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作 者:金颂峰 宫丽鸿[2] 肖福龙 吕童 Jin Songfeng;Gong Lihong;Xiao Fulong;Lyu Tong(Lia-oning University of Traditional Chinese Medicine,Liaoning,Shenyang 110079,China)
机构地区:[1]辽宁中医药大学,辽宁沈阳110079 [2]辽宁中医药大学附属医院,辽宁沈阳110032
出 处:《中国中医急症》2020年第10期1732-1734,共3页Journal of Emergency in Traditional Chinese Medicine
基 金:国家中医药管理局国家中医临床研究基地业务建设科研专项课题(JDZX2015033);辽宁省科学技术基金项目(20180530016);辽宁省特聘教授项目(辽委发〔2017〕3号)。
摘 要:目的基于细胞凋亡探讨搜风祛痰方对心肌缺血再灌注大鼠冠脉微循环内皮功能的影响。方法将140只SPF级健康SD大鼠随机分为4组:假手术组、模型组、西药组、中药组,每组35只。于药物干预后建立缺血再灌注模型,其中假手术组穿线但不结扎。ELISA法测血清前列环素(PGI2)、血栓素A2(TXA2)的含量。RT-PCR法测B细胞淋巴瘤2家族蛋白2(Bcl-2)、B细胞淋巴瘤/白血病2关联X(Bax)mRNA的表达。结果相比假手术组,模型组TXA2含量与Bcl-2 mRNA、Bax mRNA表达提高,PGI2含量下降(P<0.05)。相比模型组,中药组、西药组TXA2含量和Bax mRNA表达下降,PGI2含量和Bcl-2 mRNA表达增加(P<0.05)。结论搜风祛痰方可抑制细胞凋亡、保护缺血再灌注大鼠冠脉微循环内皮功能,这可能与上调PGI2含量及Bcl-2 mRNA表达,下调TXA2含量及Bax mRNA表达相关。Objective:To investigate the effect of Soufeng Qutan Decoction on the apoptosis of coronary microcirculatory endothelial cells in rats with myocardial ischemia-reperfusion injury.Methods:A total of 140 healthy SPF SD rats were randomly divided into the sham operation group,model group,perindopril group and Soufeng Qutan Decoction group,35 rats in each group.After treatment with corresponding drugs,the sham operation group was not ligated,and the other groups were ligated to establish ischemia-reperfusion models.The contents of serum PGI2 and TXA2 were detected by ELISA.The contents of Bcl-2 and Bax mRNA were measured by RT-PCR.Results:Compared with the sham operation group,the contents of TXA2,Bcl-2 mRNA and Bax mRNA were increased,and the contents of PGI2 were decreased in the model group(P<0.05).Compared with the model group,the contents of TXA2 and Bax mRNA were decreased,and the contents of PGI2 and Bcl-2 mRNA were increased in Soufeng Qutan Decoction group and perindopril group(P<0.05).Conclusion:Soufeng Qutan Decoction can inhibit the apoptosis of endothelial cells in coronary microcirculation in rats with myocardial ischemia-reperfusion injury and protect the endothelial function.Its mechanism may be related to the up-regulation of PGI2 and Bcl-2 mRNA expression,as well as down-regulation of TXA2 and Bax mRNA contents.
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