AIM:To study the activity alteration of matrix metalloproteinases (MMPs) in the rat cardiomyopathy induced by L
thyroxine
and involved mechanism. METHOD: Male Sprague Dawley rats were randomly divided into three groups and administrated suspension of L
thyroxine (sc,0.4 mg/kg·d -1 ) for consecutive 10 d except for normal group. L thyroxine treated rats were given CPU 0213(po, 100 mg/kg·d -1 )in group CPU 0213 for 3 d. The whole collagen content, MDA and SOD in myocardium were measured. Relative left ventricular activity level of MMPs was determined by substrate zymography. Furthermore, relative left ventricular mRNA level of proα2 (Ⅰ) collagen were detected with semi quantitative RT PCR. RESUIT: The whole collagen content and proα2 (Ⅰ) collagen mRNA expression were
decreased in L thyroxine group and increased in the group CPU 0213. In L thyroxine group the activity of SOD was decreased but increased in CPU 0213 group and the content of MDA in L thyroxine group was increased but decreased in CPU 0213 group. The activity of MMPs (MMP 2, MMP 9) was downregulated in L thyroxine group and CPU 0213 group had litter effect on the activity of MMPs. CONCLUSION:Myocardial hypertrophy induced by L Thyroxin, a kind of cardiac hypertrophy that is accompanied by less cardiac fibrosis is mediated partly by ET 1. In L thyroxine induced hypertrophic myocardium oxidative stress is enhanced. CPU 0213 could inhibit oxidative stress and increase collagen content. The hypertrophic myocardium mechanic induced by L thyroxine was related to ET 1.