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机构地区:[1]河南大学医学院病理生理教研室 [2]开封95936部队医院
出 处:《河南大学学报(医学版)》2007年第1期37-38,44,共3页Journal of Henan University:Medical Science
摘 要:目的:观察金属硫蛋白(metallothionein MT)对同型半胱氨酸(homocysteine Hcy)损伤血管内皮细胞的保护作用及机制。方法:培养血管内皮细胞,培养液中分别加入Hcy及Hcy+MT孵育血管内皮细胞,自动生化分析仪测培养液乳酸脱氢酶(LDH)漏出量,硫代巴比妥酸法测细胞丙二醛(MDA)含量,化学比色方法测超氧化物歧化酶(SOD)活力。结果:与对照组相比,Hcy组细胞LDH及蛋白漏出增加,细胞MDA含量明显升高(P<0.01);外源性给予MT(10-9mol/L,5×10-9mol/L,10-8mol/L)呈浓度依赖性地抑制Hcy引起的血管内皮细胞损伤,与Hcy组比,LDH漏出分别降低16.3%(P<0.05)、23.5%(P<0.01)和37.2%(P<0.01)。MDA含量分别减少15.8%(P<0.05)、21.1%(P<0.01)和36.8%(P<0.01)。结论:MT拮抗Hcy对血管内皮细胞的脂质过氧化损伤。Objective: To observe the protective effect and possible mechanism of metallothionein against homocysteineinduced vascular endothelial cell injury. Methods: Human vascular endothelial cells (VECs) were cultured, LDH leakage of VECs were measured , and the content of MDA of VECs was calculated. Results: Hey not only increased LDH and protein leakage of cultured VECs . but also increased level of MDA of cultured VECS . Exogenous MT (10-9mol L^-1, 5 × 10^-9mol L^-1, 10^-8mol L^-1) could inhibit Hcy-induced VECs injury in dose-dependent manner. LDH leakage decreased by 16.3 % ( P 〈 0.05) ,23.5% ( P 〈 0.01 ) and 37.2% ( P 〈 0.01 ) . The level of MDA decreased 15.8% (P 〈 0.05) ,21. 1% (P 〈 0.01) and 36. 8% (P 〈 0.01) , respectively compared with the control group. Conclusion: Metallothionein can diminish Hcy-induced vascular endothelial cell lipid hyperoxidative injury.
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