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小檗碱对酒精所致心肌细胞凋亡的影响研究 被引量:4

Effect of BBR on Myocardial Cell Apoptosis Induced by Alcohol
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摘要 目的:探讨小檗碱对酒精损伤性大鼠心肌细胞凋亡的影响及可能机制。方法:取无特定病原体(SPF)雄性SD大鼠随机分为空白对照组、酒精组、酒精组+小檗碱保护组(简称保护组),12周后检验血清肌钙蛋白T(cTnT)、肌酸激酶(CK)、C反应蛋白(CRP)浓度水平,HE染色观察心肌病理学改变,RT-PCR法检测心肌组织中细胞凋亡及凋亡相关基因-B细胞白血病/淋巴瘤-2基因(Bcl-2)和Bcl相关蛋白(Bax)的表达。结果:与对照组比较,酒精组血清cTnT、CK、CRP均明显升高,显微镜下心肌细胞肿胀,心肌纤维排列紊乱,心肌间质炎细胞浸润,Bcl-2表达减弱,Bax表达明显增强,差异有统计学意义。保护组与酒精组相比,血清cTnT、CK、CRP升高不明显,显微镜下部分心肌细胞肿胀,排列紊乱,心肌间质无炎性细胞浸润,Bcl-2表达明显增强,Bax表达减弱。结论:酒精性心肌损伤中存在细胞凋亡,小檗碱可抑制心肌细胞凋亡,减少酒精对心肌的损伤,达到保护心肌的作用。 Objective To study the effects of berberine( BBR) on apoptosis of the myocardial cell by alcohol and its possible mechanisms. Methods The Sprague-Dawley( SD) male rats were randomly divided into the control group,Alcohol group,alcohol and BBR group( protect group). After 12 weeks,levels of the serum CTnT,CK and CRP were tested,changes of myocardial pathological were observed by HE stain,the RT-PCR was be used to measure myocardial cell apoptosis and expression of apoptosis-associated gene such as Bcl-2 and Bax. Results Compared with control group,the alcohol group showed significantly high levels of serum CTnT,CK and CRP. The myocardial cells were swollen,myocardial fibers were disarrayed,and inflammatory cells were infiltrated in myocardial interstitial under the microscope. There was significant difference among expression of Bcl-2 decreased and Bax up-regulated. The serum CTnT,CK,CRP in protect group was little higher than alcohol group,under the microscope,part of myocardial cells were swollen,myocardial fibers still disarrayed,inflammatory cells were absented in myocardial interstitial,there was significant difference among expression of Bcl-2 up-regulated and Bax decreased. Conclusion There are apoptosis in myocardial injury by alcohol,BBR can protects myocardial cell from alcohol damage and decreases apoptosis.
出处 《湖南师范大学学报(医学版)》 2014年第1期38-41,共4页 Journal of Hunan Normal University(Medical Sciences)
基金 长沙市科技局指导性科技计划项目(K12ZD006-33)
关键词 小檗碱 SD大鼠 酒精性心肌损伤 细胞凋亡 RT-PCR berberine SD rat alcoholic myocardial injury apoptosis RT-PCR
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