Abstract
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 H2O2-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 H2O2-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.
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