Protective Effects and Mechanism of Cyclocarya Paliurus Polysaccharides on Diabetic Mice

BAI Yuxiao; QIN Jianshe; LIU Xin; DING Shuai; WU Chunyang; OUYANG Jingfeng

Abstract：Objective To investigate the hypoglycemic effect of cyclocarya paliurus polysaccharides (CPP) on streptozotocin (STZ)-induced diabetic mice and the possible mechanisms involved. Methods Diabetic mouse models were prepared by intraperitoneal injection of STZ. The high,medium,and low dose groups of CPP were orally administered with corresponding CPP doses,and the positive control group was orally administered metformin hydrochloride for 2 weeks. The general condition of the mice was recorded during this period,and body weight,fasting blood glucose (FBG),and oral glucose tolerance (OGT) were measured on days 0,7,and 14. Biochemical indicators in serum were measured using a biochemical analyzer after 2 weeks. ELISA was used to detect serum insulin and C-peptide levels. Pancreatic tissue from the mice was stained with HE for pathological examination. Immunohistochemistry was used to detect the expression of silent information regulator 1 (Sirt1) and adenosine monophosphate-activated protein kinase (AMPK) in pancreatic tissue. Western blot was used to measure the protein levels of nuclear factor erythroid2-related factor (Nrf2) in pancreatic tissue. Results Compared to the normal group,the FBG,area under the blood glucose curve (AUC),total cholesterol (TC),triglycerides (TG),creatinine (CRE),malondialdehyde (MDA),low-density lipoprotein cholesterol (LDL-C) levels and activities were significantly increased in the model group (P<0.01),while high-density lipoprotein cholesterol (HDL-C) and superoxide dismutase (SOD) activities were significantly decreased (P<0.01). C-peptide and insulin levels were also decreased. The pancreatic structure was disrupted,and the protein expression of Sirt1,Nrf2,and phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK) in pancreatic tissue was significantly reduced (P<0. 05). After 14 days of drug intervention,compared to the model group,the serum indicators in all CPP dose groups showed significant improvement,with notable recovery in HDL-C,C-peptide,and insulin levels (P<0. 05),indicating a significant protective effect of CPP on pancreatic damage. Conclusion CPP can effectively reduce blood glucose levels in diabetic mice,improve pancreatic tissue damage,and its mechanism may be related to the activation of the Sirt1/AMPK/Nrf2 signaling pathway by CPP.