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N-乙酰-L-半胱氨酸对亚砷酸钠诱导的内皮细胞凋亡的防治作用 被引量:6

Effects of N-acetyl-L-cysteine on endothelial cells apoptosis induced by Ars
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摘要 目的 全身炎症反应综合征时内皮细胞 (ECs)凋亡是许多继发性损伤发生、发展的重要环节 ,观察N -乙酰 -L -半胱氨酸 (NAC)对ECs凋亡的防治作用。 方法 采用亚砷酸钠(Ars)在体外诱导ECs凋亡 ,应用流式细胞术测定凋亡细胞比例、细胞间黏附分子ICAM - 1表达和细胞内氧化状态水平 ,以及NAC处理后上述指标的改变。 结果  80 μmol LArs及 16 0 μmol LArs浓度时应用NAC可以使凋亡细胞百分率分别从 (2 5 .7± 2 .0 ) %、(5 4.4± 11.1) %降低至 (2 0 .4±1.3) %、(33 .1± 6 .5 ) % (P <0 .0 5 ) ,同时使ICAM - 1表达下降 ,40 μmol LArs及 80 μmol LArs浓度时应用NAC可以使细胞内氧化状态恢复到对照水平。 结论 NAC可以显著防治Ars诱导的内皮细胞凋亡 ,其防治作用可能与调节ICAM - Objective This study was designed to test the hypothesis that the N-acetyl-L-cysteine (NAC) may modulate human endothelial cells (ECs) apoptosis. Methods Ars was used to induce ECs apoptosis in vitro. ECs apoptosis, ICAM-1 expression and oxidative state and their changes after NAC treatment were detected by flow cytometry. Results When Ars was added at the concentration of 80 μmol/L and 160 μmol/L, NAC could significantly attenuate ECs apoptosis with the apoptosis rate from 25.7%±2.0% and 54.4% ±11.1% to 20.4%±1.3% and 33.1%±6.5%, respectively ( P <0.05). Meanwhile, ICAM-1 expression was also decreased. NAC could resume oxidative state to control level as 40 μmol/L and 80 μmol/L of Ars were added. Conclusions These data indicate that NAC, possibly through its regulation of ICAM-1 expression and oxidative state, can prevent ECs dysfunction and cells apoptosis.
出处 《中华创伤杂志》 CAS CSCD 北大核心 2000年第5期302-304,共3页 Chinese Journal of Trauma
关键词 内皮细胞 细胞凋亡 半胱氨酸 NAG 全身炎症反应 Endothelial cell Apoptosis Acetylcysteine
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