Mirzoev Timur M, Tyganov Sergey A, Shenkman Boris S
Myology Laboratory, Institute of Bio-Medical Problems of the Russian Academy of Sciences, 123007, Moscow, Russian Federation.
Muscle Nerve. 2017 Mar;55(3):393-399. doi: 10.1002/mus.25235. Epub 2016 Aug 6.
The purpose of our study was to assess the contribution of insulin growth factor-1-dependent and phosphatidic acid-dependent signaling pathways to activation of protein synthesis (PS) in rat soleus muscle during early recovery from unloading.
Wistar rats were divided into: Control, 14HS [14-day hindlimb suspension (HS)], 3R+placebo (3-day reloading + saline administration), 3R+Wort (3-day reloading + wortmannin administration), 3R+But (3-day reloading + 1-butanol administration). SUnSET and Western blot analyses were used in this study.
Wortmannin and 1-butanol induced a decrease in protein kinase B (phospho-Akt) and the rate of PS (P < 0.05) versus Control. In 3R+placebo and 3R+Wort, phosphorylation of glycogen synthase kinase 3 beta (phospho-GSK-3β) was increased versus Control (P < 0.05). Wortmannin administration during reloading did not alter phospho-p70S6K (70 kDa ribosomal protein S6 kinase) versus 3R+placebo. In 3R+But, there was a decline in phospho-GSK-3β versus 3R+placebo and Control. In 3R+But, there was a decrease in phopho-p70S6K (P < 0.05) versus 3R+placebo.
These results suggest that PS activation during 3-day reloading following 14HS involves both Akt-dependent and Akt-independent pathways. Muscle Nerve 55: 393-399, 2017.
我们研究的目的是评估胰岛素生长因子-1依赖性和磷脂酸依赖性信号通路在大鼠比目鱼肌卸载后早期恢复过程中对蛋白质合成（PS）激活的贡献。
将Wistar大鼠分为：对照组、14HS组[14天 hindlimb 悬吊（HS）]、3R+安慰剂组（3天再负荷+生理盐水给药）、3R+渥曼青霉素组（3天再负荷+渥曼青霉素给药）、3R+丁醇组（3天再负荷+1-丁醇给药）。本研究采用SUnSET和蛋白质印迹分析。
与对照组相比，渥曼青霉素和1-丁醇使蛋白激酶B（磷酸化Akt）和PS速率降低（P<0.05）。与对照组相比，3R+安慰剂组和3R+渥曼青霉素组中糖原合酶激酶3β（磷酸化GSK-3β）的磷酸化增加（P<0.05）。再负荷期间给予渥曼青霉素与3R+安慰剂组相比，磷酸化p70S6K（70 kDa核糖体蛋白S6激酶）未改变。与3R+安慰剂组和对照组相比，3R+丁醇组中磷酸化GSK-3β下降。与3R+安慰剂组相比，3R+丁醇组中磷酸化p70S6K降低（P<0.05）。
这些结果表明，14HS后3天再负荷期间PS激活涉及Akt依赖性和Akt非依赖性途径。《肌肉与神经》55: 393-399, 2017。
