Objective

Cerebrovascular disease is one of the major diseases that seriously harm human health currently. The purpose of this study is to find an effective treatment and clarify its mechanism of action to provide a new idea and drug target for the clinical treatment of ischemic cerebrovascular disease.

Methods

The microglia cell line (BV2 cell line) was cultured in vitro. Prepare a hypoxia ischemia cell model by OGD and simulate the pathophysiological process of ischemic cerebrovascular disease in vivo. According to the techniques of LDH Cytotoxicity Assay Kit, flow cytometry of Annexin V-FITC Apoptosis Detection Kit, Laser Confocal Fluorescence Immunostaining (Double staining method),

enzyme-linked immunosorbent assay (ELISA), and Western blotting, BV2 cells are observed through morphology and function changes induced by OGD. Moreover, these techniques were used to analyze changes in key proteins expression of signal transduction pathway in ischemic cerebrovascular disease, to explore the mechanism of gastrodin on ischemic cerebrovascular disease, and to elucidate the available ways for cell protection following ischemia and hypoxia.

Results

Gastrodin has no obvious toxic effect on BV-2 cells under physiological conditions. The death rate of BV-2 cells increases as the time of hypoxia increase. In the absence of oxygen, Gastrodin has a protective effect on the survival of BV-2 cells. This protective effect is related to the reduction of apoptosis rate. It can also improve the hypoxic tolerance of BV-2 cells, and there is no obvious Gastrodin dose-dependence. Moreover, Gastrodin has dual effects on BV-2 cells. The dual role of Gastrodin is closely related to the expression of several proteins which can affect the MAPK signal transduction pathway.

Conclusion

Gastrodin has a dual effect on microglia with OGD. On the one hand, Gastrodin can inhibit the inflammatory cytokines secreted by microglia and aggravate the inflammatory response; on the other hand, Gastrodin can promote the secretion of protective cytokines from microglia to reduce the inflammatory response.

中文翻译：

---

天麻素对氧葡萄糖剥夺下BV2细胞的作用及其机制

目的

脑血管疾病是当前严重危害人类健康的主要疾病之一。这项研究的目的是找到一种有效的治疗方法，并阐明其作用机理，为缺血性脑血管病的临床治疗提供新的思路和药物靶标。

方法

小胶质细胞系（BV2细胞系）在体外培养。通过OGD制备缺氧缺血细胞模型，并模拟体内缺血性脑血管疾病的病理生理过程。根据LDH细胞毒性测定试剂盒的技术，膜联蛋白V-FITC细胞凋亡检测试剂盒的流式细胞仪，激光共聚焦荧光免疫染色（双重染色法），

酶联免疫吸附测定（ELISA）和Western印迹法，通过OGD诱导的形态和功能变化观察BV2细胞。此外，这些技术还用于分析缺血性脑血管疾病中信号转导途径的关键蛋白表达的变化，探讨天麻素对缺血性脑血管疾病的作用机制，并阐明缺血和缺氧后细胞保护的可用方法。

结果

天麻素在生理条件下对BV-2细胞无明显毒性作用。BV-2细胞的死亡率随着缺氧时间的增加而增加。在没有氧气的情况下，天麻素对BV-2细胞的存活具有保护作用。这种保护作用与凋亡率的降低有关。它也可以提高BV-2细胞的低氧耐受性，并且没有明显的天麻素剂量依赖性。此外，天麻素对BV-2细胞具有双重作用。天麻素的双重作用与可能影响MAPK信号转导途径的几种蛋白质的表达密切相关。

结论

天麻素与OGD对小胶质细胞有双重作用。一方面，天麻素能抑制小胶质细胞分泌的炎性细胞因子，加剧炎症反应。另一方面，天麻素可促进小胶质细胞分泌保护性细胞因子，从而减轻炎症反应。