目的 研究注射用丹參多酚酸（SAFI）對過氧化氫（H₂O₂）誘導(dǎo)的人臍靜脈內(nèi)皮細(xì)胞（HUVEC）損傷的保護(hù)作用及機(jī)制。方法 體外培養(yǎng)HUVEC，設(shè)置對照組、模型組、SAFI（0.05、0.10、0.20、0.40、0.80 mg/mL）組，對照組及模型組不加藥，繼續(xù)培養(yǎng)24 h，模型組及SAFI組分別加入1 mmol/L H₂O₂作用1 h，對照組不加H₂O₂。CCK-8法檢測HUVEC增殖；酶聯(lián)免疫吸附法（ELISA）測定細(xì)胞間黏附因子（ICAM-1）、血管細(xì)胞黏附因子（VCAM-1）、丙二醛（MDA）、乳酸脫氫酶（LDH）、超氧化物歧化酶（SOD）的含量；TUNEL染色法觀察HUVEC凋亡狀態(tài)；Western blotting法檢測凋亡相關(guān)蛋白Bcl-2、Bax的變化。結(jié)果 與模型組比較，質(zhì)量濃度大于0.1 mg/mL的SAFI組細(xì)胞存活率顯著增加（P<0.05）；質(zhì)量濃度大于0.2 mg/mL的SAFI組LDH、MDA水平顯著降低，SOD水平顯著增加（P<0.05）；0.4、0.8 mg/mL的SAFI組ICAM-1、VCAM-1水平顯著降低（P<0.05）；TUNEL染色結(jié)果顯示，0.4、0.8 mg/mL的SAFI顯著抑制凋亡；Western blotting結(jié)果顯示，0.4、0.8 mg/mL的SAFI組Bcl-2蛋白表達(dá)顯著升高（P<0.05），Bax蛋白表達(dá)顯著下降（P<0.05）。結(jié)論 SAFI對H₂O₂誘導(dǎo)的HUVEC損傷有保護(hù)作用，主要是通過提高SOD含量，降低氧化指標(biāo)LDH、MDA以及炎癥因子ICAM-1、VCAM-1水平，調(diào)節(jié)凋亡蛋白Bax、Bcl-2的表達(dá)發(fā)揮作用。

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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