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目的研究表没食子儿茶素(epigallocatechin-3-gallate,EGCG)对化学缺氧损伤PC12细胞的保护作用。方法建立氯化钴(Co Cl2)诱导PC12细胞化学缺氧损伤模型,实验分为对照组、EGCG组、缺氧组和联合组,通过测定细胞活力、细胞凋亡率、超氧化物歧化酶(superoxide dismutase,SOD)活性、细胞上清液中乳酸脱氢酶(lacticdehydrogenase,LDH)含量及Bcl-2、Akt蛋白表达,探讨EGCG对受损细胞的保护作用。结果氯化钴作用后,缺氧组细胞存活率较对照组降低(P<0.05),联合组细胞存活率较缺氧组升高(P<0.05);缺氧组细胞凋亡增加至34.2%,EGCG干预后,细胞凋亡率降至23.5%;缺氧组细胞SOD活性较对照组降低(P<0.05),EGCG干预后可提高氯化钴诱导的细胞SOD活性降低,差异具有统计学意义(P<0.05)。缺氧组细胞上清液中的LDH活力增高,与对照组比较,差异有统计学意义(P<0.05);EGCG处理后能降低氯化钴引起的上清液中LDH活力增加(P<0.05)。缺氧组细胞Bcl-2表达降低(P<0.05),EGCG处理后能抑制氯化钴诱导的Bcl-2表达降低(与缺氧组比较P<0.05),并提高细胞p-Akt的表达(与缺氧组比较P<0.05),各组总的Akt表达量均无改变。结论本缺氧模型可诱导PC12细胞凋亡,EGCG对缺氧损伤PC12细胞具有明显的保护作用。
Objective To study the protective effect of epigallocatechin-3-gallate (EGCG) on PC12 cells damaged by chemical hypoxia. Methods The model of chemical hypoxic injury induced by cobalt chloride (Co Cl2) was established in rats. The experiment was divided into control group, EGCG group, hypoxia group and combination group. The cell viability, apoptosis rate and superoxide dismutase superoxide dismutase (SOD), the content of lactic dehydrogenase (LDH) and the expression of Bcl-2 and Akt in the cell supernatant, and to explore the protective effect of EGCG on the damaged cells. Results After treatment with cobalt chloride, the cell viability in hypoxia group was lower than that in control group (P <0.05). The survival rate of cells in combination group was higher than that in hypoxia group (P <0.05), and the apoptosis rate in hypoxia group increased to 34.2% (P <0.05). After EGCG intervention, the apoptosis rate of cells decreased to 23.5%. The activity of SOD in hypoxia group was lower than that of control group (P <0.05). The EGCG intervention could decrease the activity of SOD induced by cobalt chloride, the difference was statistically significant (P <0.05). The activity of LDH in supernatant of hypoxia group was higher than that in control group (P <0.05), and the activity of LDH in supernatant induced by cobalt chloride was decreased after EGCG treatment (P <0.05 ). The expression of Bcl-2 was decreased in hypoxia group (P <0.05). After treatment with EGCG, the decrease of Bcl-2 expression was inhibited by cobalt chloride (P <0.05 compared with hypoxia group) and the expression of p-Akt Compared with hypoxia group, P <0.05), the expression of Akt in each group had no change. Conclusion The hypoxia model can induce the apoptosis of PC12 cells. EGCG has a protective effect on hypoxic injury of PC12 cells.