本文選題：AR阻斷劑 + mTOR通路�。� 參考：《中國運動醫(yī)學(xué)雜志》2015年02期

【摘要】：目的:通過阻斷雄激素受體(AR)并結(jié)合運動,探討雄激素對運動骨骼肌哺乳動物雷帕霉素靶蛋白(m TOR)信號通路的影響特點。方法:30只7周齡雄性SD大鼠,適應(yīng)性訓(xùn)練后隨機分為5組:安靜對照組(C)、AR阻斷劑組(F)、運動組(E)、AR阻斷劑運動組(EF)、假手術(shù)組(S)。F、EF組于實驗前3 d頸部皮下包埋氟他胺釋緩劑,E、EF組進行為期10 d的中等強度運動,于末次運動后6 h取趾長伸肌,測定肌球蛋白重鏈(MHC)蛋白表達(dá)及AR、m TOR、核糖體S6蛋白激酶(p70S6K)、真核起始因子4E結(jié)合蛋白(4EBP1)基因及蛋白和磷酸化表達(dá)。結(jié)果:F組體重與C組相比顯著下降(P0.01),E組無顯著差異。F組MHC含量與C組相比顯著下降(P0.05),E組則顯著升高(P0.05);EF組與E組相比顯著下降(P0.01)。F組AR m RNA、p-AR與C組相比顯著下降(P0.01),E組顯著升高(P0.05),EF組與E組相比顯著下降(P0.01)。F組m TOR、p70S6K、4EBP1 m RNA與C組相比均顯著下調(diào)(P0.05,P0.01,P0.05),E組則顯著上調(diào)(P0.05),EF組與E組相比顯著下降(P0.01)。F組p-m TOR、p-4EBP1、4EBP1與C組相比均顯著下降(P0.01,P0.01,P0.05),E組p-m TOR、m TOR、p-p70S6K顯著增加(P0.01,P0.01,P0.05),EF組與E組相比顯著下降(P0.01)。結(jié)論:阻斷AR可顯著抑制m TOR通路活性,運動則促進m TOR通路活性增強,阻斷AR后運動并不能誘導(dǎo)m TOR通路活性增強,表明雄激素對運動骨骼肌m TOR通路的作用主要經(jīng)AR介導(dǎo)的非基因途徑進行。
[Abstract]:Aim: to investigate the effects of androgen on the signaling pathway of rapamycin target protein (rapamycin) in the exercise skeletal muscle mammal by blocking androgen receptor ARA and combined with exercise. Methods 30 7 week-old male SD rats were selected. After adaptive training, the rats were randomly divided into five groups: the control group (n = 5), the control group (n = 10), and the control group (n = 10), the sham operation group (n = 10) and the control group (n = 10). The muscle extensor digitorum longus was taken at 6 h after the last exercise. The expression of myosin heavy chain (MHCC) protein and the expression of ARMTOR, ribosomal S6 protein kinase p70S6KN, eukaryotic initiation factor 4E binding protein 4EBP1) and protein and phosphorylation were measured. Results there was no significant difference in body weight between group F and group C. The content of MHC in group F was significantly lower than that in group C. The content of MHC in group F was significantly higher than that in group C, but it was significantly higher in group E than in group E. The level of AR m RNAp-AR in group F was significantly lower than that in group E (P 0.01) and that in group E was significantly lower than that in group C (P 0.01). The decrease of P0.05P0.05FEF group was significantly lower than that of E group P0.01U. F group decreased P0.01P0.01K4EBP1 m RNA, compared with C group, P0.05P0.01K4EBP1 m RNA was significantly down-regulated, while P0.05P0.01P0.05E group significantly up-regulated the decrease of P0.05TORP-4P1P1EB4EBP1 compared with E group. P0.01P0.01P0.01P0.05EBP1 decreased P0.01P0.01P0.05EBP1 and P0.01P0.01P0.05EBP1 significantly decreased compared with E group and P0.05P0.01P0.05EBP1 decreased P0.01P0.01K4EBP1 significantly lower than that of E group and P0.05P0.01P0.05EBP1 decreased P0.01P0.01P0.05EBP1 and P0.01P0.01P0.05EBP1 significantly decreased compared with E group. Compared with E group, the increase of P0.01P0.01P0.01P0.05F decreased significantly (P 0.01). Conclusion: blocking AR can significantly inhibit the activity of m TOR pathway, while exercise can enhance the activity of m TOR pathway, but after blocking AR, it can not induce the increase of m TOR pathway activity. The results showed that the effect of androgen on the m TOR pathway of exercise skeletal muscle was mainly mediated by AR-mediated non-gene pathway.
【作者單位】： 北京體育大學(xué);國家體育總局運動醫(yī)學(xué)研究所;
【基金】：國家自然科學(xué)基金項目(31071034) 中央高�；究蒲袠I(yè)務(wù)費專項資金資助課題(2014BS019)
【分類號】：R87

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