中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2013年
12期
1052-1055
,共4页
王勇%杨健%钟枢哲%刘金钢
王勇%楊健%鐘樞哲%劉金鋼
왕용%양건%종추철%류금강
糖尿病,实验性%胃促生长素%胰岛β细胞%内质网应激
糖尿病,實驗性%胃促生長素%胰島β細胞%內質網應激
당뇨병,실험성%위촉생장소%이도β세포%내질망응격
Diabetes mellitus,experimental%Ghrelin%Pancreas β-cells%Endoplasmic reticulum stress
目的 探讨胃促生长素(ghrelin)各亚型对高糖诱导的大鼠INS-1胰岛β细胞损伤的影响.方法 大鼠INS-1胰岛β细胞分别在正常血糖组(5.6 mmol/L葡萄糖)、高糖组(33.3 mmol/L葡萄糖)、乙酰化胃促生长素组(33.3 mmol/L葡萄糖+10 nmol/L乙酰化胃促生长素)、非乙酰化胃促生长素组(33.3mmol/L葡萄糖+10 nmol/L非乙酰化胃促生长素)孵育不同时间后,应用MTT法检测细胞存活率,分光光度计检测caspase-3活性,激光共聚焦检测GRP78,细胞色素c表达并观察细胞形态.结果 高糖刺激可增加胰岛β细胞凋亡,caspase-3、GRP78、细胞色素C表达增高;乙酰化胃促生长素或非乙酰化胃促生长素均可抑制caspase-3、GRP78、细胞色素c表达,并进而抑制胰岛β细胞凋亡(均P<0.05).结论 胃促生长素可通过抑制内质网应激和线粒体功能障碍改善持续性高糖引起的大鼠INS-1胰岛β细胞损伤.
目的 探討胃促生長素(ghrelin)各亞型對高糖誘導的大鼠INS-1胰島β細胞損傷的影響.方法 大鼠INS-1胰島β細胞分彆在正常血糖組(5.6 mmol/L葡萄糖)、高糖組(33.3 mmol/L葡萄糖)、乙酰化胃促生長素組(33.3 mmol/L葡萄糖+10 nmol/L乙酰化胃促生長素)、非乙酰化胃促生長素組(33.3mmol/L葡萄糖+10 nmol/L非乙酰化胃促生長素)孵育不同時間後,應用MTT法檢測細胞存活率,分光光度計檢測caspase-3活性,激光共聚焦檢測GRP78,細胞色素c錶達併觀察細胞形態.結果 高糖刺激可增加胰島β細胞凋亡,caspase-3、GRP78、細胞色素C錶達增高;乙酰化胃促生長素或非乙酰化胃促生長素均可抑製caspase-3、GRP78、細胞色素c錶達,併進而抑製胰島β細胞凋亡(均P<0.05).結論 胃促生長素可通過抑製內質網應激和線粒體功能障礙改善持續性高糖引起的大鼠INS-1胰島β細胞損傷.
목적 탐토위촉생장소(ghrelin)각아형대고당유도적대서INS-1이도β세포손상적영향.방법 대서INS-1이도β세포분별재정상혈당조(5.6 mmol/L포도당)、고당조(33.3 mmol/L포도당)、을선화위촉생장소조(33.3 mmol/L포도당+10 nmol/L을선화위촉생장소)、비을선화위촉생장소조(33.3mmol/L포도당+10 nmol/L비을선화위촉생장소)부육불동시간후,응용MTT법검측세포존활솔,분광광도계검측caspase-3활성,격광공취초검측GRP78,세포색소c표체병관찰세포형태.결과 고당자격가증가이도β세포조망,caspase-3、GRP78、세포색소C표체증고;을선화위촉생장소혹비을선화위촉생장소균가억제caspase-3、GRP78、세포색소c표체,병진이억제이도β세포조망(균P<0.05).결론 위촉생장소가통과억제내질망응격화선립체공능장애개선지속성고당인기적대서INS-1이도β세포손상.
Objective To examine whether ghrelin has beneficial effect on survival of pancreatic INS-1 beta cell.Methods Rat INS-1 cells were cultured separately in 5.6 mmol/L glucose (NG group),33.3 mmol/L glucose (HG group),33.3 mmol/L glucose plus 10 nmol/L acylated ghrelin (HG+AG group),and 33.3 mmol/L glucose plus 10 μmol/L unacylated ghrelin(HG+UG group).After being incubated for different hours,cell suvival rate was determined by MTT.Activity of caspase-3 was estimated by spectrophotometry,activity of GRP78,and cytochrome c was analyzed by confocal microscopy.Results Both acylated ghrelin and unacylated ghrelin inhibited the rise in activity of GRP78,caspase-3,and cytochrome c induced by sustained high glucose.Conclusions These findings indicate that ghrelin is able to inhibit endoplasmic reticulum stress and mitochondrial dysfunction of INS-1 β-cell caused by persistent high glucose,and the effect of ghrelin is not affected by acylation.