中国医科大学学报
中國醫科大學學報
중국의과대학학보
JOURNAL OF CHINA MEDICAL UNIVERSITY
2015年
2期
119-122,126
,共5页
增食欲素A%增食欲素受体1%细胞增殖%AKT信号通路%胰岛β细胞
增食欲素A%增食欲素受體1%細胞增殖%AKT信號通路%胰島β細胞
증식욕소A%증식욕소수체1%세포증식%AKT신호통로%이도β세포
orexin A%orexin receptor 1%cell proliferation%AKT signaling pathway%pancreas isletβcells
目的:探讨增食欲素A(Orexin A)通过增食欲素受体1(OX1R)和AKT/PKB信号传导途径对胰岛细胞增殖的干预效应。方法体外培养的大鼠INS?1胰岛素瘤细胞暴露于不同浓度的Orexin A,OX1R拮抗剂(SB334867)、PI3K拮抗剂(渥曼青霉素)和AKT拮抗剂(PF?04691502)干预Orexin A的作用,测定INS?1的细胞增殖、凋亡、胰岛素分泌、OX1R蛋白活性及AKT蛋白磷酸化水平。结果 Orexin A(10-10~10-6 mol/L)可刺激INS?1细胞的增殖和活化,防止细胞凋亡,并增加胰岛素的分泌;Orexin A (10-10~10-6 mol/L)增强了INS?1细胞内AKT的磷酸化,SB334867(10-6 mol/L)、渥曼青霉素(10-8 mol/L)和PF?04691502(10-6 mol/L)可以减弱Orexin A的作用。结论 INS?1细胞内Orexin A通过Orexin A?OX1R的介导而活化AKT信号通路,促进细胞增殖。
目的:探討增食欲素A(Orexin A)通過增食欲素受體1(OX1R)和AKT/PKB信號傳導途徑對胰島細胞增殖的榦預效應。方法體外培養的大鼠INS?1胰島素瘤細胞暴露于不同濃度的Orexin A,OX1R拮抗劑(SB334867)、PI3K拮抗劑(渥曼青黴素)和AKT拮抗劑(PF?04691502)榦預Orexin A的作用,測定INS?1的細胞增殖、凋亡、胰島素分泌、OX1R蛋白活性及AKT蛋白燐痠化水平。結果 Orexin A(10-10~10-6 mol/L)可刺激INS?1細胞的增殖和活化,防止細胞凋亡,併增加胰島素的分泌;Orexin A (10-10~10-6 mol/L)增彊瞭INS?1細胞內AKT的燐痠化,SB334867(10-6 mol/L)、渥曼青黴素(10-8 mol/L)和PF?04691502(10-6 mol/L)可以減弱Orexin A的作用。結論 INS?1細胞內Orexin A通過Orexin A?OX1R的介導而活化AKT信號通路,促進細胞增殖。
목적:탐토증식욕소A(Orexin A)통과증식욕소수체1(OX1R)화AKT/PKB신호전도도경대이도세포증식적간예효응。방법체외배양적대서INS?1이도소류세포폭로우불동농도적Orexin A,OX1R길항제(SB334867)、PI3K길항제(악만청매소)화AKT길항제(PF?04691502)간예Orexin A적작용,측정INS?1적세포증식、조망、이도소분비、OX1R단백활성급AKT단백린산화수평。결과 Orexin A(10-10~10-6 mol/L)가자격INS?1세포적증식화활화,방지세포조망,병증가이도소적분비;Orexin A (10-10~10-6 mol/L)증강료INS?1세포내AKT적린산화,SB334867(10-6 mol/L)、악만청매소(10-8 mol/L)화PF?04691502(10-6 mol/L)가이감약Orexin A적작용。결론 INS?1세포내Orexin A통과Orexin A?OX1R적개도이활화AKT신호통로,촉진세포증식。
Objective To investigate the interference effects of orexin A on cell proliferation of the insulin?secreting beta?cell line(INS?1 cells) through the orexin receptor 1(OX1R)and the AKT/PKB signaling pathway. Methods INS?1 cells were exposed to different concentrations of orexin A in vitro,and treated with OX1R antagonist(SB334867),PI3K antagonist(wortmannin),or AKT antagonist(PF?04691502). The INS?1 cell proliferation and apoptosis,insulin secretion,OX1R protein activity and AKT phosphorylation level were determined. Results Orexin A(10-10 to 10-6 mol/L)stimulated the proliferation and activation of INS?1 cells,prevented apoptpsis,and increased insulin secretion. Additionally,AKT phosphorylation was stimulated by orexin A(10-10 to 10-6 mol/L). The OX1R antagonist SB334867(10-6 mol/L),the PI3K antagonist wortmannin (10-8 mol/L)and the AKT antagonist PF?04691502(10-6 mol/L)weakened the effects of orexin A. Conclusion Orexin A activated the AKT sig?naling pathway through the mediation of orexin A?OX1R,and promoted cell proliferation in INS?1 cells.