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机构地区:[1]北华大学附属医院心内科,吉林吉林132011 [2]北华大学附属医院病理科,吉林吉林132011
出 处:《中国现代医学杂志》2008年第4期420-422,共3页China Journal of Modern Medicine
基 金:吉林市科委资助项目(No:2001035)
摘 要:目的bFGF对大鼠急性心肌梗死(AMI)时心肌细胞内Bcl-2、Bax表达的影响,并探讨其发生机制。方法实验动物随机分为假手术组,缺血+生理盐水组,缺血+bFGF组,结扎大鼠左冠状动脉复制AMI模型。术前分别注入生理盐水及bFGF,于结扎后2、4和8h处死动物,采用免疫组织化学方法检测大鼠缺血区心肌细胞内Bcl-2、Bax蛋白的表达水平。结果在急性心肌梗死后第2、4h时,缺血+bFGF组心肌细胞Bcl-2蛋白的表达(141.75±26.91)‰,(125.63±24.09)‰明显高于缺血+生理盐水组(15.63±5.05)‰,(42.12±14.08)‰,P<0.01,Bax蛋白表达(11.25±3.80)‰,(30.87±8.05)‰明显低于缺血+生理盐水组(32.62±6.61)‰,(83.638±9.84)‰,P<0.05。结论bFGF可促进AMI时心肌细胞内Bcl-2的表达、抑制Bax的表达,对心肌细胞具有保护作用。[Objective] To study the effects of basic fibroblast growth factor (bFGF) to Bel-2 and Bax expression in myocardial cells on acute myocardial infarction in rats and then discuss its mechanisms. [Methods] The experiment animals were randomly divided into three groups, sham operated group, ischemic + saline group and ischemic + bFGF group. The acute myocardial infarction rat model was established by left coronary artery ligation. The rats were treated with saline or bFGF before coronary artery occlusion. The rats were killed at 2 h, 4 h, and 8 h after coronary artery occlusion. Bcl-2 and Bax in myocardial cells were detected by inmmnohistochemical staining. [Resuits] The amount of Bcl-2 protein expression of myocardial cells of ischemic + bFGF groups at 2 h (141.75± 26.91)‰ or 4 h (125.63±24.09)‰ was significantly higher than that in ischemic + Saline groups [2 h (15.63± 5.05)‰, 4 h(42.12±14.08)‰] P 〈0.01, after coronary artery occlusion; However the amount of Bax protein expression in ischemic + bFGF groups at 2 h (11.25±3.80)‰ and 4 h (30.87±8.05)‰ were lower than that in ischemic + saline group (2h: 32.62±6.61‰) (4 h: 83.638±9.84‰),(P 〈0.05). [Conclusion] bFGF has protective roles to myocardial cells of acute myocardial infarction in rats by promoting Bcl-2 expression and inhibiting Bax expression.
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