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目的探讨雌马酚对PC12细胞缺氧/复氧损伤的保护作用及机制。方法以PC12细胞为研究对象,构建体外神经元缺氧/复氧损伤模型,用雌马酚进行干预。MTT法检测细胞活力,比色法测定细胞培养上清液中乳酸脱氢酶(LDH)活性和丙二醛(MDA)含量,免疫细胞化学法检测活性氧(ROS)含量,Western blotting检测缺氧/复氧损伤的PC12细胞内NADPH氧化酶2(gp91phox)和磷酸化Src(p-Src)激酶的表达。结果雌马酚可有效减轻缺氧/复氧引起的PC12细胞损伤,降低缺氧/复氧损伤细胞培养上清液中LDH的活性和MDA的含量,明显抑制ROS的生成及gp91~(phox)和p-Src的表达。结论雌马酚通过抑制p-Src激酶和gp91~(phox)表达,减少ROS生成,从而对PC12细胞缺氧/复氧损伤产生保护作用。
Objective To investigate the protective effect and mechanism of equol on hypoxia / reoxygenation injury in PC12 cells. Methods PC12 cells were used as the research object to establish an in vitro model of neuronal hypoxia / reoxygenation injury with equol. Cell viability was measured by MTT assay. Lactate dehydrogenase (LDH) activity and malondialdehyde (MDA) content in cell culture supernatants were determined by colorimetric assay. Reactive oxygen species (ROS) were detected by immunocytochemistry. / Reoxygenation injury in PC12 cells NADPH oxidase 2 (gp91phox) and phosphorylated Src (p-Src) kinase expression. Results Equol can effectively reduce the hypoxia / reoxygenation-induced injury of PC12 cells and decrease the activity of LDH and the content of MDA in the cell culture supernatant of hypoxia / reoxygenation injury, and significantly inhibit the production of ROS and the expression of gp91 ~ (phox) And p-Src expression. Conclusion Equol has a protective effect on hypoxia / reoxygenation injury in PC12 cells by inhibiting the expression of p-Src kinase and gp91 ~ (phox) and decreasing the production of ROS.