本文選題：失神經(jīng) + 肌萎縮��； 參考：《山西醫(yī)科大學(xué)》2012年碩士論文

【摘要】：背景：周圍神經(jīng)損傷后，骨骼肌失神經(jīng)支配將不可避免地發(fā)生骨骼肌萎縮，嚴(yán)重阻礙肢體的功能恢復(fù)。采取有效措施延緩肌肉萎縮，以等待再生神經(jīng)的重新支配是臨床亟待解決的問(wèn)題，而直至目前，失神經(jīng)骨骼肌萎縮的發(fā)生機(jī)制仍不清楚。 目的:探討失神經(jīng)大鼠腓腸肌細(xì)胞中FoxO3a及MAFbx的表達(dá)規(guī)律。 方法：72只Wistar大鼠隨機(jī)分為12組，每組6只，切斷大鼠右側(cè)坐骨神經(jīng)，左側(cè)行坐骨神經(jīng)探查術(shù)，分別于術(shù)后0、1、2、3、4、5、6、7、10、14、21、28天處死一組大鼠，完整取出雙側(cè)腓腸肌，以分析天平稱重，求出右側(cè)與左側(cè)的比值后，冷凍于-70℃冰箱保存。分別使用實(shí)時(shí)熒光定量PCR法和Western Blot法對(duì)其中的FoxO3a和MAFbx的基因和蛋白及253位磷酸化的FoxO3a（pFoxO3aS253）進(jìn)行檢測(cè)。 結(jié)果:失神經(jīng)后骨骼肌迅速發(fā)生萎縮，失神經(jīng)14天后肌濕重約下降50%，28天后肌濕重僅存正常時(shí)的30%。MAFbx的基因表達(dá)在失神經(jīng)第四天達(dá)到峰值（39.1倍），其后逐漸下降至正常。FoxO3a的基因表達(dá)在失神經(jīng)第五天達(dá)到峰值（7.06倍），而后緩慢下降，但仍高表達(dá)。FoxO3a和MAFbx的蛋白含量隨失神經(jīng)時(shí)間的延長(zhǎng)逐漸升高，而FoxO3a和磷酸化水平逐漸下降，失神經(jīng)28天時(shí)pFoxO3aS253的量只有失神經(jīng)0天時(shí)的60.1%。 結(jié)論：FoxO3a的磷酸化調(diào)節(jié)和MAFbx的表達(dá)改變與失神經(jīng)骨骼肌萎縮關(guān)系密切，，可以作為藥物治療和基因治療的靶點(diǎn)之一。
[Abstract]:Background: after peripheral nerve injury, denervated skeletal muscle will inevitably cause atrophy of skeletal muscle, which seriously hinders the recovery of limb function. It is an urgent clinical problem to take effective measures to delay muscle atrophy and wait for the regenerative nerve to be innervated. Until now, the mechanism of denervated skeletal muscle atrophy is still unclear. Objective: to investigate the expression of FoxO3a and MAFbx in gastrocnemius muscle cells of denervated rats. Methods Seventy-two Wistar rats were randomly divided into 12 groups, 6 rats in each group, the right sciatic nerve was transected, and the left sciatic nerve was explored on the left side. One group of rats were killed on the 1st and 2nd day after operation, and the bilateral gastrocnemius muscles were removed completely to weigh them. The ratio of right side to left side was calculated and frozen in-70 鈩

本文編號(hào)：1916315