目的 探讨D-半乳糖（D-gal）致衰小鼠胰腺结构与功能变化。 方法 2月龄雄性C57BL/6J小鼠随机分为两组，每组10只。衰老组：小鼠皮下注射D-gal（120mg/kg），每天1次，共42 d；对照组：小鼠皮下注射等时与等量生理盐水。衰老模型建立完成第2天，采外周血测定空腹血糖（FBG）与空腹胰岛素（FINS）水平；称小鼠体重（g）与胰腺湿重（mg）计算胰腺脏器指数；石蜡切片，HE染色观察胰腺光学显微镜下形态；制备胰腺冷冻切片，检测衰老相关β-半乳糖苷酶（SA-β-Gal）染色阳性胰腺细胞的相对吸光度（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；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）的含量。 结果 衰老组小鼠FBG显著升高，FINS水平降低；胰腺湿重和胰腺脏器指数明显升高；胰腺光学显微镜下结构未见显著改变，但胰岛内单个有核细胞所占面积增加；胰腺SA-β-Gal染色阳性细胞数显著增加；AGEs阳性表达区域RA值明显升高；SOD与T-AOC含量显著降低，MDA含量显著升高。 结论 D-gal复制衰老小鼠可致其胰腺损伤，其机制与D-gal致胰腺组织细胞的氧化应激损伤有密切关系。

Objective To investigate the structural and functional changes of pancreas in D-galactose(D-gal)-induced aging mice. Methods Two-month-old male C57BL/6J mice were randomly divided into aging and control groups, 10 mice per group. The aging group was injected D-gal ［120 mg/(kg·d)］ for 42 days by continuous subcutaneous injection. The control group was injected saline with the same dosage. On the 2nd day after the aging model was established, the level of fasting blood glucose (FBG) and fasting insulin (FINS) in peripheral blood were detected. The body weight(g) and wet pancreatic weight(mg) were weighted to measure pancreas organ index. Microscopic structures of the pancreatic tissue were observed after HE staining. Frozen sections of pancreas were prepared to detect the aging ofsenescence-related β-galactosidase (SA-β-Gal) positive pancreas cells. Advanced glycation end products (AGEs) and its relative absorbance (RA) of pancreas tissue were assayed by immunohistochemistry. Superoxide dismutase (SOD), malonaldehyde (MDA) and total antioxidant capacity (T-AOC) in the pancreas tissue homogenate were assayed. Results Levels of FBG, pancreas wet weight and organ index in the aging group were significantly increased compared with the control group. The level of FINS was significantly decreased. Although the structural change of pancreas was not obvious, but the proportion of the area occupied by mononuclear cells in the pancreas islet was markedly increased. The contents of SOD and T-AOC were decreased and the level of MDA was increased in pancreatic tissue homogenate. Compared with the control group, the numbers of SA-β-Gal positive cells and the content of SOD and AGEs positive region were markedly increased in the aging group. Conclusion The structural and functional damages of pancreas exist in D-gal-induced aging mice. The mechanisms may be closely related to oxidative-stress damage.