[1]薛君力 代喆 曾姣娥 徐焱成.RIP140在姜黄素抑制MIN6细胞凋亡中的 作用机制[J].国际内分泌代谢杂志,2018,38(03):154-157162.[doi:10.3760/cma.j.issn.1673-4157.2018.03.003]
　Xue Junli*,Dai Zhe,Zeng Jiao'e,et al.Role of RIP140 in the inhibition of curcumin on apoptosis in MIN6 cells[J].International Journal of Endocrinology and Metabolism,2018,38(03):154-157162.[doi:10.3760/cma.j.issn.1673-4157.2018.03.003]
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RIP140在姜黄素抑制MIN6细胞凋亡中的 作用机制()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
38
期数:
2018年03期
页码:
154-157162
栏目:
论著
出版日期:
2018-05-20

文章信息/Info

Title:
Role of RIP140 in the inhibition of curcumin on apoptosis in MIN6 cells
作者:
薛君力 代喆 曾姣娥 徐焱成
434020 湖北省荆州市中心医院内分泌科(薛君力、曾姣娥); 430071 武汉大学中南医院内分泌科(代喆、徐焱成)
Author(s):
Xue Junli*;  Dai Zhe;  Zeng Jiao'e;  Xu Yancheng.*
Department of Endocrinology, Jingzhou Central Hospital, Jingzhou 434020, China
关键词:
受体相互作用蛋白140;  姜黄素;  胰岛β细胞;  细胞凋亡
Keywords:
Receptor interaction protein 140;  Curcumin;  Islet β cells;  Apoptosis
DOI:
10.3760/cma.j.issn.1673-4157.2018.03.003
摘要:
目的 明确受体相互作用蛋白140(RIP140)在姜黄素抑制胰岛β细胞株MIN6细胞凋亡中的作用。方法 将MIN6细胞分为对照组、高糖高脂处理组、姜黄素干预组、O-RIP140-MIN6组(过表达RIP140细胞株)、GFP-MIN6组(对照细胞株)。除对照组外,其余各组细胞给予25 mmol/L葡萄糖+500 μmol/L棕榈酸处理24 h。姜黄素干预组与O-RIP140-MIN6组、GFP-MIN6组均在25 mmol/L葡萄糖+500 μmol/L棕榈酸处理24 h前给予20 μmol/L姜黄素预处理2 h。流式细胞仪检测细胞凋亡率、Western印迹检测B细胞淋巴瘤-2(Bcl-2)、细胞外信号调节激酶(ERK)及其磷酸化水平。结果 与对照组相比,高糖高脂处理组RIP140蛋白表达、细胞凋亡率及ERK磷酸化水平均明显增加、Bcl-2表达下降(F=22.42～111.43,P均<0.01); 与高糖高脂处理组相比,姜黄素干预组细胞凋亡率及RIP140蛋白表达均明显下降、ERK磷酸化水平明显降低,Bcl-2表达升高(F=22.42～111.43,P均<0.01); 与GFP-MIN6组相比,O-RIP140-MIN6组细胞凋亡率明显升高(t=7.16, P<0.01)、ERK的磷酸化水平升高(t=8.37,P<0.01),Bcl-2表达降低(t=5.88,P<0.05)。结论 姜黄素通过下调RIP140的表达来抑制高糖高脂诱导的胰岛β细胞凋亡。
Abstract:
Objective To investigate the role of receptor interaction protein 140(RIP140)in the inhibition of curcumin on apoptosis in MIN6 cells.Methods MIN6 cells were divided into five groups: control group, high glucose and lipid group, curcumin group, O-RIP140-MIN6 group(MIN6 cells with overexpressed RIP140)and GFP-MIN6 group(empty vector group). Except for control group, all other groups were treated with 25 mmol/L glucose and 500 μmol/L palmitic acid for 24 hours. Cells in curcumin group, O-RIP140-MIN6 group and GFP-MIN6 group were pretreated with 20 μmol/L curcumin for 2 hours before the treatment of 25 mmol/L glucose and 500 μmol/L palmitic acid for 24 hours. Apoptosis rate was detected by flow cytometry, the expression of B-cell lymphoma 2(Bcl-2), extracellular regulated protein kinases(ERK)and phosphated-ERK were tested by Western blotting.Results Compared with control group, the expression of RIP140 protein, apoptosis rate and the level of phosphated-ERK were significantly increased whereas the expression of Bcl-2 was decreased in high glucose and lipid group(F=22.42-111.43, all P<0.01). However, compared with high glucose and lipid group, the apoptosis rate and the expression of RIP140 and phosphated-ERK were inhibited whereas the expression of Bcl-2 was increased in curcumin group(F=22.42-111.43, all P<0.01). Compared with GFP-MIN6 group, the apoptosis rate(t=7.16, P<0.01)and the level of phosphated-ERK(t=8.37, P<0.01)were increased and the expression of Bcl-2(t=5.88,P<0.05)was decreased in O-RIP140-MIN6 group.Conclusion Curcumin inhibits glucolipotoxicity-induced apoptosis in islet β cells via the downregulation of RIP140 expression.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金(81170769,81370872); 湖北省卫生计生科研基金(WJ2016-YZ-06)
通信作者:徐焱成,Email: xjl100901@whu.edu.cn
更新日期/Last Update: 2018-03-30