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衰老模型小鼠胰腺結(jié)構(gòu)與功能的變化

發(fā)布時(shí)間:2019-01-11 08:19
【摘要】:目的探討D-半乳糖(D-gal)致衰小鼠胰腺結(jié)構(gòu)與功能變化。方法 2月齡雄性C57BL/6J小鼠隨機(jī)分為兩組,每組10只。衰老組:小鼠皮下注射D-gal(120mg/kg),每天1次,共42 d;對(duì)照組:小鼠皮下注射等時(shí)與等量生理鹽水。衰老模型建立完成第2天,采外周血測定空腹血糖(FBG)與空腹胰島素(FINS)水平;稱小鼠體重(g)與胰腺濕重(mg)計(jì)算胰腺臟器指數(shù);石蠟切片,HE染色觀察胰腺光學(xué)顯微鏡下形態(tài);制備胰腺冷凍切片,檢測衰老相關(guān)β-半乳糖苷酶(SA-β-Gal)染色陽性胰腺細(xì)胞的相對(duì)吸光度(RA);免疫組織化學(xué)法觀察胰腺組織晚期糖基化終產(chǎn)物(AGEs)的RA;制備胰腺組織勻漿檢測超氧化物歧化酶(SOD)、總抗氧化能力(T-AOC)和丙二醛(MDA)的含量。結(jié)果衰老組小鼠FBG顯著升高,FINS水平降低;胰腺濕重和胰腺臟器指數(shù)明顯升高;胰腺光學(xué)顯微鏡下結(jié)構(gòu)未見顯著改變,但胰島內(nèi)單個(gè)有核細(xì)胞所占面積增加;胰腺SA-β-Gal染色陽性細(xì)胞數(shù)顯著增加;AGEs陽性表達(dá)區(qū)域RA值明顯升高;SOD與T-AOC含量顯著降低,MDA含量顯著升高。結(jié)論 D-gal復(fù)制衰老小鼠可致其胰腺損傷,其機(jī)制與D-gal致胰腺組織細(xì)胞的氧化應(yīng)激損傷有密切關(guān)系。
[Abstract]:Objective to investigate the changes of pancreatic structure and function in aging mice induced by D-galactose (D-gal). Methods two-month old male C57BL/6J mice were randomly divided into two groups with 10 mice in each group. Aging group: mice were subcutaneously injected with D-gal (120mg/kg) once a day for 42 days; control group: mice were subcutaneously injected with the same amount of normal saline. On the second day after the establishment of the aging model, fasting blood glucose (FBG) and fasting insulin (FINS) were measured in peripheral blood, and the pancreatic organ index was calculated by weight (g) and wet weight (mg) of pancreas. Paraffin sections, HE staining to observe the morphology of pancreas under optical microscope; preparation of frozen sections of pancreas to detect relative absorbance of pancreatic cells with SA- 尾-Gal staining The content of total antioxidant activity (T-AOC) of superoxide dismutase (SOD),) and malondialdehyde (MDA) in pancreatic tissue homogenate was determined by immunohistochemical method. Results in aging group, FBG was significantly increased, FINS level was decreased, wet weight of pancreas and pancreatic organ index were significantly increased, the structure of pancreas was not changed significantly under optical microscope, but the area of single nucleated cells in pancreatic islets increased. The number of SA- 尾-Gal positive cells in pancreas was significantly increased, the RA value of AGEs positive region was significantly increased, the contents of SOD and T-AOC were significantly decreased, and MDA content was significantly increased. Conclusion D-gal replication can induce pancreatic injury in aging mice, and its mechanism is closely related to oxidative stress injury of pancreatic tissue cells induced by D-gal.
【作者單位】: 重慶醫(yī)科大學(xué)干細(xì)胞與組織工程研究室組織學(xué)與胚胎學(xué)教研室;
【基金】:國家自然科學(xué)基金(30973818,81673748)
【分類號(hào)】:R-332;R339.38

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