WANG Zhentao1, HAN Lihua1, CHAI Songbo1, et al. Effect of Kangxian Yixin Formula on MMP-1 and TIMP-1 Expressions in Dilated Cardiomyopathy Heart Failure Rats[J]. Journal of Traditional Chinese Medicine2011, 52(16): 1406-1408.
WANG Zhentao1, HAN Lihua1, CHAI Songbo1, et al. Effect of Kangxian Yixin Formula on MMP-1 and TIMP-1 Expressions in Dilated Cardiomyopathy Heart Failure Rats[J]. Journal of Traditional Chinese Medicine2011, 52(16): 1406-1408.DOI: 10.13288/j.11-2166/r.2011.16.019.
Objective To observe the effect of Kangxian Yixin Formula(Formula for relieving fibrosis and tonifying the heart) on the expression of myocardial matrix metalloproteinase-1(MMP-1) and tissue inhibitor of metalloproteinase-1(TIMP-1).Methods One hundred Wistar male rats were randomized into normal group
10 rats
and model group
90 rats.The dilated cardiomyopathy models were established by raising with furazolidone solution for 8 weeks.Then 70 successfully made models were randomized into 5 groups
i.e.model group
captopril group
Kangxian Yixin Formula high-dose and low-dose groups
and integrated Chinese and western medicine group
with 14 in each.The models were given normal saline
captopril 10.125mg/kg
Kangxian Yixin Formula 18.8g/kg or 4.7 g/kg
and the mixture of Kangxian Yixin Formula high-dose and captopril respectively as intervention for 8 weeks.Six rats of each group randomly selected were treated with immunohistochemical staining for measuring the expressions of MMP-1 and TIMP-1.Results Compared with the model group
the MMP-1 expression in the integrated Chinese and western medicine group
Kangxian Yixin Formula high-dose group
and captopril group was significantly down-regulated(P<0.05)
the TIMP-1 expression up-regulated(P<0.05).MMP-1 expression in the Kangxian Yixin Formula low-dose group was down-regulated(P<0.05)
while its TIMP-1 expression was not different from that in the model group(P>0.05).Conclusion Kangxian Yixin Formula could effectively down-regulating MMP-1 expression and up-regulating TIMP-1 expression.This may be one of its functional mechanisms in inhibiting the remodeling of ventricle of heart through relieving the myocardial fibrosis of dilated cardiomyopathy heart failure rats.