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目的:研究环氧合酶2(COX2)在心肌纤维化中的表达及意义。方法:注射盐酸异丙肾上腺素(Iso)15mg.kg-1复制大鼠心肌坏死模型,用MD-100自动生化分析仪检测大鼠血清天冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、肌酸激酶(CK)及肌酸激酶同工酶(CK-MB)的含量。通过免疫组化染色分析心肌COX2蛋白表达,RT-PCR分析COX2mRNA表达。结果:与正常对照组比较,注射Iso后4h血清LDH、CK及CK-MB达高峰(P<0.05),6hAST达高峰(P<0.05)。COX2蛋白表达随病变程度的加重而增加,与正常对照组比较差异有显著性(P<0.05)。COX2mRNA表达结果显示,注射Iso后2～12h,COX2mRNA表达有逐渐增加趋势,但与正常对照组比较差异无显著性(P>0.05);注射Iso后24～48h,COX2mRNA表达较正常对照组明显增加(P<0.05);48h后mRNA表达逐渐下降,3周后仍未降至正常,但与正常对照组比较差异无显著性(P>0.05)。结论:COX2的蛋白表达及COX2mRNA水平在缺血性坏死心肌中明显增加,提示COX2的表达与纤维化程度有关联,可能参与了心肌纤维化的过程。
Objective: To study the expression of cyclooxygenase 2 (COX2) in myocardial fibrosis and its significance. Methods: Myocardial necrosis model was established by injecting isoproterenol (Iso) 15mg.kg-1 into rat heart. Serum aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzyme (CK-MB). The expression of COX2 protein was analyzed by immunohistochemistry and COX2 mRNA was analyzed by RT-PCR. Results: Compared with the normal control group, serum LDH, CK and CK-MB peaked at 4h after injection of Iso (P <0.05), and peaked at 6h (P <0.05). The expression of COX2 protein increased with the severity of the disease, compared with the normal control group, the difference was significant (P <0.05). The expression of COX2 mRNA showed that the COX2 mRNA expression gradually increased from 2 to 12 hours after injection of Iso, but there was no significant difference compared with the normal control group (P> 0.05); COX2 mRNA expression was significantly increased from 24 to 48 hours after injection of Iso (P <0.05). After 48 hours, the mRNA expression gradually decreased and did not drop to normal level after 3 weeks, but there was no significant difference compared with the normal control group (P> 0.05). CONCLUSION: The expression of COX2 protein and the level of COX2 mRNA in myocardium of ischemic necrosis are significantly increased, suggesting that the expression of COX2 is correlated with the degree of fibrosis and may be involved in the process of myocardial fibrosis.