Expression of MMP and TIMP in the Development of Exercise-induced Cardiac Damage and Fibrosis / 中国运动医学杂志

ABSTRACT

Objective To determine the expression of matrix metalloproteinase-1 (MMP-1) and its inhibitor in the development of exercise-induced atrial fibrosis.Methods Totally 48 eight-week-old male adult sprague-dawley rats were randomly divided into a control(C) group and a highly intensive exercise(H) group,each of 24.Group C was fed normally,while group H took one hour treadmill running with the gradient of 10°and speed of 28 m/min every weekday,lasting 5 weeks.The mRNA and protein expression of MMP-1 and matrix metalloproteinase tissue inhibitor-1 (TIMP-1) were detected using the real-time PCR and Western blotting.Results The MMP-1 expression of group H increased significantly after 8 weeks' training,compared to the control group.However,there was no significant difference in MMP-1 expression between group C and H after 12 or 16 weeks of training.The MMP-1 mRNA expression decreased with the extending of exercise,and that of group H after 16 weeks' training was significantly lower than 8 weeks' (P＜0.05).The TIMP-1 expression had an increasing trend without significance after 8-week exercise.After 12 and 16-week exercise,the mRNA and protein expression of TIMP-1 increased significantly(P＜0.01 and P＜0.05).The TIMP-1 mRNA and protein expression increased gradually with the extension of exercise,and the TIMP-1 mRNA expression of group H after 16 weeks of training was significantly higher than that after 8 weeks(P＜0.01).The ratio of MMP-1/TIMP-1 mRNA and protein increased at first and decreased afterwards.The ratio of MMP-1/TIMP-1 of group H after 16 weeks of exercise was significantly lower than group C at the same time point,and group H after 8 weeks' Conclusion After a long-term high-intensity exercise,the MMP-1 expression of atrial first increases and then decreases,while the TIMP-1 expression increases gradually.Moreover,such exercise can induce disbalance between MMP-1 and TIMP-1,maybe due to the molecular pathological mechanism of exercise-induced atrial damage and fibrosis.