本文選題：離心運動 + 低氧　； 參考：《北京體育大學(xué)》2016年博士論文

【摘要】：目的：觀察急性離心運動后大鼠腓腸肌Dystrophin表達(dá)及相應(yīng)信號通路變化,并驗證低氧是否通過此信號通路調(diào)控Dystrophin表達(dá),為高住低訓(xùn)提供理論依據(jù)。方法：研究一：70只雄性SD大鼠分安靜對照組、常氧運動后常氧恢復(fù)24H、48H、72H組和常氧運動后低氧暴露24H、48H、72H組。運動組大鼠進(jìn)行一次間歇性離心運動后,于不同環(huán)境下恢復(fù)。研究二：72只雄性SD大鼠分為安靜對照組、ERK1/2抑制劑24H、48H組；ERK1／2安慰劑24H、48H組；AKT抑制劑24H、48H組和AKT安慰劑24H、48H組。除安靜對照組外,其他組在運動后進(jìn)行低氧暴露。采用免疫組化、Western blot、qRT-PCR等方法檢測大鼠腓腸肌細(xì)胞膜完整性、Dystrophin mRNA及蛋白表達(dá)、ERK1/2和AKT/mTOR通路的蛋白表達(dá)。結(jié)果：(1)離心運動后低氧暴露,大鼠腓腸肌陽性細(xì)胞率在各時間點與常氧恢復(fù)組比較,呈現(xiàn)顯著性上升、下降再上升的趨勢。(2)急性離心運動后,Dystrophin蛋白含量在各組中未出現(xiàn)顯著性變化；Dystrophin mRNA表達(dá)水平顯著性降低,且低氧暴露組mRNA水平低于常氧恢復(fù)組；ERK和AKT/mTOR通路蛋白及磷酸化水平存在時相性差異,低氧暴露組ERK通路蛋白及磷酸化水平變化趨勢與Dystrophin mRNA表達(dá)一致。(3)注射MEK靶向抑制劑可在運動后48h阻斷ERK通路蛋白及磷酸化水平,抵消低氧通過ERK1/2信號傳導(dǎo)途徑調(diào)控Dystrophin mRNA的作用。而AKT靶向抑制劑在運動后24h即已抑制了AKT的表達(dá),但對Dystrophin沒有顯著影響。結(jié)論：(1)離心運動后急性低氧暴露可加劇骨骼肌細(xì)胞膜損傷。隨著低氧暴露時間的延長,機(jī)體產(chǎn)生了短暫適應(yīng),細(xì)胞膜完整性得到一定恢復(fù)。(2)急性離心運動后24h-72h, Dystrophin蛋白表達(dá)無明顯變化,基因含量顯著下降。(3)低氧可通過ERK1/2信號通路調(diào)控Dystrophin mRNA表達(dá),進(jìn)而調(diào)節(jié)Dystrophin蛋白表達(dá)。ERK1/2信號通路與Dystrophin mRNA間存在負(fù)向調(diào)節(jié)作用。(4)AKT/mTOR信號傳導(dǎo)通路在低氧對Dystrophin蛋白表達(dá)影響中并不占據(jù)主導(dǎo)調(diào)控地位。
[Abstract]:Aim: to observe the changes of dystrophin expression and signal pathway in gastrocnemius muscle after acute centrifugation, and to verify whether hypoxia regulates the expression of dystrophin through this signaling pathway, which provides a theoretical basis for high living and low training. Methods: a total of 70 male Sprague-Dawley rats were divided into two groups: the control group, the normal oxygen recovery group after normoxic exercise, and the control group, which were exposed to hypoxia after normoxic exercise. The rats in the exercise group recovered in different environments after an intermittent eccentric exercise. In this study, 72 male Sprague-Dawley rats were divided into two groups: the quiet control group with ERK1 / 2 inhibitor 24H, the control group with ERK1 / 2 placebo 24H4H 48H and the AKT placebo with 24Hn48H and the AKT placebo 24H with 48H. In addition to quiet control group, other groups were exposed to hypoxia after exercise. The expression of dystrophin mRNA and protein in rat gastrocnemius muscle cell membrane was detected by Western blottit qRT-PCR, and the protein expression of ERK1 / 2 and AKT / mTOR pathway was detected. Results (1) compared with normoxic recovery group, the positive cell rate of gastrocnemius muscle increased significantly in rats exposed to hypoxia after centrifugation. There was no significant change in Dystrophin protein content after acute centrifugation. There was no significant change in Dystrophin mRNA expression in each group. The mRNA levels in hypoxia group were lower than those in normoxic recovery group, and the protein and phosphorylation levels of ERK and AKT / mTOR pathway were significantly lower than those of normoxic recovery group. The changes of ERK pathway protein and phosphorylation level in hypoxic exposure group were consistent with the expression of dystrophin mRNA. (3) injection of MEK targeting inhibitor could block ERK pathway protein and phosphorylation at 48 h after exercise, and counteract the effect of hypoxia on regulating Dystrophin mRNA through ERK1 / 2 signal transduction pathway. AKT-targeted inhibitors inhibited AKT expression 24 hours after exercise, but had no significant effect on dystrophin. Conclusion (1) Acute hypoxic exposure after eccentric exercise can aggravate the damage of skeletal muscle cell membrane. With the prolongation of hypoxic exposure time, the body had a transient adaptation, cell membrane integrity was recovered to some extent.) after 24 h-72 h of acute centrifugation, the expression of dystrophin protein did not change significantly. Hypoxia can regulate the expression of dystrophin mRNA through ERK1 / 2 signaling pathway. Furthermore, the regulation of Dystrophin protein expression. ERK1 / 2 signaling pathway and Dystrophin mRNA has negative regulatory effect. The AKT / mTOR signal transduction pathway does not play a dominant role in the effect of hypoxia on dystrophin protein expression.
【學(xué)位授予單位】：北京體育大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：G804.2

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相關(guān)期刊論文 前2條

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本文編號：1999954