摘要
目的 :观察川芎嗪对儿茶酚胺诱导大鼠心肌损伤时心肌细胞Bcl 2和Fas蛋白表达的影响。方法 :采用皮下多点注射异丙肾上腺素 (ISO ,5mg·kg- 1)每天 1次 ,连续 3d ,诱导大鼠心肌损伤 ,采用免疫组化方法检测Bcl 2和Fas蛋白的水平 ,并利用图像分析系统分析蛋白阳性表达区域平均光密度值。结果 :损伤组和川芎嗪保护组心肌细胞Bcl 2蛋白表达较对照组均显著升高 (P <0 .0 1 ) ,损伤组Fas蛋白水平较对照组也显著升高 (P <0 .0 1 ) ,川芎嗪保护组的Fas蛋白水平较损伤组显著下降 (P <0 .0 1 ) ,且Bcl 2 Fas比值也较损伤组和对照组明显增加。川芎嗪保护组的病理损伤程度明显低于损伤组。结论 :川芎嗪可抑制儿茶酚胺诱导的心肌损伤时心肌细胞中促凋亡基因Fas的表达 ,提高心肌细胞中Bcl 2
AIM: To observe the influence of tetramethylpyrazine on the ex pression of Bcl-2 and Fas proteins in myocardial injury induced by catecholamin e in rats. METHODS: 36 Wistar rats were divided into 3 groups: c ardiac injury group (n=12), tetramethylpyrazine treated group ( n=12) and control group (n=12).The rat card iac injury was induced by the subcutaneous injection of isoproterenol (ISO, 5 mg·kg -1 ·d -1 ). Bcl-2 and Fas protein was identified by immunoh istochemical technique and the mean optical density (OD) values of the positive fields of protein expression were quantitatively examined by ima ge analysis system. RESULTS: The expression of Bcl-2 protein wa s increased significantly in the cardiac injury group and tetramethylpyrazine tr eated group as compared with that of the control group (P< 0.0 1 ). There were no significant difference in the Bcl-2 protein expression betw een the tetramethylpyrazine treated group and cardiac injury group (P> 0.05 ), but the expression of Fas protein was decreased significantly i n the tetramthylpyrazine treated group as compared with that of the cardiac inju ry group (P< 0.05 ). The protein expression ratio of Bcl-2/Fa s was increased significantly in the tetramethylpyrazine treated group as compar ed with those of the cardiac injury group and the control group.The myocardium pathological damage was decreased significantly in the tetramethylpyrazine treat ed group. CONCLUSION: Tetramethylpyrazine can significantly inhi bit the expression of pro-apoptotic Fas protein and raise the ratio of Bcl-2/F as protein cardiomyocytes.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2004年第2期197-200,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
江西省自然科学基金资助题 (№ 0 0 4 0 0 54)