Study On Antidiabetic Effect Of Schisandra Chinensis Acidic Polysaccharide

Objective:To observe the therapeutic effect of Schisandra chinensis acidic polysaccharide（SCAP）on type 1 diabetes mellitus（T1DM）in mouse induced by streptozotocin（STZ）,H₂O₂-induced MIN6 cell injury model and type 2 diabetes mellitus（T2DM）in rat induced by high-fat diet（HFD）with STZ and explore its underlying mechanism.Methods:（1）T1DM model in mouse was established by traperitoneal injection with STZ（30 mg/kg）for 5 d and was treated with SCAP 4 weeks.The levels of fasting blood glucose（FBG）and fasting insulin（FINS）,malondialdehyde（MDA）content and superoxide dismutase（SOD）activity in the serum were tested.The pathological changes of the mice’s pancreas issue were performed by hematoxylin-eosin（HE）staining.The expressions of P-JNK,JNK,Bcl-2,BAX and Cleaved Caspase-3 in mice’s pancreas tissue were detected by Western blotting analysis,to investigate the therapeutic effect and mechanism of SCAP on T1DM.（2）H₂O₂-induced MIN6 cell injury models was established.The cell apoptosis was assessed by Caspase-3 activity and annexin V/PI staining in injury MIN6 cells induced by H₂O₂.The expressions of Bcl-2,BAX and Cleaved Caspase-3 in MIN6 cells were detected by Western blotting analysis,to investigate the effect of SCAP onβ-cells apoptosis.（3）T2DM model in rat was developed by giving a high-fat diet（HFD）combined with low-dose STZ,and was treated with SCAP 8 weeks.FBG,FINS,triglycerides（TG）,total cholesterol（TC）,low-density lipoprotein cholesterol（LDL-C）,high-density lipoprotein cholesterol（HDL-C）,MDA and SOD levels in the rat’s serum were measured.Oral glucose tolerance test（OGTT）was performed.The pathological changes of the rat’s pancreas issue were performed by HE staining.The expression of P-JNK、JNK、BAX、Bcl-2 and Cleaved Caspase-3 in pancreatic islet were observed by Western blotting method,to investigate the therapeutic effect of SCAP on T2DM and explore the underlying mechanism of protection of SCAP onβ-cells apoptosis.Results:（1）SCAP could decrease the level of FBG and MDA,increase the content of FINS and SOD,and improve the pathological changes in the pancreatic islet in STZ induced T1DM mice.Western blotting results indicated that SCAP treatment inhibited the up-regulation of P-JNK,BAX and Cleaved Caspase-3 protein,increased the expression of Bcl-2 in STZ induced T1DM mice.（2）SCAP could decreased Caspase-3 activity in MIN6 cells significantly.Flow cytometry analysis indicated that SCAP significantly improvedβ-cells apoptosis.SCAP treatment inhibited the up-regulation of BAX and Cleaved Caspase-3 protein,increased the expression of Bcl-2 in MIN6 cells.（3）SCAP could decrease the level of FBG and MDA,increase the content of FINS and SOD,decrease the level of TC,TG and LDL-C in the T2DM rat’s serum significantly（P<0.01 or P<0.05）,and increase HDL-C levels.SCAP improved the pathological changes in rat’s pancreatic islet.Furthermore,SCAP inhibited the up-regulation of P-JNK,BAX and Cleaved Caspase-3 proteins,and increased Bcl-2 protein expression.Conclusions:SCAP has a therapeutic effect on T1DM in mice induced by STZ and T2DM in rats induced by HFD combined with STZ.SCAP has a protect effect on MIN6 cell injury induced by H₂O₂.This mechanism might be mediated through preventing the apoptosis ofβ-cells via inhibiting the expression of JNK signal pathway.