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作 者:苏丽华[1,2,3] 王璇琳[2] 贺敏[2] 李伟静[2] 任素萍[2] 王春燕[3] 乔志新[2] 丁雪洁[2] 何跃忠[3] 于群[2]
机构地区:[1]中南大学湘雅二医院急诊科,湖南长沙410011 [2]军事医学科学院野战输血研究所,北京100850 [3]军事医学科学院附属医院急诊科,北京100071
出 处:《中国医药导报》2014年第12期21-24,F0003,共5页China Medical Herald
摘 要:目的研究黑青稞籽皮提取物对心肌细胞缺氧/复氧(H/R)损伤的保护作用及其机制。方法取大鼠胚胎心肌细胞(H9c2),随机分为5组:正常对照组(C组)、缺氧/复氧组(H/R组)、缺氧/复氧+低、中、高剂量药物组(H/R+L、M、H组)。流式细胞术检测细胞凋亡、细胞线粒体跨膜电位(ΔΨm)和细胞内活性氧(ROS)产生情况;Western blot方法检测B细胞淋巴瘤/白血病-2基因(Bcl-2),Bcl-2相关X蛋白(Bax),总丝氨酸苏氨酸蛋白激酶(tAkt)和磷酸化丝氨酸/苏氨酸蛋白激酶(pAkt)蛋白表达变化。结果药物组[(H/R+L)组至(H/R+H组)]细胞凋亡比例为(26.7±2.9)%至(6.1±1.1)%,较H/R组[(57.3±10.4)%]明显降低,差异有统计学意义(P<0.05);与H/R组比较,药物组ΔΨm升高,差异有高度统计学意义(P<0.01),ROS水平下降,差异有高度统计学意义(P<0.01),Bcl-2及pAkt表达升高,Bax及tAkt表达无明显变化。结论黑青稞籽皮提取物对心肌细胞缺氧/复氧损伤具有保护作用,可抑制心肌细胞凋亡,其可能与Bcl-2/Bax调控和激活磷脂酰肌醇-3激酶/丝氨酸苏氨酸蛋白激酶(PI3K-Akt)信号通路有关。Objective To investigate the protective effect of black barley pericarp extract on cardiomyocytes against hy- poxia/reoxygenation injury and to elucidate its underlying mechanism. Methods Cultured rat cardiac myoblast cells H9c2 were randomly divided into 5 groups: normal control group (C group), hypoxia/reoxygenation injury group (H/R group), and H/R followed by drug treatment with low/median/high dose group (HR+L, +M, +H group). Cell apoptosis, mitoehondrial transmembrane potential (Aψm) and the generation of intracellular ROS were monitored by flow cytome- ter. The protein levels of Bel-2, Bax, tAkt and pAkt in H9e2 cells were observed by Western blot assay. Results It was shown that black barley pericarp extract could reduce the apoptosis rate compared with H/R group cells [H/R group: (57.3+10.4)%, drug treat group (H/R+L) group--*(H/R+H) group: (26.7+2.9)% to (6.1+1.1)%, P 〈 0.05], rescue the loss of mitochondrial transmembrane potential (P 〈 0.01), and inhibit the production of ROS (P 〈 0.01). Drug treatments in- creased the expression levels of Bcl-2 and pAkt rather than H/R group cells, accompanied with no changes in the ex- pression levels of Bax and tAkt. Conclusion Black barley periearp extract can protect eardiomyocytes against hypoxia/ reoxygenation injury and suppress the apoptosis of cardiomyoeytes, which may relate to Bcl-2/Bax regulation and PI3K-Akt activation pathway.
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