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作 者:何磊[1] 张靓[2] 曹苏[2] 康焕菊[2] 沈施仁[2]
机构地区:[1]南通大学附属医院药剂科,226001 [2]南通大学附属医院麻醉科,226001
出 处:《江苏医药》2011年第13期1498-1501,共4页Jiangsu Medical Journal
基 金:江苏省卫生厅科技项目(Z201018);南通大学自然科学基金项目(10Z048)
摘 要:目的观察二氮嗪预处理对大鼠缺氧-复氧(H-R)心肌微血管内皮细胞(MMECs)Fractalkine(FKN)和p53 mRNA表达的影响。方法培养SD大鼠MMECs,分为四组:正常对照组(N组)、H-R组、二氮嗪组(DZ组)、二氮嗪+mitoKATP特异性阻断剂5-羟葵酸预处理组(DZ+5-HD组)。DZ组和DZ+5-HD组分别加入二氮嗪100μmol/L、二氮嗪100μmol/L+5-羟葵酸100μmol/L预处理2 h,然后和H-R组同样进行H-R 2 h。观察凋亡细胞形态,测定细胞凋亡率和活力、RT-PCR检测FKN和p53 mRNA转录水平。结果与N组比较,H-R组细胞凋亡率显著升高,细胞增殖率显著下降,p53 mRNA和FKN mRNA表达显著增强(P<0.01);与H-R组比较,DZ组细胞凋亡率显著降低,细胞增殖率显著增强(P<0.05),FKN mRNA和p53 mRNA表达显著降低(P<0.01);DZ+5-HD组取消了DZ组的作用。结论二氮嗪预处理通过抑制细胞凋亡,促使细胞增殖,下调FKN mRNA和p53 mRNA表达而实现对H-R MMECs损伤的保护。Objective To investigate the effects of diazoxide pretreatment on the expressions of FKN mRNA and p53 mRNA in rat myocardium microvascular endothelial cells undergoing hypoxia-reoxygenation(H-R).Methods The SD rat myocardium microvascular endothelial cells were randomly divided into 4 groups of normal control(group N),H-R(underwent H-R for 2h),H-R+DZ(pretreated with diazoxide 100μmol/L) and H-R+DZ+5-HD(pretreated with diazoxide 100μmol/L and 5-hydroxydecanoate 100μmol/L).The cell vitality,apoptosis rate and expressions of FKN mRNA and p53 mRNA were detected at the end of reoxygenation.Results Compared with group N,the cell vitality was significantly decreased,apoptotic rate increased and the expressions of FKN mRNA and p53 mRNA up-regulated in group H-R(P0.01).Compared with group H-R,the cell vitality was significantly increased(P0.05),apoptosis rate decreased(P0.01),the expressions of FKN mRNA and p53 mRNA down-regulated in group DZ(P0.01),which were inhibited by 5-HD in group H-R+DZ+5-HD.Conclusion Diazoxide pretreatment can reduce H-R injury in rat cardiac microvascular endothelial cells through inhibiting apoptosis,promoting cell proliferation and down-regulating the expressions of FKN mRNA and p53 mRNA.
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