p38的磷酸化调控有关。