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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蛋白表达并与病理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干预缺血心肌Ｆｏｓ蛋白阳性细胞数明显减少，再灌注９０ｍｉｎ分别为（４６７．５０±４５０．１０）个／张和（１７１．０２±１６０．８０）个／张（Ｐ＜０．０１）．③ＭＩＲ６０ｍｉｎ时，心肌细胞水肿，糖原颗粒减少，线粒体肿大，空化，肌丝片状溶解，断裂．ＴＭＰ干预ＭＩＲ６０ｍｉｎ时，心肌细胞缺血性改变似有减轻，线粒体肿大，空化，肌丝轻度疏松，未见到肌丝片状溶解．结论：ＭＩＲ可诱导缺血心肌Ｆｏｓ蛋白表达，ＴＭＰ干预可使缺血心肌Ｆｏｓ蛋白表达明显减弱，心肌细胞缺血损伤减轻．
OBJECTIVE: To study the expression of Fos protein and its histopathological changes during myocardial ischemia-reperfusion (MIR) in rats and to observe the effect of ligustrazine (TMP) on the expression of Fos protein at MIR. Methods: The rat MIR model was used to detect the Fos protein expression in different stages of MIR by immunohistochemical ABC method and compared with histopathological changes. Results: ①Fos protein was expressed in non-ischemic myocardium. Fos protein expression was induced at MIR60min and peaked at 90min, mainly distributed on the epicardial side. ② Compared with MIR rats, the number of Fos protein positive cells in ischemic myocardium decreased significantly after TMP intervention, and the numbers of Fos protein positive cells in TMP intervention group were (467.50 ± 450.10) / (171.02 ± 160.80) / Zhang (P <0.01). ③ MIR60min, myocardial cell edema, glycogen particles decreased, mitochondria swelling, cavitation, myoflagelin dissolution, rupture. TMP intervention MIR60min, ischemic changes seem to reduce myocardial cells, mitochondria swelling, cavitation, mild myxelastosis, did not see the sheet-like lysis. Conclusion: MIR can induce the expression of Fos protein in ischemic myocardium. TMP can attenuate the expression of Fos protein in ischemic myocardium and relieve the myocardial ischemia.