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作 者:李浩亮 许邦龙[1] 胡广全[1] 高峰[1] LI Hao-liang;XU Bang-long;HU Guang-quan(Department of Cardiovascular Medicine,Second Affiliated Hospital of Anhui Medical University,Hefei 230601,Anhui)
机构地区:[1]安徽医科大学第二附属医院心血管内科,安徽合肥230601
出 处:《安徽医专学报》2024年第3期78-81,共4页Journal of Anhui Medical College
基 金:安徽省高等学校科学研究项目(编号:2022AH050771)。
摘 要:目的:探讨灯盏花素对急性心肌梗死(AMI)大鼠的心肌保护作用及其分子机制。方法:将32只SD大鼠随机均分为假手术组、AMI组、AMI+灯盏花素组,AMI+灯盏花素+LY294002组。通过超声心动图、TUNEL染色、ELISA、Western blot和qRT-PCR等多种检测方法,探究各组大鼠的心功能、心肌细胞凋亡率、心肌损伤程度、凋亡相关分子以及PI3K/Akt信号通路的表达情况。结果:与假手术组比较,AMI组大鼠的心脏收缩功能降低,心肌细胞凋亡率显著增加,心肌损伤严重;与AMI组比较,AMI+灯盏花素组的上述病理改变明显减轻;当加入PI3K的特异性抑制剂LY294002后,灯盏花素对AMI大鼠的治疗作用被削弱。结论:灯盏花素可能是通过激活PI3K/Akt信号通路抑制心肌细胞凋亡,从而减轻AMI导致的大鼠心肌损伤,改善心功能。Objective:To explore the effects of breviscapine in myocardial protection and its molecular mechanism in rats with acute myocardial infarction(AMI).Methods:Thirty-two SD rats were randomly and equally divided into sham-operated group,AMI group,AMI+breviscapine group,AMI+breviscapine+LY294002 group,8 rats in each group.Echocardiography,TUNEL staining,ELISA,Western blot and qRT-PCR were used to investigate the cardiac function,myocardial apoptosis rate,myocardial injury degree,the expression of apoptosis-related molecules and PI3K/Akt signaling pathway in rats of each group.Results:Compared with the sham-operated group,rats in the AMI group showed reduced cardiac contractile function,significantly increased apoptosis rate,severe myocardial injury,while compared with the AMI group,the AMI+breviscapine group showed the above pathological changes were significantly reduced(P<0.05);when LY294002,a specific inhibitor of PI3K,was added,the therapeutic effect of breviscapine on AMI was diminished.Conclusion:Breviscapine may inhibit cardiomyocyte apoptosis through activation of PI3K/Akt signaling pathway,thereby reducing myocardial injury caused by AMI and improving cardiac function.
关 键 词:灯盏花素 急性心肌梗死 PI3K/AKT信号通路 细胞凋亡
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