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
2011年
10期
844-848
,共5页
柴佳妮%徐明彤%薛声能%唐菊英%姜力丹%何爽%李焱%严励
柴佳妮%徐明彤%薛聲能%唐菊英%薑力丹%何爽%李焱%嚴勵
시가니%서명동%설성능%당국영%강력단%하상%리염%엄려
血管紧张素Ⅱ%血管紧张素(1-7)%胰岛β细胞%胰岛素信号通路
血管緊張素Ⅱ%血管緊張素(1-7)%胰島β細胞%胰島素信號通路
혈관긴장소Ⅱ%혈관긴장소(1-7)%이도β세포%이도소신호통로
Angiotensin Ⅱ%Angiotensin-( 1-7)%Pancreatic β cell%Insulin signaling pathway
目的 研究血管紧张素Ⅱ、血管紧张素(1-7)对胰岛β细胞胰岛素信号通路的影响.方法 小鼠胰岛β细胞株NIT-1予(1)0、10-7、10-6、10-5和10-4 mol/L浓度血管紧张素Ⅱ处理24h;(2)0、10-7、10-6、10-5和10-4mol/L浓度血管紧张素(1-7)处理24h;(3)血管紧张素Ⅱ、血管紧张素(1-7)联合处理24h,分为对照、10-5 mol/L血管紧张素Ⅱ、10-6 mol/L血管紧张素(1-7)、10-5 mol/L血管紧张素Ⅱ+10-6 mol/L血管紧张素(1-7)组.Western印迹检测胰岛素受体β亚基酪氨酸磷酸化(IR-β-Tyr)及蛋白激酶β丝氨酸磷酸化(Akt-Ser)水平.结果 血管紧张素Ⅱ浓度10-5和10-4mol/L时,胰岛素刺激的IR-β-Tyr、Akt-Ser表达显著降低;不同浓度血管紧张素(1-7)作用下,胰岛素刺激的IR-β-Tyr、Akt-Ser表达与对照组相比无差异;加入血管紧张素(1-7)共同孵育可逆转血管紧张素Ⅱ对Akt-Ser表达的抑制,而血管紧张素Ⅱ对IR-β-Tyr表达的抑制无效应.结论 在β细胞中,血管紧张素Ⅱ抑制胰岛素信号传导,血管紧张素(1-7)可拮抗血管紧张素Ⅱ对胰岛素刺激的Akt-Ser的抑制.
目的 研究血管緊張素Ⅱ、血管緊張素(1-7)對胰島β細胞胰島素信號通路的影響.方法 小鼠胰島β細胞株NIT-1予(1)0、10-7、10-6、10-5和10-4 mol/L濃度血管緊張素Ⅱ處理24h;(2)0、10-7、10-6、10-5和10-4mol/L濃度血管緊張素(1-7)處理24h;(3)血管緊張素Ⅱ、血管緊張素(1-7)聯閤處理24h,分為對照、10-5 mol/L血管緊張素Ⅱ、10-6 mol/L血管緊張素(1-7)、10-5 mol/L血管緊張素Ⅱ+10-6 mol/L血管緊張素(1-7)組.Western印跡檢測胰島素受體β亞基酪氨痠燐痠化(IR-β-Tyr)及蛋白激酶β絲氨痠燐痠化(Akt-Ser)水平.結果 血管緊張素Ⅱ濃度10-5和10-4mol/L時,胰島素刺激的IR-β-Tyr、Akt-Ser錶達顯著降低;不同濃度血管緊張素(1-7)作用下,胰島素刺激的IR-β-Tyr、Akt-Ser錶達與對照組相比無差異;加入血管緊張素(1-7)共同孵育可逆轉血管緊張素Ⅱ對Akt-Ser錶達的抑製,而血管緊張素Ⅱ對IR-β-Tyr錶達的抑製無效應.結論 在β細胞中,血管緊張素Ⅱ抑製胰島素信號傳導,血管緊張素(1-7)可拮抗血管緊張素Ⅱ對胰島素刺激的Akt-Ser的抑製.
목적 연구혈관긴장소Ⅱ、혈관긴장소(1-7)대이도β세포이도소신호통로적영향.방법 소서이도β세포주NIT-1여(1)0、10-7、10-6、10-5화10-4 mol/L농도혈관긴장소Ⅱ처리24h;(2)0、10-7、10-6、10-5화10-4mol/L농도혈관긴장소(1-7)처리24h;(3)혈관긴장소Ⅱ、혈관긴장소(1-7)연합처리24h,분위대조、10-5 mol/L혈관긴장소Ⅱ、10-6 mol/L혈관긴장소(1-7)、10-5 mol/L혈관긴장소Ⅱ+10-6 mol/L혈관긴장소(1-7)조.Western인적검측이도소수체β아기락안산린산화(IR-β-Tyr)급단백격매β사안산린산화(Akt-Ser)수평.결과 혈관긴장소Ⅱ농도10-5화10-4mol/L시,이도소자격적IR-β-Tyr、Akt-Ser표체현저강저;불동농도혈관긴장소(1-7)작용하,이도소자격적IR-β-Tyr、Akt-Ser표체여대조조상비무차이;가입혈관긴장소(1-7)공동부육가역전혈관긴장소Ⅱ대Akt-Ser표체적억제,이혈관긴장소Ⅱ대IR-β-Tyr표체적억제무효응.결론 재β세포중,혈관긴장소Ⅱ억제이도소신호전도,혈관긴장소(1-7)가길항혈관긴장소Ⅱ대이도소자격적Akt-Ser적억제.
Objective To evaluate the effect of angiotensin Ⅱ ( Ang Ⅱ ),angiotensin- (1-7) [ Ang- ( 1-7 ) ],and co-action of Ang Ⅱ and Ang-( 1-7 ) on β cell insulin signaling pathway.Methods Mouse pancreatic β cell line NIT-1 was incubated with( 1 )0,10-7,10-6,10-s,10-4 mol/L concentrations of Ang Ⅱ for 24 h ; ( 2 )0,10-7,10-6,10 -5,10-4 mol/L concentrations of Ang- ( 1-7 ) for 24 h; ( 3 ) co-administration of Ang Ⅱ and Ang- ( 1-7 ) was divided into control,10-5mol/L Ang Ⅱ,10-6mol/L Ang-( 1-7 ),10-5mol/L Ang Ⅱ + 10-6mol/L Ang-( 1-7 ) group.Tyrosine phosphorylation of insulin receptor β subunit(IR-β-Tyr) and serine phophorylation of protein kinase B(Akt-Ser) were detected by Western blot.Results Insulin-stimulated IR-β-Tyr and Akt-Ser phosphorylation was significantly decreased in Ang Ⅱ 10-5 and 10-4 mol/L group; no significant changes in insulin-stimulated IR-β-Tyr and Akt-Ser phosphorylation were detected between Ang-( 1-7 ) treatment groups and control; Ang-( 1-7 ) blocked the inhibitory effect of Ang Ⅱ on Akt-Ser phosphorylation,yet exerted no effect on Ang Ⅱ-induced IR-β-Tyr phosphorylation inhibition.Conclusion Ang Ⅱ significantly inhibits insulin signaling pathway in β cell; Ang-( 1-7 ) reverts the inhibitory effect of Ang Ⅱ on insulin-stimulated Akt-Ser phosphorylation in β cell.
