| 摘要: |
| 目的 观察丹酚酸A 对H2O2所致大鼠脑微血管内皮细胞（RCMECs）氧化损伤的保护作用，并探讨其可能的作用机
制。方法 分离并培养大鼠脑微血管内皮细胞，用H2 O2 损伤的方法建立氧自由基损伤模型。采用丹酚酸A 进行干预后，分别测定细胞培养液中乳酸脱氢酶（LDH）活性、血栓素B2（TXB2）水平、6- 酮基前列腺素1α（6-keto-PGF1α）的含量，以及细胞内和培养液中脂质过氧化产物丙二醛（MDA）含量和超氧化物歧化酶（SOD）的活性。结果 H2O2致RCMECs 氧化损伤后，细胞LDH 释放水平、TXB2和MDA 的含量均明显增加，同时6-keto-PGF1α 含量和SOD 活性显著下降；而丹酚酸A 预处理后能呈浓度依赖性的降低RCMECs 氧化损伤后LDH 水平、TXB2含量和细胞内外的MDA 含量，提高受损细胞6-keto-PGF1α 的表达和细胞内外SOD 活性。结论 丹酚酸A 对H2O2所致RCMECs 氧化损伤具有保护作用，其机制可能与其抗氧化作用有关。 |
| 关键词: 丹酚酸A H2O2 氧自由基损伤 脑微血管内皮细胞 |
| DOI： |
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| Protective effects of salvianol acid A on hydrogen peroxide-induced oxidative injury of rat cerebral microvascular endothelial cells |
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YI Zhihong,BAI Yang,CHEN Lisun,XU Feng,CHEN Lijiang
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Keqiao Traditional Chinese Medicine Hospital
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| Abstract: |
| Objective To investigate the protective effects of salvianol acid A (Sal A) on hydrogen peroxide-induced oxidative injury in rat cerebral microvascular endothelial cells (RCMECs). Methods RCMECs were isolated and cultured; the cultured cells were treated with hydrogen peroxide to induce the oxidative injury. Different concentrations of SalA were added in cell culture to intervene the cell injury. Lactate dehydrogenase(LDH), malondialdelyde(MDA) and superoxide dismutase(SOD)activities
were measured by automatic biochemistry analyzer. Radioimmunoassay was applied to measure the thromboxane B2(TXB2) and 6-keto-prostaglandin F1α(6-keto-PGF1α). Results After incubated with 0.125 mmol/L hydrogen peroxide for 0.5h, the viability of RCMECs was significantly inhibited, the LDH, MDA and TXB2 levels in culture supernatant were significantly increased,while 6-keto-PGF1α and SOD levels were decreased. Pre-incubated with different concentrations of SalA for 20h significantly
decreased the levels of LDH, MDA and TXB2, and increased 6-keto-PGF1α level and the activity of SOD. Conclusion SalA can protect RCMECs against hydrogen peroxide-induced injury in a concentration-dependent manner, which may be associated with its antioxidant effects. |
| Key words: Salvianol acid A Hydrogen peroxide Oxygen free radical injury Cerebral microvascular endothelial cell |
