Aim To explore the regulating effect of Shengmaisan on insulin resistance and inflammation factors in rat with type 2 diabetes. Methods The Sprague Dawley rats were induced by feeding high fat diet after injection with Santa Terezinha (STZ) in order to copy the model and then they were randomly divided into six groups, the normal control group, the model control group, the Aspirin group and the low-dose, middle-dose and high-dose of Shengmaisan treatment groups. The low-dose, middle-dose and high-dose of Shengmaisan treatment groups were respectively given 4.7 g/(kg·d),9.4 g/(kg·d) and 18.8 g/(kg·d) of Shengmaisan decoction by gavage. Aspirin group was given 0.2 g/(kg·d) of aspirin suspension by gavage. The model control group and normal control group were given equivalent dose of normal saline by gavage. After four weeks administration, the fasting blood-glucose(FBG),fasting insulin(FINS),insulin sensitivity index(ISI) and homeostasis model assessment-estimated insulin resistance(HOMA-IR) were observed, and the content of serum tumor necrosis factor-α (TNF-α ), plasminogen activator inhibitor-1(PAI-1), interleukin-6(IL-6), C-reaction protein (CRP) were assayed by ELISA. Results After four weeks of medication, levels of FBG,FINS and HOMA-IR were remarkably decreased and ISI were remarkably increased in middle-dose treatment group, high-dose treatment group and aspirin group compared with the model control group (P＜0.05); Compared with aspirin group, levels of FBG,FINS,HOMA-IR were increased in low-dose treatment group, while remarkably decreased in middle-dose treatment group and high-dose treatment group; levels of ISI were decreased in low-dose treatment group, while remarkably increased in middle-dose treatment group and high-dose treatment group (P＜0.05); Compared with model control group, the content of serum TNF-α, PAI-1, IL-6, CRP were significantly lower in low-dose, middle-dose and high-dose treatment groups and aspirin group (P＜0.05). Conclusion Shengmaisan has certain protective effects on improving insulin resistance in type 2 diabetic rats by a mechanism that may be associated with the inhibition of inflammatory factors release.