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[Objective] To explore protective effects of naringin on myocardial structure function with STZ-induced diabetic cardiomyopathy in rats via regulation of peroxisome proliferation factor receptor γ (PPARγ) and its possible mechanism. [Method] 80 male Wister experimental rats of Type 2 diabetic cardiomyopathy of 6-week old were randomly divided into five groups of 16 each, including the model control group, low-, medium-, high-dose naringin treatment groups, PPARγ agonist pioglitazone treatment group. 16 normal rats were used as the normal control. After oral administration of different doses of naringin (40, 20, 10 mg/kg·d), the expression of PPARγ was tested by immunohistochemistry and the expression of peripheral blood B brain natriuretic peptide (BNP) and cardiac troponin I (cTnI) were detected by quantitative immunofluorescence. The myocardial cell ultra-structure was observed under the transmission electron microscope. [Result] ① In the model control group, the enhanced PPARγ expression was prominently stained in endothelial cells and myocardial cell cytoplasm area. Compared with the normal control group, oral glucose tolerance test (OGTT) was positive, the level of heart/body weight, FFA, HOMA-iR, GSP and BNP increased, and the myocardial cell ultra-structure was injured in diabetes cardiomyopathy model control group. ② Compared with the model control group, the enhanced PPARγ expression were down-regulated, PPARγ positive vascular density weaken and the corresponding gray value increased (P<0.05), the injury in the myocardial cell ultra-structure and OGTT ameliorated, the level of heart/body weight, FFA, HOMA-iR, GSP and BNP decreased in the medium- or high-dose naringin and pioglitazone treatment groups. ③ Compared with the pioglitazone treatment group, the level of decrease was better in BNP but poor in HOMA-iR in the high-dose naringin treatment group (P<0.05). [Conclusion] Naringin could ease the injury in the myocardial cell ultra-structure. Its mechanisms may be associated to regulating myocardial PPARγ express mediated improvement of insulin resistance, blocking activation of FFA and inhibiting BNP.