ABSTRACT
Objective To explore the effect of D-galactose(D-gal) on murine pancreatic injury and its pathogenesis.Methods C57BL/6J mice were randomly divided into control group and D-gal model group [D-gal 120 mg/(kg · d) for 42 days].On the 2nd day after drug injection completed,the peripheral blood was taken for measuring the level of fasting blood glucose(FBG) and fasting insulin(FINS);and then the organ index of pancreas was calculated by the ratio of pancreatic wet weight(mg) and mouse body weight(g);HE stain was routinely prepared to observe the histologic structure of pancreatic tissue;the TEM was used to analyze ultrastructural changes of pancreatic cells;the pancreatic frozen sections were prepared to test senescence-associated β-galactosidase (SA-β-gal) and its relative absorbance(RA) of positively stained cells in the pancreatic islets;immunohistochemistry assays to study advanced glycation end products (AGEs) and its RA;pancreas tissue homogenate was made to detect the content of superoxide dismutase(SOD),malonaldehyde(MDA) and total antioxidant capacity(T-AOC).Results In D-gal group mice,the FBG increased(P＜0.05) and FINS reduced;pancreas wet weight and organ increased obviously (P＜0.01);light microscopic structure of the pancreas presented without typical pathologic change,however the single nucleated cell's area within the islet was increased significantly(P＜0.05);the pancreas endocrine and exocrine cells were showed the ultrastructure damaged and lipofuscin formation increased;the RA of positive pancreas cells in SA-β-gal staining increased(P＜0.05);the RA of AGEs positive regional expression markedly increased (P＜0.01);the content of SOD and T-AOC decreased (P ＜ 0.05),the content of MDA increased (P ＜ 0.01).Conclusions Aging mice model replicated by D-gal can cause the pancreatic injury,its mechanisms may be closely related to oxidative injury of pancreatic cells caused by D-gal.