Polysaccharides from Anemarrhena asphodeloides Bge. improve glucose and lipid metabolism in diabetic rats via the PPAR-γ/NF-κB pathway

We aim to investigate the therapeutic effects of polysaccharides from Anemarrhena asphodeloides Bge. (DT) on glucose and lipid metabolism in type 2 diabetic (T2DM) rats and explore its underlying mechanisms, with a focus on the modulation of transforming growth factor-β1 (TGF-β1), nuclear factor-κB (NF-κB), and peroxisome proliferator-activated receptor-γ (PPAR-γ) expression. The T2DM rat model was established using a high-fat and high-sucrose diet combined with intraperitoneal injection of streptozotocin (STZ). The T2DM rats were randomly divided into the model control (DM) group and different DT administration groups. Fasting blood glucose (FBG), fasting serum insulin (FINS), total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels were measured. Then, serum inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were quantified. Hepatic histopathology was assessed by hematoxylin-eosin (HE) staining. PPAR-γ expression in adipose tissue was detected via immunohistochemistry, while hepatic TGF-β1 and NF-κB mRNA levels were analyzed using reverse transcription polymerase chain reaction (RT-PCR) and Western blot (WB). DT significantly reduced the FBG, FINS, and dyslipidemia, such as TC, TG, and LDL-C levels in T2DM rats, along with decreased serum IL-6 and TNF-α levels. HE staining revealed attenuated hepatic damage in DT-treated groups. Mechanistically, DT downregulated hepatic TGF-β1 and NF-κB expression while upregulating PPAR-γ in adipose tissue. DT may ameliorate glucose and lipid metabolic disorders in T2DM rats by modulating the PPAR-γ/NF-κB pathway, with suppressing hepatic inflammatory responses via TGF-β1/NF-κB inhibition and enhancing adipose tissue metabolic regulation via PPAR-γ activation.