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作 者:孙婷[1] 史红霞[2] 孙秀菊[2] 田华[3] 刘同美[3]
机构地区:[1]潍坊医学院诊断学教研室 [2]潍坊医学院附属医院 [3]潍坊医学院病理生理学教研室
出 处:《潍坊医学院学报》2007年第2期131-133,共3页Acta Academiae Medicinae Weifang
摘 要:目的观察在慢性压力负荷性心力衰竭大鼠心肌细胞凋亡的改变和凋亡蛋白Bcl-2,Bax,Bcl-XS,Bcl-XL的变化及意义。方法20只大鼠随机分为心力衰竭组(心衰组)10只、对照组10只,缩窄鼠的腹主动脉复制慢性压力负荷性心力衰竭模型。18周后测量血流动力学指标后,处死大鼠,取心脏。称左、右心室重量。原位脱氧核糖核酸酶末端标记法检测细胞凋亡;免疫组化法和免疫印迹法测Bcl-2,Bax,Bcl-XS,Bcl-XL蛋白表达。结果心衰组心肌细胞凋亡明显增加(P<0.01),Bax,Bcl-XS表达增加,Bcl-2表达减低,Bcl-XL无明显变化。结论在慢性压力负荷诱导的心力衰竭大鼠发生心肌细胞凋亡与Bcl-XS/XL蛋白的比例增加,Bcl-2/Bax比率降低有关。Objective To examine the changes and significant of apoptosis, pro-apoptotic Bax, Bcl- XS and anti-apoptotic Bcl-2, Bcl-XL protein expression in chronic pressure overload heart failure in rats. Methods Twenty rats were randiomied divide into 2 groups : heart failure ( HF ) group( n = 10) and sham operation group( n = 10) .The rat model of chronic pressure overload HF was induced by transverse abdominal aortic constriction. These rats were killed after measurement of haemodynamie parameters and the hearts were removed.The left and right ventricles were dissected and weighed separately. Apoptosis was assessed using TUNEL method. The monitoring of proapoptotic Bax, Bcl- XS, and antiapoptotic Bcl-2, Bcl-XL proteins were determined by Western blot and immunohistochemistry. Results In HE rats, there was significant ( P 〈 0.01) systolic dysfunction compared to sham. Myocardial apoptosis was significantly increased( P 〈 0.01 ) . Bax and Bcl- XS were significantly elevated in heart failure rats. The expression of Bcl-2 was significantly reduced. Express of Bcl-XL was not insignificant. The Bcl-2 to Bax ratio was reduced and Bcl-XS to Bcl-XL ratio was increased. Conclusion These data suggest that increased cardiomyocyte-specific apoptosis Bax,and Bcl-XS expression and reduced Bcl-2 and the Bcl-2 to Bax ratio and increased Bcl-XS to Bcl-XL ratio in chronic pressure overload HF, may be mechanism contributing heart failure.
分 类 号:R541.6[医药卫生—心血管疾病]
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