缺血再灌注大鼠心肌Fos蛋白表达及川芎嗪的作用

目的：研究大鼠心肌缺血再灌注（ＭＩＲ）时Ｆｏｓ蛋白表达与其病理组织学改变，并观察川芎嗪（ＴＭＰ）对ＭＩＲ时Ｆｏｓ蛋白表达的作用。方法：采用大鼠ＭＩＲ模型，用免疫组化ＡＢＣ法检测ＭＩＲ过程中不同时期Ｆｏｓ蛋白表达并与病得组织学改变进行对照分析．结果：（１）非缺血心肌无Ｆｏｓ蛋白表达，ＭＩＲ６０ｍｉｎ可诱导Ｆｏｓ蛋白表达，９０ｍｉｎ时达高峰，主要分布在心外膜侧。（２）与ＭＩＲ大鼠相比，ＴＭＰ干预缺血心

Effects of tetramethylpyrazine on Fos protein expression of myocardial ischemia reperfusion in rats

AIM: To study the relationship between Fos protein expression and myocardial ischemical changes, and to observe the effects of tetramethylpyrazine (TMP) on Fos protein expression of the myocardial ischemic reperfusion (MIR) in rats. METHODS: Using an experimental MIR in SpragueDawley (SD), the myocardial cellular expression of Fos protein in different phases of MIR and effects of TMP on MIR were observed by immunohistochemical staining in conjunction with histopathological analysis of rat hearts. RESULTS: (1) No Fos proteinexpression was found in noischemic myocardial tissues. Fos protein expression was first observed mainly in the nuclei of subepicardial myocardiac cells 60 minutes after MIR and reached its peak by 90 minutes; (2) Compared with that of rats with MIR, Fos protein expression of MIR rats with TMP decreased significantly, and the number of Fos immunopasitive cells also decreased markedly 90 minutes after MIR of rats treated with TMP as revealed by computerized image analysis, (from 467.5450.10/section to 171.02160.80/section, P<0.01); (3) Sixty minutes after MIR, some ischemic changes were morphologically confirmed, such as edema in myocardial cells, swollen mitochondria with empty cavities and broken myocardial fibrils with partial lysis. But in the TMP group, though some ischemic changes still exist, they were alleviated. CONCLUSION: MIR can induce Fos protein expression in injured myocardiac cells and Fos protein expression will increase with the extension of reperfusion and the aggravation of the injured cells. The administration of TMP can markedly decrease Fos protein expression and alleviate histopathological changes of myocardial ischemia.