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目的:探讨大鼠急性心肌梗死(AMI)后心肌纤维化和TGF-Β1表达及炎症反应的分子机制。方法: 建立大鼠AMI模型及假手术组,于术后第1、4和8周末测血流动力学后取心脏。RT-PCR和免疫组化SABC法检测 FGF-Β1岛基因和蛋白的表达。用氯胺T法测心肌组织羟脯氨酸的含量。心肌病检观察心肌组织炎症细胞浸润情况。结果:与假手术组相比,AMI后第1、4和8周末血流动力学有明显改变(P<0．01)。在梗死区、交界区和非梗死区羟脯氨酸和TGF-Β1基因和蛋白表达均增高(P<0．05),第1周的表达高于第4和8周。羟脯氨酸和TGF-Β1蛋白表达呈现明显正相关(R=0．75-0．99,P<0．05)。AMI后第1周梗死区和交界区炎症细胞浸润明显,第4和8周心肌炎症细胞减少。TGF-Β1在梗死后1’周时主要见于心肌细胞、中性粒细胞、巨噬细胞和部分淋巴细胞的胞浆内表达,在4 周和8周见于成纤维母细胞及间质。结论:AMI后心肌细胞、炎症细胞、成纤维母细胞胞浆及基质中TGF-Β1表达增高,与羟脯氨酸的变化及炎症过程存在联系,可能在AMI后心室重塑和心肌炎性修复过程中起重要作用。
Objective: To investigate the molecular mechanism of myocardial fibrosis and TGF-β1 expression and inflammatory response after acute myocardial infarction (AMI) in rats. Methods: AMI rats and sham-operation group were established. At the end of the 1st, 4th and 8th week after operation, the hemodynamics were measured and the heart was taken. The expression of FGF-Β1 island genes and proteins was detected by RT-PCR and immunohistochemical SABC method. The content of hydroxyproline in myocardial tissue was measured by chloramine T method. Cardiomyopathy Check myocardial tissue inflammatory cell infiltration. Results: At the end of the 1st, 4th, and 8th week after AMI, there was a significant change in hemodynamics compared with the sham operation group (P <0.01). The expression of hydroxyproline and TGF-β1 gene and protein were increased in the infarct area, junctional area and non-infarcted area (P <0.05), and the expression in the first week was higher than that in the 4th and 8th week. Hydroxyproline and TGF-β1 protein expression showed a significant positive correlation (R = 0.75-0.99, P <0.05). In the first week after AMI, infiltration of inflammatory cells in the infarct area and junctional area was obvious, and myocardial inflammatory cells decreased in the 4th and 8th week. TGF-Β1 was mainly expressed in the cytoplasm of cardiomyocytes, neutrophils, macrophages and some lymphocytes 1 week after infarction, and was found in fibroblasts and stroma at 4 weeks and 8 weeks. CONCLUSION: The expression of TGF-β1 in the cytoplasm and matrix of myocardial cells, inflammatory cells and fibroblasts after AMI is increased, which is related to the change of hydroxyproline and the inflammatory process. It may be related to the process of ventricular remodeling and myocarditis repair after AMI Play an important role.