| Objective To observe the effect of IRS-2 expression in diabetic rat pancreatic beta cells after rosiglitazone sodium treatment and explore the regulated effect of rosiglitazone sodium to survival pancreatic beta cells.Methods 58 rats were randomly assigned as control group(group A),diabetes mellitus group(group B)and rosiglitazone sodium-treated group(group C).STZ were administered intraperitoneally at a dose of 60mg/kg for both group B and group C.After 72 hours,animals with FBG≥16.7mmol/L were served as diabetic models.Each group was executed two animals after being successfully built diabetic models,and the animal of group C were treated with rosiglitazone sodium(7mg/kg.d-1)gastric perfusion.After rosiglitazone sodium treatment,two animals from each group were executed in 2-,4-,6-,8week and the rest animals were all executed in the end of 10 week.Pancreas samples were removed and preserved for subsequent use.Fasting blooding samples were collected for the assessment of FBG and INS levels.Histopathology and ultrastructrure of pancreatic islets were observed by light microscopy and transmission electron microscopy respectively.The expression levels for INS,IRS-2 in pancreatic islets were measured by immunohistochemistry.Results After rosiglitazone sodium treatment,the changes of group C were shown as follow:(1)the INS levels of blood were gradually increased,and the increased FBG levels were gradually decreased.(2)The pancreatic islets area and the mass of beta cells were increased.(3)The sizes of pancreatic islet were enlarged,and the configuration became normal little by little.Furthermore,the expression levels of INS in pancreatic islets were raised significantly higher than that of group B after two weeks treatment with rosiglitazone sodium.(4)The expression levels of IRS-2 in pancreatic islets were higher than group B,meanwhile,it also paralleled to FINS and the expression levels of INS in pancreatic islets. Conclusions(1)Rosiglitazone sodium can mostly increase beta cells mass in experimental diabetic SD rats by promoting the proliferation of survival beta cells.(2)The mechanism of action of rosiglitazone sodium may be related with the upregulated expression of IRS-2 in pancreatic islet. |
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