北京体育大学学报
北京體育大學學報
북경체육대학학보
Journal of Beijing University of Physical Education
2015年
2期
48~53
,共null页
运动 雄激素 AR阻断剂 ERK1/2通路
運動 雄激素 AR阻斷劑 ERK1/2通路
운동 웅격소 AR조단제 ERK1/2통로
exercise; androgen; AR inhibitor; ERK1/2 pathway
目的：通过阻断AR,以探讨雄激素对运动骨骼肌ERK1/2通路的影响特点。方法：7周龄雄性SD大鼠30只,随机分为对照组、AR阻断剂组、运动组、AR阻断剂运动组、假手术组。AR阻断剂组于颈部皮下包埋氟他胺释缓剂,运动组进行10 d中等强度运动,于末次运动后6 h取趾长伸肌进行指标测定。结果：与对照组相比,AR阻断剂组趾长伸肌湿重、肌纤维横截面积、AR mRNA及p-AR^Ser210均显著下降（p〈0.01-0.05）,MEK1/2、ERK1/2、P90^RSK的mRNA及蛋白磷酸化水平未有显著变化。运动组AR及ERK1/2通路的mRNA及蛋白磷酸化水平则显著增加（p〈0.05）,而其趾长伸肌湿重、肌纤维横截面积并未有显著变化。AR阻断剂运动组各指标与运动组相比均显著下降（p〈0.01-0.05）,而与AR阻断剂组相比均未有显著变化。结论：阻断AR可显著抑制运动骨骼肌湿重、横截面积及AR的基因和磷酸化表达,证实雄激素对运动骨骼肌的促蛋白合成作用主要经AR介导;AR阻断剂可显著抑制运动骨骼肌ERK1/2通路激活,提示雄激素经AR介导发挥非基因作用。该研究对雄激素促进运动骨骼肌蛋白合成的非基因作用提供一定实验依据。
目的：通過阻斷AR,以探討雄激素對運動骨骼肌ERK1/2通路的影響特點。方法：7週齡雄性SD大鼠30隻,隨機分為對照組、AR阻斷劑組、運動組、AR阻斷劑運動組、假手術組。AR阻斷劑組于頸部皮下包埋氟他胺釋緩劑,運動組進行10 d中等彊度運動,于末次運動後6 h取趾長伸肌進行指標測定。結果：與對照組相比,AR阻斷劑組趾長伸肌濕重、肌纖維橫截麵積、AR mRNA及p-AR^Ser210均顯著下降（p〈0.01-0.05）,MEK1/2、ERK1/2、P90^RSK的mRNA及蛋白燐痠化水平未有顯著變化。運動組AR及ERK1/2通路的mRNA及蛋白燐痠化水平則顯著增加（p〈0.05）,而其趾長伸肌濕重、肌纖維橫截麵積併未有顯著變化。AR阻斷劑運動組各指標與運動組相比均顯著下降（p〈0.01-0.05）,而與AR阻斷劑組相比均未有顯著變化。結論：阻斷AR可顯著抑製運動骨骼肌濕重、橫截麵積及AR的基因和燐痠化錶達,證實雄激素對運動骨骼肌的促蛋白閤成作用主要經AR介導;AR阻斷劑可顯著抑製運動骨骼肌ERK1/2通路激活,提示雄激素經AR介導髮揮非基因作用。該研究對雄激素促進運動骨骼肌蛋白閤成的非基因作用提供一定實驗依據。
목적：통과조단AR,이탐토웅격소대운동골격기ERK1/2통로적영향특점。방법：7주령웅성SD대서30지,수궤분위대조조、AR조단제조、운동조、AR조단제운동조、가수술조。AR조단제조우경부피하포매불타알석완제,운동조진행10 d중등강도운동,우말차운동후6 h취지장신기진행지표측정。결과：여대조조상비,AR조단제조지장신기습중、기섬유횡절면적、AR mRNA급p-AR^Ser210균현저하강（p〈0.01-0.05）,MEK1/2、ERK1/2、P90^RSK적mRNA급단백린산화수평미유현저변화。운동조AR급ERK1/2통로적mRNA급단백린산화수평칙현저증가（p〈0.05）,이기지장신기습중、기섬유횡절면적병미유현저변화。AR조단제운동조각지표여운동조상비균현저하강（p〈0.01-0.05）,이여AR조단제조상비균미유현저변화。결론：조단AR가현저억제운동골격기습중、횡절면적급AR적기인화린산화표체,증실웅격소대운동골격기적촉단백합성작용주요경AR개도;AR조단제가현저억제운동골격기ERK1/2통로격활,제시웅격소경AR개도발휘비기인작용。해연구대웅격소촉진운동골격기단백합성적비기인작용제공일정실험의거。
Objective： The purpose of this study was to investigate the effects of androgen on ERK1 /2 pathway in exercise skeletal muscle through blocking AR. Methods： Thirty seven-week old male SD rats were randomly divided into control group,AR inhibitor group,exercise group,AR inhibitor ＋ exercise group and sham group. AR inhibitor group rats were implanted subcutaneously with a flutamide release pellet,and exercise group rats participated in 10 days moderate intensity exercise. Extensor Digitorum Longus（ EDL） was isolated at 6 h after the last exercise. Results： Compared with control group,the wet weight and CSA of EDL,AR mRNA and p-AR^Ser210 in AR inhibitor group were significantly decreased（ Ps〈 0. 05）,and the mRNA and phosphorylation level of MEK1 /2,ERK1 /2 and p90 ^RSK had no significant changes. The mRNA and phosphorylation level of AR,ERK1 /2 pathway in exercise group significantly raised（ P 〈0. 05）,while the wet weight and CSA of EDL had no significant changes. All indexes in AR inhibitor ＋ exercise group were lower than in exercise group（ Ps〈 0. 05）,but had no differences compared with AR inhibitor group. Conclusions： AR inhibitor can significantly inhibit the expressions of wet weight,CSA,AR mRNA and phosphorylation of EDL,which demonstrated that the promotion of androgen on exercise skeletal muscle is mediated by AR. AR inhibitor can significantly inhibit ERK1 /2 pathway,which indicated that androgen activating ERK1 /2 pathway in exercise skeletal muscle is mediated by AR.
