基础医学与临床 ›› 2017, Vol. 37 ›› Issue (7): 912-917.

• 研究论文 • 上一篇    下一篇

D-半乳糖致小鼠胰腺损伤

黄杰,董照瀛,许梦雄,晏红,陈粼波,王璐,王亚平   

  1. 重庆医科大学
  • 收稿日期:2016-08-18 修回日期:2016-11-01 出版日期:2017-07-05 发布日期:2017-06-23
  • 通讯作者: 王亚平 E-mail:ypwangcq@aliyun.com
  • 基金资助:
    国家自然科学基金资助项目;重庆医科大学大学生科学研究与创新实验项目

Murine pancreatic injury induced by D-galactose

  • Received:2016-08-18 Revised:2016-11-01 Online:2017-07-05 Published:2017-06-23

摘要: 目的 探讨D-半乳糖(D-gal)对小鼠胰腺的损伤及其机制。方法 C57BL/6J小鼠随机分为对照组和D-gal组(D-gal 120 mg/kg,qd×42)。注射完成第二天,采外周血测定空腹血糖(FBG)与空腹胰岛素(FINS)水平;称小鼠体质量(g)与胰腺湿重(mg)计算胰腺脏器指数;HE染色观察胰腺组织形态学;透射电镜观察胰腺细胞超微结构;制备冷冻切片,衰老相关β-半乳糖苷酶(SA-β-Gal)染色检测胰岛内染色阳性细胞的相对吸光度(RA);免疫组织化学法观察胰腺组织晚期糖基化终产物(AGEs)的RA值;制备胰腺组织匀浆检测超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)和丙二醛(MDA)含量。结果 D-gal组小鼠FBG显著升高(P<0.05),FINS水平降低;胰腺湿重和胰腺脏器指数明显升高(P<0.01);胰腺光镜结构无显著损伤,但胰岛内单个有核细胞所占面积增加(P<0.05);胰腺内外分泌部显示细胞超微结构损伤,脂褐素明显沉积;胰腺SA-β-Gal染色阳性细胞的RA值增加(P<0.05);AGEs阳性表达区域RA值升高(P<0.01);SOD与T-AOC含量降低(P<0.05),MDA含量升高(P<0.01)。结论 D-gal复制衰老小鼠模型可致胰腺损伤,可能机制与D-gal致胰腺细胞氧化应激损伤有关。

关键词: D-半乳糖, 衰老模型, 胰腺, 氧化损伤, 小鼠

Abstract: Objective To explore the effect of D-galactose(D-gal)on murine pancreatic injury and its mechanism.Methods C57BL/6J mice were randomly divided into Control group and D-gal model group(D-gal 120mg/kg/d for 42 days).On the 2nd day after drug injection completed,the peripheral blood were taken for measuring the level of fasting blood glucose(FBG) and fasting insulin(FINS);and then the organ index of pancreas were calculated by the ratio of pancreatic wet weight(mg) and mouse body weight(g);HE stain were routinely prepared to observe the histologic structure of pancreatic tissue;the transmission electron microscopy 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; mmunohistochemistry 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 markedly(P<0.05) and FINS reduced; pancreas wet weight and organ index raised 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 obviously(P<0.05); the RA of AGEs positive regional expression markedly increased(P<0.01); the content of SOD and T-AOC decreased obviously(P<0.05), the content of MDA increased markedly(P<0.01). Conclusion 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.

Key words: D-Galactose, aging model, pancreas, oxidative injury, mice

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