has the effect of lowering blood glucose and improving insulin resistance (IR). However, its underlying mechanism remains unclear. In this study, a rat model of type 2 diabetes (T2D) was created to explore whether
acidic polysaccharide (SCAP) would improve the IR in T2D rats by inhibiting inflammation. A combination of a high-fat diet and low dose of streptozotocin (STZ, 30 mg/kg, intraperitoneally) were administered to rats for establishing the T2D model. Then, these T2D rats were orally administered with SCAP (25, 50, or 100 mg/kg) for 8 weeks. The results indicated that SCAP significantly lowered the fasting blood glucose, elevated the fasting insulin, and improved glucose tolerance. SCAP also decreased the serum interleukin-1
), interleukin-6 (IL-6), tumor necrosis factor-
), C-reactive protein (CRP), and nuclear factor-
B) levels, as well as their mRNA expression in the liver tissue. Further, SCAP significantly inhibited the upregulation of phosphorylated c-Jun N-terminal kinase (p-JNK) and NF-
B protein, and it increased phosphorylated insulin receptor substrate-1 (p-IRS-1), phosphorylated phosphatidylinositol 3-kinase (p-PI3K), and phosphorylated protein kinase B (p-AKT) protein expression levels significantly. These results suggest that SCAP improves the IR in T2D rats by inhibiting inflammation.