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目的:研究基质金属蛋白酶(MMPs)及金属蛋白酶组织抑制因子(TIMPs)在阿霉素心肌病(ADR DCM)大鼠左室心肌中的表达与意义。方法:雄性Wistar大鼠分两组:正常对照组(n=10)和ADR DCM组(n =25)。ADR DCM模型建立方法:阿霉素2.5mg/kg,尾静脉注射,每周1次,连续10周。12周时进行超声检测 评价其心功能,硫代巴比妥酸法检测丙二醛(MDA)含量,逆转录 聚合酶链反应、Western印迹分析检测MMP 2、 MMP 9及TIMP 1的表达。结果:ADR DCM组大鼠死亡率40%,左室舒张末期内径及收缩末期内径增加,左室 短轴缩短率明显下降,MDA含量增加(P<0.01)。ADR DCM组大鼠左室心肌MMP 2、MMP 9mRNA及蛋白 水平表达较正常对照组明显升高(P<0.01),而TIMP 1的表达在两组间均无统计学意义(P>0.05)。结论: ADR DCM左室心肌MMPs表达上调,MMPs可能参与ADR DCM左室重构和心力衰竭的发生发展。
Objective: To investigate the expression of MMPs and TIMPs in left ventricular myocardium of adriamycin-induced cardiomyopathy (ADR DCM) rats. Methods: Male Wistar rats were divided into two groups: normal control group (n = 10) and ADR DCM group (n = 25). ADR DCM model establishment method: doxorubicin 2.5mg / kg, tail vein injection once a week for 10 weeks. The heart function was evaluated by sonography at 12 weeks. The content of malondialdehyde (MDA) was detected by thiobarbituric acid method. The expression of MMP-2, MMP-9 and TIMP-1 were detected by reverse transcription polymerase chain reaction and Western blot analysis. Results: The mortality of ADR DCM group was 40%, the diameter of end-diastole and the end-systolic diameter of left ventricle were increased, the shortening rate of left ventricular short axis was significantly decreased and MDA content was increased (P <0.01). The mRNA and protein expressions of MMP-2 and MMP-9 in left ventricular myocardium in ADR DCM group were significantly higher than those in normal control group (P <0.01), while TIMP-1 expression was not significantly different between the two groups (P> 0.05). Conclusion: MMPs expression in left ventricular myocardium of ADR DCM is up-regulated. MMPs may be involved in the development of left ventricular remodeling and heart failure in ADR DCM.