Triptolide attenuate cardiac hypertrophy and elevate Foxp3 expression in mice

Aim To explore the role of transcription factor Foxp3 and the regulating effect of triptolide （TP） in the progression of myocardial hypertrophy in mice. Methods Fifty male mice were randomly divided into 5 groups, i. e., normal control group, myocardial hypertrophy model group and TP （10, 30, 90μg · kg^-1） treated groups. Myocardial hypertrophy was induced by isoprenaline （ISO） 5 mg kg^-1 once daily for 14 days. Triptolide was giv- en intraperitoneally once daily. Left ventricle tissue was subjected to HE staining and chemiluminescence technique to assess effects on hypertrophy, fibrosis and inflammation, quantitative assessment of hypertrophy regulatory genes were performed by qPCR and WB. Results After 14 days of treatment, myocardial expressions of Foxp3 and CD4 were significantly reduced in the model group compared with controls. The expression level of TGFβ1 in control group was lower, while that in model group increased obviously. TP could significantly lessen myocardial tissue damage, and reduce the heart index and left ventricular index. Compared with model group, TP （30, 90 μg · kg^-1 ） significantly increased myocardial expression ratio of α-MHC to β-MHC, reduced serumal levels of BNP and troponin I, elevated mRNA and protein expressions of Foxp3 and CD4 in myocardial tissue and reduced the protein expression of TGFβ1 by comparison of those in model group. Conclusion TP can effectively ameliorate myocardial damage and inhibit left ventricular remodeling through elevating the expression of CD4 and Foxp3 and decreasing that of TGF-β.