Objective: To analysis the molecular mechacnism of the signal transduction Calcineurin-nuclear factor of activated T cells (CaN-NFAT3) in the treatment of heart failure with Sini decoction. Method: Sixty SPF grade SD rats were dividied into control group (n＝10)and model group(n＝50). Adriamycin was given intraperitoneally to fifty to copy the model of heart failure.The heart failure rats were divided into model group and Sini decoction treating group(high

middle and low dose group).Giving Sini decoction to the treatment groups for eight days

CaN activity kit and calcium content kit

NFATc protein relatively express kit

respectively

were used to detect the activity of CaN and calcium NFAT3 expression of the dephosphorylation protein. Result: Compared with model group

the activity of CaN in high dose group and middle dose group was obviously lower. The calcium content increased significantly. In the rats myocardial tissue

the light density ratio of dephosphorylation NFATc/β-actin was lower than model group (P<0.05). Conclusion: The CaN-NFAT3 signal transduction pathways may be suppressed

which can explay the key molecular mechanism of Sini decoction in treatmentof heart failure.