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机构地区:[1]绍兴市柯桥区中医医院神经内科,312030 [2]正大青春宝药业有限公司研究所
出 处:《浙江医学》2015年第11期951-954,共4页Zhejiang Medical Journal
摘 要:目的观察丹酚酸A对H_2O_2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H_2O_2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B_2(TXB_2)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 H_2O_2致RCMECs氧化损伤后,细胞LDH释放水平、TXB_2和MDA的含量均明显增加,同时6一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、TXB_2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H_2O_2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。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)ac- tivities were measured by automatic biochemistry analyzer. Radioimmunoassay was applied to measure the thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 a (6-keto-PGF1 ~ ). Results After incubated with 0.125 mmol/L hydrogen peroxide for 0.5 h, the viability of RCMECs was significantly inhibited, the LDH, MDA and TXB2 levels in culture supernatant were significantly in- creased, while 6-keto-PGF1 a and SOD levels were decreased. Pre-incubated with different concentrations of SalA for 20h sig- nificantly decreased the levels of LDH, MDA and TXB2, and increased 6-keto-PGF1 a level and the activity of SOD. Conclusion SalA can protect RCMECs against hydrogen peroxide-induced injury in a concentration-dependent manner, which may be as- sociated with its antioxidant effects.
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