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[1]马立荣,李建宁,栾延松,等.Bcl-2、Bax、Insulin在高脂诱导C57BL/6J小鼠胰岛损伤中的表达[J].宁夏医科大学学报,2018,(04):393-397.[doi:10.16050/j.cnki.issn1674-6309.2018.04.005]
 MA Lirong,LI Jianning,LUAN Yansong,et al.Expression of Bcl-2,Bax and Insulin in Pancreatic Islet Injury of C57BL/6J Mice Induced by High Fat Diet[J].Ningxia Medical University,2018,(04):393-397.[doi:10.16050/j.cnki.issn1674-6309.2018.04.005]
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Bcl-2、Bax、Insulin在高脂诱导C57BL/6J小鼠胰岛损伤中的表达(PDF)
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《宁夏医科大学学报》[ISSN:1005-8486/CN:64-1029/R]

卷:
期数:
2018年04期
页码:
393-397
栏目:
论 著
出版日期:
2019-09-30

文章信息/Info

Title:
Expression of Bcl-2,Bax and Insulin in Pancreatic Islet Injury of C57BL/6J Mice Induced by High Fat Diet
作者:
马立荣12 李建宁12 栾延松12 李雨涵12 宋 辉13 杨 怡12
(1. 宁夏医科大学基础医学院生物化学与分子生物学系,银川 750004; 2. 宁夏医科大学内分泌研究所, 银川 750004; 3. 宁夏医科大学基础医学院细胞生物学与遗传学系,银川 750004)
Author(s):
MA Lirong12 LI Jianning12 LUAN Yansong12 LI Yuhan12 SONG Hui13 YANG Yi12
(1. Department of Biochemistry and Molecular Biology,School of Basic Medical Science, Ningxia Medical University,Yinchuan 750004; 2. Institute of Endocrinology,Ningxia Medical University,Yinchuan 750004; 3.Department of Cell Biology and Genetics,School of Basic Medical Science, Ningxia Medical University,Yinchuan 750004)
关键词:
高脂胰岛损伤细胞凋亡胰岛素
Keywords:
high fat dietpancreas injurycell apoptosisinsulin
分类号:
R817.4
DOI:
10.16050/j.cnki.issn1674-6309.2018.04.005
文献标志码:
A
摘要:
目的 探讨细胞凋亡因子在高脂引起的小鼠胰岛损伤中的表达。方法 雄性C57BL/6J小鼠分高脂饮食组(HFD)和低脂饮食对照组(LFD),每组6只,喂养12周时尾部取血进行葡萄糖耐量实验(GTT)及胰岛素耐量实验(ITT)检测胰岛功能。持续喂养至20周时处死取胰腺组织用于透射电镜,苏木素-伊红(haematoxylin-eosin,HE)染色观察胰岛形态;免疫组化(immunohistochemical,IHC)检测Bcl-2、Bax及Insulin蛋白表达水平。结果 喂养12周后,小鼠GTT和ITT显示,HFD组小鼠葡萄糖负荷时的血糖水平高于LFD 组(P<0.05)。注射胰岛素后,HFD组小鼠血糖下降缓慢且血糖水平仍较LFD组高(P<0.05)。HE结果显示HFD组小鼠胰岛数量和体积较LFD组减少,形态损伤严重。电镜下观察HFD组胰岛β细胞超微结构受损较LFD组严重,HFD组β细胞形态不规则,细胞核固缩,染色质边集,有大量电子密度较小的脂滴堆积,其中胰岛细胞胞浆内胰岛素分泌颗粒减少。免疫组化的结果显示:HFD组Bcl-2表达低于低脂组,同时HFD组Bax表达高于LFD组,而HFD组胰岛中的Insulin表达低于LFD组(P<0.01)。结论 高脂导致C57BL/6J小鼠胰岛细胞结构功能损伤,影响胰岛素的合成与分泌,并且增加细胞凋亡。Bcl-2 及Bax 在胰岛细胞凋亡中起一定的作用,并可能与高脂饮食有关。
Abstract:
Objective To investigate the expression of apoptotic factors in islets of mice induced by high fat. Methods C57BL/6J male mice were divided into high fat diet group(HFD) and low fat diet control group (LFD),with 6 rats in each group. At 12 weeks, the glucose tolerance and insulin tolerance test were used to detect the islet function. The pancreas tissue was sacrificed at 20 weeks for transmission electron microscopy, and haematoxylin-eosin(HE) staining was used to observe the morphology of the islet,and the expression of Bcl-2,Bax and Insulin protein was detected by immunohistochemical(IHC). Results After 12 weeks of feeding,glucose tolerance and insulin tolerance test in mice showed that the glucose level of HFD group was higher than that of group LFD(P<0.05). After injection of insulin, blood glucose in group HFD decreased slowly and blood glucose level was higher than that in group LFD(P<0.05). HE results showed that the number and volume of islets in HFD group were lower than those in LFD group,and the morphological damage was serious. Under electron microscope,the ultrastructure of islet beta cells in group HFD was damaged more seriously than that in group LFD. In group HFD,the morphology of beta cells was irregular,nuclear condensation, chromatin set, and a large number of small electron density lipid droplets accumulated, and insulin secreting granules in the islet cell cytoplasm decreased. The results of immunohistochemistry showed that the expression of Bcl-2 in group HFD was lower than that in low fat group, while the expression of Bax in group HFD was higher than that in group LFD,and the expression of Insulin in group HFD was lower than that in group LFD(P<0.01). Conclusion High fat can induce structural damage of islet cells in C57BL/6J mice, affect insulin synthesis and secretion, and increase cell apoptosis. Bcl-2 and Bax play a role in the apoptosis of islet cells and may be related to the high fat diet.

参考文献/References:


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备注/Memo

备注/Memo:
收稿日期:2017-11-22
基金项目:宁夏自然科学基金(NZ16066);宁夏医科大学科学研究基金(XY2017001);宁夏高等学校一流学科建设资助项目(NXYLXK2017B07)
作者简介: 马立荣(1983-) ,女,宁夏人,在读硕士研究生。
通信作者: 杨怡(1973-),女,甘肃人,教授,博士,从事内分泌与代谢性疾病机制研究。E-mail: yangyi73422@163.Com
更新日期/Last Update: 2018-04-30