Effect Of Rosiglitazone Sodium On The Apoptosis Of Beta Cells In Rats With Experimental Type 1 Diabetic Mellitus

Objective:To explore the effect of rosiglitazone sodium on the apoptosis of pancreatic beta cells in rats with experimental type 1 diabetic mellitus.Methods:72 SD rats were randomly assigned as normal control group(group A,n=24),diabetes mellitus group(groupB,n=24) and RSG natrium treatment group(group C,n=24).STZ were administered intraperitoneally at a dose of 65mg/kg body weight for group B and group C.We determined FBG levels of rats in 3 days,and those,with FBG≥16.7mmol/L were served as diabetes models.Then RSG natrium were given to the rats in group C via intragastric administration at a dose of 7mg/kg.d^-1,while solvent were applied at the same dose and method to group A and B.Three days after the administration of STZ and 2-,5-,7- 10- and 13 weeks after the administration of RSG natrium,4 rats out of groups were put to death respectively.Blood samples were collected for the assessment of FBG and FINS.Pancreas specimens were removed and preserved in the same time for subsequent use.The morphologic changes were observed under light and electron microscopes.The apoptosis of beta cell was evaluate by TUNEL assay and the levels of expression for Insulin and Fasl were performed by immunohistochemistry.Results:Two weeks after RSG treatment,the decreased levels of weight and FINS increased while the elevated FBG levels decreased gradually in group C comparing with group B(all P＜0.05).The functional beta cell mass were raised. The amount of secretory granule in beta cells increased simultaneously.The levels of expression for INS in the pancreas islet was higher significantly than that in group B(P＜0.05).The relative index of apoptosis of beta cells in group C was lower than group B(P＜0.05).The upgraded levels of Fasl were downgraded. The positive area density of Fasl has a negetive correlation with the levels of INS expressing in the islets(r=-0.67,P＜0.01),but a positive correlation with the relative index of apoptosis of beta cells(r=0.71,P＜0.02).Conclusions:Rosiglitazone natrium can inhibit or down regulate the apoptosis of beta cells to some extent in experimental type 1 diabetic rats,and one of the mechanisms was probably through inhibiting the apoptosis pathway of Fas/Fasl.