Objective To explore the effects of the calmodulin dependent protein kinase Ⅱ (CaMKⅡ) regulated by Kudiezi on cardiac function and myocardial fibrosis in rats with heart failure (HF).

Methods Forty SD rats were randomly divided into 4 groups: the control group, HF group, kudiezi group and kudiezi + activated CaMKⅡ group, with 10 rats in each group. Echocardiography was used to detect the cardiac function indexes: LVEF, LVSF, LVEDD, LVESD. HE staining was used to detect the pathological changes of myocardial tissue. Myocardial fibrosis was detected by Masson staining. The protein levels of CaMKⅡ, α-SMA and Collagen Ⅲ in myocardial tissue were detected by Western blotting. RT-qPCR was used to detect the mRNA level of CaMKⅡ in myocardial tissue. ELISA was used to detect the serum levels of cTnI and BNP. The free calcium in myocardial tissue was detected by colorimetry.

Results Compared with the control group, the LVEF and LVSF in the HF group decreased, the LVEDD and LVESD increased (P ＜ 0.05), the structure of myocardial tissue was loose and disordered, the collagen fiber infiltration in myocardial space increased (P ＜ 0.05), the CaMKⅡ protein and mRNA levels in myocardial tissue increased, and the levels of α-SMA and Collagen Ⅲ protein and serum cTnI and BNP increased (P ＜ 0.05). Compared with the HF group, the LVEF and LVSF in the Kudiezi group increased, the LVEDD and LVESD decreased (P ＜ 0.05), the degree of disorder of myocardial tissue decreased, the collagen fiber infiltration in myocardial space increased (P ＜ 0.05), the CaMKⅡ protein and mRNA levels in myocardial tissue decreased, and the levels of α-SMA and Collagen Ⅲ protein and serum cTnI and BNP significantly decreased (P ＜ 0.05). Compared with the Kudiezi group, the protein levels of α-SMA and Collagen Ⅲ in myocardial tissue and serum levels of cTnI and BNP increased in the kudiezi + Urocortin Ⅱ group (P ＜ 0.05).

Conclusions Kudiezi can down-regulate the level of CaMKⅡ, and improve the cardiac function and myocardial fibrosis in HF rats.