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作 者:牛春雨[1] 赵自刚[1] 陈瑞华[1] 张静[1] 张玉平[1] 刘艳凯[1]
机构地区:[1]河北北方学院病理生理学教研室,河北张家口075029
出 处:《中国病理生理杂志》2008年第2期294-297,共4页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.30370561);河北省自然科学基金资助项目(No.C2004000649)
摘 要:目的:观察休克淋巴液对大鼠肺微血管内皮细胞(PMVECs)凋亡相关基因表达的影响,探讨休克淋巴液诱导PMVECs细胞凋亡的分子机制。方法:无菌条件下复制大鼠重症失血性休克模型,引流休克时肠系膜淋巴液或收集门静脉血,同时引流正常的淋巴液或正常门静脉血作为对照。以不同处理因素与第3代原代培养的PMVECs共同孵育,应用流式细胞仪检测细胞凋亡率,RT-PCR检测凋亡相关基因bcl-2、bax及fas、fas L的表达。结果:4%终浓度的休克淋巴液作用4 h后,PMVECs凋亡率为9.86%±3.24%,显著高于其它组(P<0.01);4%终浓度的休克淋巴液作用6 h后,PMVEC的fas、fas L、baxmRNA表达高于其它组、bcl-2mRNA表达低于其它组(P<0.01)。结论:休克淋巴液可诱导大鼠PMVECs凋亡,其机制与凋亡促进基因fas、fas L、bax表达增强、凋亡抑制基因bcl-2表达降低有关。AIM: To observe the effects of shock lymph on apoptosis relative gene expressions of pulmonary micro - vascular endothelial cells (PMVECs) , and explore its mechanism. METHODS : The model of severe hemorrhagic shock was established by maintaining the blood pressure of rats in the condition of sepsis, mesentery lymph and shock portal vein blood was taken out. As control, mesentery lymph, portal vein blood of normal rats was taken out. The primary PMVECs of passages 3 were treated by different treatment factors, respectively. The apoptosis rate was analyzed by flow cytometry, and the expressions of relative genes of apoptosis such as fas, fas L, bcl - 2 and bax were detected by RT - PCR. RESULTS : The apoptosis rate of PMVECs was 9.86% ± 3.24% after exposed to shock lymph at the final concentration of 4% for 4 hours and significantly higher than that in control ( P 〈 0.01 ). The expression levels offas, fas L and bax mRNA were higher and bcl-2 mRNA was lower in shock lymph group than those in control group. CONCLUSION: The results demonstrated that the apoptosis of PMVECs of rats was induced by shock lymph, and its mechanism relate to high expression of apoptosis accelerative genes such asfas, fas L, bax mRNA and low expression of apoptosis inhibitory gene bcl -2.
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