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The aim of the present study was to examine the effects of atorvastatinon p38 phosphorylation and cardiac remodeling after myocardial infarction in rats. A total of 43 rats were randomly divided into the control, sham operation, post-modeling medication (medication) and post-modeling non-medication (non-medication) groups. The control group did not receive any treatment. Anterior descending arteries of the rats in the medication and non-medication groups were ligated, and threading at the anterior descending arteries was conducted for the rats in the sham operation group. Atorvastatin (10 mg/kg) was given daily to the rats in the medication group, and an equivalent amount of normal saline was given daily to the rats in the sham operation group. Four weeks later, the cardiac function, morphological changes in the myocardial cells, and the expression of tumor necrosis factor-α (TNF-α) and p38 in each group was detected. At 4 weeks after treatment, the myocardial infarction size, fibrosis and myocardial necrosis of the rats in the medication group was examined compared with those in the non-medication group (P<0.05). The cardiac function of the rats in the non-medication group was significantly lower than that of the rats in the control and sham groups (P<0.05), while it was obviously elevated in the medication group compared with that in the non-medication group (P<0.05). The expression of TNF-α and phosphorylated p38 of the left ventricle in the non-medication group was higher than that in the control group (P<0.05), while it was obviously reduced in the non-medication group compared with that in the control group (P<0.05). Atorvastatin can improve cardiac remodeling after myocardial infarction in rats, which may be associated with its inhibition of p38 phosphorylation and its decrease of TNF-α expression. [ABSTRACT FROM AUTHOR]