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作 者:穆晶[1] 王红霞[1] 邱笑违[1] 王艳霞[1] 芦玲巧[1] 张立克[1]
机构地区:[1]首都医科大学病理生理教研室,北京100069
出 处:《微循环学杂志》2008年第3期25-27,F0003,共4页Chinese Journal of Microcirculation
基 金:北京市自然科学基金(7062007)
摘 要:目的:探讨11,12-环-二十碳三烯酸(11,12-EET)对缺氧大鼠血管平滑肌细胞(VSMC)增殖和凋亡的影响。方法:采用贴块法体外培养大鼠主动脉VSMC,将细胞分为常氧对照组(Con组),缺氧模型组(H组),EET组(EET组)和EET-缺氧组(EET-H组),以MTT法测定VSMC的增殖率,以流式细胞术观察VSMC细胞周期及凋亡率,Western blot方法检测Bax的表达。结果:与Con组比较,H组VSMC增殖率升高(P<0.01),EET组VSMC存活率降低(P<0.01);EET-H组细胞增殖率低于H组(P<0.01)。与Con组相比,H组G0/G1期VSMC细胞比例减少(P<0.05),S期细胞比例增加(P<0.05);EET组较Con组G0/G1期细胞比例增加(P<0.05);与H组相比,EET-H组G0/G1期细胞比例增加(P<0.05),S期和G2/M期细胞比例减少(P<0.05)。EET-H组VSMC凋亡率高于H组(P<0.05)、Con组(P<0.05)及EET组(P<0.05)。EET组Bax的表达高于Con组(P<0.05);与H组比较,EET组及EET-H组Bax的表达均升高(P<0.01)。结论:外源性给予11,12-EET有抑制缺氧VSMC增殖和促进缺氧VSMC凋亡双重作用。11,12-EET可能通过对VSMC增殖和凋亡的调控,影响血管损伤后血管重构。Objective:To explore the effect of 11,12-EET on the proliferation and apoptosis in hypoxia vascular smooth muscle cells(VSMC).Method:VSMCs were cultured by explant method and were divided into four groups:Con group,H group,EET group and EET-H group.MTT colorimetric assay was used to detect the proliferation viability of VSMC.The cell cycle and cell apoptosis rate were detected by flow cytometry assay.Western blotting method was used to detect the expression of Bax.Results:The cell proliferation viability of H group was higher than Con group(P<0.01),EET group was lower than Con group(P<0.01),EET-H group was lower than H group(P<0.01);In H group,the percentage of cells in G0/G1 phase was decreased(P< 0.05),the percentage of cells in S phase was increased(P< 0.05)compared with Con group.EET group compared with Con group,EET-H group compared with H group the percentage of cells in G0/G1 phase was increased(P< 0.05),the percentage of cells in S phase was decreased(P< 0.05).The apoptosis rate of EET-H group was higher than H group(P< 0.05),Con group(P< 0.05)and EET group.The expression of Bax in EET group was higher than Con group(P< 0.05),in EET-H group,the expression of Bax was higher than H group(P< 0.01).Conclusion:11,12-EET inhibits the proliferation of VSMC induced by hypoxia and enhances apoptosis of hypoxia VSMC,which may affect on vascular remodeling after injury.
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