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目的探讨PM_(2.5)对人脐静脉内皮细胞(EA.hy926)的影响及黄芩苷的保护作用及机制。方法于2015年3月采集广州城区雾霾天气时的大气PM_(2.5),以不同质量浓度(0、50、200、400μg/ml)染毒EA.hy926细胞24 h,检测细胞存活率、凋亡率、丙二醛(MDA)含量、超氧化物歧化酶(SOD)及乳酸脱氢酶(LDH)活力、细胞内p-p38 MAPK、Bax、Bcl-2蛋白表达。另外分别以黄芩苷(15、30、60μg/ml)和p38 MAPK通路特异性阻滞剂SB203580 20μmol/L预处理细胞,再加入200μg/ml PM_(2.5)染毒24 h,检测上述指标,探讨黄芩苷的干预作用及机制。结果与对照组比较,PM_(2.5)染毒后可降低EA.hy926细胞存活率和SOD活力,增加MDA含量及LDH活力,上调p-p38 MAPK蛋白表达及Bax/Bcl-2蛋白,差异均有统计学意义(P<0.05);黄芩苷干预可增加EA.hy926细胞存活率和SOD活力,降低MDA含量及LDH活力,下调p-p38 MAPK蛋白表达及Bax/Bcl-2蛋白,差异均有统计学意义(P<0.05)。结论黄芩苷可通过抑制p38 MAPK通路,减轻PM_(2.5)对EA.hy926细胞的损伤。
Objective To investigate the effect of PM 2.5 on human umbilical vein endothelial cells (EA.hy926) and the protective effect of baicalin and its mechanism. Methods The atmospheric PM_ (2.5) was collected during the haze days in Guangzhou city in March 2015. The cells were treated with 0, 50, 200 and 400 μg / ml of 0, 50, 200 and 400 μg / ml for 24 h, (P <0.01), MDA content, superoxide dismutase (SOD) and lactate dehydrogenase (LDH) activity, p-p38 MAPK, Bax and Bcl- In addition, the cells were pretreated with baicalin (15, 30, 60μg / ml) and p38 MAPK channel-specific blocker SB203580 20μmol / L, respectively, and then treated with 200μg / ml PM 2.5 for 24 hours Intervention of Baicalin and Its Mechanism. Results Compared with the control group, PM 2.5 could reduce the survival rate of EA.hy926 cells and increase the activity of SOD, increase the content of MDA and LDH, and up-regulate the expression of p-p38 MAPK and Bax / Bcl-2 protein (P <0.05). The intervention of baicalin increased the survival rate of EA.hy926 cells and the activity of SOD, decreased the content of MDA and the activity of LDH, decreased the expression of p-p38 MAPK protein and Bax / Bcl-2 protein Significance (P <0.05). Conclusion Baicalin can reduce the damage of PM_ (2.5) to EA.hy926 cells by inhibiting the p38 MAPK pathway.