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Polysaccharide is a key bioactive component of Schisandra chinensis and has significant pharmacological activities. The aim of this study was to evaluate the anti-diabetic effect of acidic polysaccharide from Schisandra chinensis (SCAP). Type 2 diabetic (T2D) rats were developed by giving a high-fat diet (HFD) combined with low-dose streptozotocin (STZ), and administered orally with SCAP (25, 50 mg/kg) for 8 weeks. Fasting blood glucose (FBG), fasting insulin (FINS), triglycerides (TG), total cholesterol (TC), lowdensity lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), malondialdehyde (MDA), and superoxide dismutase (SOD) in the rat's serum were measured. Oral glucose tolerance test (OGTT) and pathological changes of pancreas were observed. Furthermore, expressions of c-Jun N-terminal kinase (JNK), B-cell lymphoma 2-associated X protein (BAX), B-cell lymphoma 2 (Bcl-2), and Cleaved Caspase-3 in pancreatic islet were detected. The results showed that SCAP decreased FBG, TG, TC, LDL-C and MDA levels, increased insulin, HDL-C levels and SOD activity, improved the pathological changes in pancreatic islet. Furthermore, SCAP inhibited the up-regulation of phosphorylated JNK, BAX and Cleaved Caspase-3 proteins, and increased Bcl-2 protein expression. These data indicate that SCAP has a therapeutic effect in T2D rats, and the mechanism may be related to its protection against β-cells apoptosis by regulating apoptosis-related proteins expression to alleviate the injury caused by the oxidative stress.

Polysaccharide, one of the main components in Schisandra chinensis, has been discovered to have an antidiabetic effect. In this study, we further observed the effect of the secondary component of Schisandra polysaccharide, acidic polysaccharide, on diabetes induced by streptozotocin (STZ) in mice and H 2 O 2 -induced MIN6 cell injury model and investigated the underlying mechanisms at the same time. The results showed that S. chinensis acidic polysaccharide (SCAP) could increase the content of fasting blood insulin and the activity of superoxide dismutase, lower the level of fasting blood glucose and malondialdehyde, and improve the pathological changes in the pancreatic islet in STZ-induced diabetic mice. SCAP decreased the percent of apoptotic cells and increased Cleaved Caspase-3 activity in H 2 O 2 -incubated cells. Furthermore, SCAP treatment inhibited the upregulation of phospho C-Jun N-terminal kinase (JNK), BAX, and Cleaved Caspase-3 protein expressions, and increased the expression of Bcl-2. These results indicate that SCAP has a therapeutic effect on STZ-induced diabetic mouse, and this protective effect may be mediated through preventing the apoptosis of β-cells via inhibiting the expression of JNK and related apoptotic proteins.