目的 研究注射用丹参多酚酸（SAFI）对过氧化氢（H₂O₂）诱导的人脐静脉内皮细胞（HUVEC）损伤的保护作用及机制。方法 体外培养HUVEC，设置对照组、模型组、SAFI（0.05、0.10、0.20、0.40、0.80 mg/mL）组，对照组及模型组不加药，继续培养24 h，模型组及SAFI组分别加入1 mmol/L H₂O₂作用1 h，对照组不加H₂O₂。CCK-8法检测HUVEC增殖；酶联免疫吸附法（ELISA）测定细胞间黏附因子（ICAM-1）、血管细胞黏附因子（VCAM-1）、丙二醛（MDA）、乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）的含量；TUNEL染色法观察HUVEC凋亡状态；Western blotting法检测凋亡相关蛋白Bcl-2、Bax的变化。结果 与模型组比较，质量浓度大于0.1 mg/mL的SAFI组细胞存活率显著增加（P<0.05）；质量浓度大于0.2 mg/mL的SAFI组LDH、MDA水平显著降低，SOD水平显著增加（P<0.05）；0.4、0.8 mg/mL的SAFI组ICAM-1、VCAM-1水平显著降低（P<0.05）；TUNEL染色结果显示，0.4、0.8 mg/mL的SAFI显著抑制凋亡；Western blotting结果显示，0.4、0.8 mg/mL的SAFI组Bcl-2蛋白表达显著升高（P<0.05），Bax蛋白表达显著下降（P<0.05）。结论 SAFI对H₂O₂诱导的HUVEC损伤有保护作用，主要是通过提高SOD含量，降低氧化指标LDH、MDA以及炎症因子ICAM-1、VCAM-1水平，调节凋亡蛋白Bax、Bcl-2的表达发挥作用。

Objective To observe the effect of Salvianolic Acids for Injection (SAFI) on the injury of human umbilical vein endothelial cells (HUVEC) induced by hydrogen peroxide (H₂O₂) and its possible mechanism. Methods HUVEC was cultured in vitro and treated with 1 mmol/L H₂O₂ for one hour to establish the HUVEC model of peroxidation damage. The control group, H₂O₂ model group and SAFI groups with different concentrations (0.05, 0.10, 0.20, 0.40, 0.80 mg/mL) for injection were set. HUVEC cell proliferation was detected by CCK-8 method. Enzyme linked immunosorbent assay (ELISA) was used to determine the contents of intercellular adhesion factor (ICAM-1), vascular cell adhesion factor (VCAM-1), malondialdehyde (MDA) and superoxide dismutase (SOD). Apoptosis status of HUVEC was evaluated by TUNEL (TdT-mediated DUTP Nick end labeling) staining. The changes of apoptosis-related proteins Bcl-2 and Bax were detected by Western blotting. Results Compared with model group, the survival rate of SAFI group with mass concentration > 0.1 mg/mL was significantly increased (P<0.05). The levels of LDH and MDA in SAFI group with mass concentration > 0.2 mg/mL were significantly decreased, while the level of SOD was significantly increased (P<0.05). The levels of ICAM-1 and VCAM-1 in 0.4 and 0.8 mg/mL SAFI group were significantly decreased (P<0.05). TUNEL staining results showed that 0.4 and 0.8 mg/mL SAFI significantly inhibited apoptosis. Western blotting results showed that Bcl-2 protein expression was significantly increased (P<0.05) and Bax protein expression was significantly decreased (P<0.05) in 0.4 and 0.8 mg/mL SAFI groups. Conclusion SAFI has a protective effect on H₂O₂-induced HUVEC injury, mainly through increasing the content of SOD, reducing the levels of oxidative indexes LDH and MDA, and inflammatory factors ICAM-1 and VCAM-1, and regulating the expression of apoptotic proteins Bax and Bcl-2.

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