Effect Of Rosiglitazone Sodium On Expression Of HGF In The Survival Pancreatic Islet Of Diabetic Rats

Objective To explore the effect of rosiglitazone sodium on expression of HGF in the survival pancreatic islet of diabetic rats.Methods 52 rats were randomly assigned as control group(group A)and diabetic control group(group B)and rosiglitazone sodium-treated diabetic group(group C).STZ were administered intraperitoneally at a dose of 65mg/kg body weight for both group B and group C and seventy two hours after that,fasting blood glucose(FBG)levels were assessed,those with FBG≥16.7mmol/l were served as diabetic models.Both group B and group C were executed 2 animals after being diabetic models,and then the group C animals were treated with rosiglitazone sodium(5mg/kg/d)via intragastric administration each day.One-,two-,four-,Seven-,and ten weeks after the administration of rosiglitazone sodium,both group B and group C were executed 4 animals respectively.Pancreas samples were removed and preserved for subsequent use.Fasting blood samples were collected for the assessment of FBG,insulin(Ins)levels.Histopathology of pancreatic islet were observed by light microscopy.The expression levels of Ins,HGF in pancreatic islet were measured by immunohistochemistry,moreover,the islet cell morphology and cell quantity were measured.Results In group C,the decreased levels of blood INS were increased over time,and the increased FBG levels were decreased gradually.The size of pancreatic islet were enlarged,and the configuration became normal little by little,furthermore,the relativeβ-cell volume were raised significantly in those animals of group C.The expression of HGF in pancreatic islet were significantly higher in group C than that of group B after two weeks treatment with rosiglitazone sodium,and the expression levels of HGF were paralleled to FBG and relativeβ-cell volume.Conclusions Rosiglitazone sodium can mostly through promoting the proliferation of beta cell to increase beta cell mass in experimental diabetic SD rats.The mechanism of action of rosiglitazone sodium may be related with the upregulated expression of HGF in pancreatic islet.