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        卒中相關(guān)性肌萎縮發(fā)生機制與研究進展

        2016-10-12 06:20:23王麗晶
        關(guān)鍵詞:肌萎縮泛素肌纖維

        王麗晶,詹 青

        1. 上海中醫(yī)藥大學附屬第七人民醫(yī)院神經(jīng)內(nèi)科,上海 200137

        2. 上海中醫(yī)藥大學附屬第七人民醫(yī)院神經(jīng)康復科,上海 200137

        卒中相關(guān)性肌萎縮發(fā)生機制與研究進展

        王麗晶1,2,詹 青1,2

        1. 上海中醫(yī)藥大學附屬第七人民醫(yī)院神經(jīng)內(nèi)科,上海 200137

        2. 上海中醫(yī)藥大學附屬第七人民醫(yī)院神經(jīng)康復科,上海 200137

        卒中;肌萎縮;發(fā)病機制

        詹 青

        E-MAIL

        zhanqing@#edu.cn

        王麗晶,詹 青. 卒中相關(guān)性肌萎縮發(fā)生機制與研究進展[J]. 神經(jīng)病學與神經(jīng)康復學雜志, 2016, 12(2):102-105.

        E-MAIL ADDRESS

        zhanqing@#edu.cn

        腦卒中會導致殘障發(fā)生。有研究表明,約50%的腦卒中患者發(fā)生偏癱,約30%的患者會失去獨立步行的能力[1]。腦卒中后肌萎縮的發(fā)生率較高,表現(xiàn)為肌肉組織萎縮和肌纖維數(shù)量減少[2],進而引發(fā)失神經(jīng)支配以及肌痙攣等肌肉異常情況[3],對患者的預后帶來嚴重的不良影響。目前認為,腦卒中后肌萎縮的發(fā)生可能與缺乏活動、廢用、炎性通路、代謝通路及神經(jīng)生長等有關(guān),其發(fā)生機制見圖1。本文旨在對有關(guān)腦卒中后肌萎縮發(fā)生機制的研究進展進行綜述,為腦卒中后肌萎縮的預防和治療提供參考依據(jù)。

        圖1 腦卒中后肌萎縮的發(fā)生機制

        1 卒中相關(guān)性肌萎縮概念的提出

        有研究證實,腦卒中后4 h就會發(fā)生肌肉組織的結(jié)構(gòu)適應性改變,隨后會導致肌肉與運動神經(jīng)元的突觸傳遞受到影響,繼而引起運動單位數(shù)量的減少,導致肌萎縮的發(fā)生[4],并持續(xù)至腦卒中后[5]。腦卒中發(fā)生1周后,健側(cè)肢體也會出現(xiàn)肌無力[6]。一般而言,隨著年齡增長出現(xiàn)的肌萎縮,通常表現(xiàn)為快肌纖維含量的增加以及慢肌纖維含量的下降,進而導致肌肉力量的下降[7];反之,腦卒中后快肌纖維的含量會下降,慢肌纖維的含量會增加[8],但目前尚不明確其發(fā)生機制。相較于其他原因所致的肌萎縮,腦卒中后肌萎縮的發(fā)生有著特殊的表現(xiàn)。基于腦卒中后肌萎縮的肌容積及其結(jié)構(gòu)的特異性改變,提出了卒中相關(guān)性肌萎縮(stroke-related sarcopenia)[9-10]這一概念,以區(qū)別于年齡相關(guān)性肌萎縮及其他原因?qū)е碌募∥s。

        2 卒中相關(guān)性肌萎縮的發(fā)生機制

        2.1 活動障礙與肌萎縮

        腦卒中后,患者處于缺乏活動的狀態(tài),而缺乏活動可導致胰島素抵抗,不僅可影響糖代謝,還可以降低胰島素的活化。KORTEBEIN等[11]的研究表明,在健康老年人中,僅僅10 d的臥床就可以導致肌蛋白合成減少30%,同時導致下肢肌肉力量下降16%,進而推測失神經(jīng)支配、攝食能力下降、活動障礙等因素能夠引起肌肉萎縮。既往的幾項研究均表明,腦卒中發(fā)生后3周至6個月就會發(fā)生肌容積減少、肌內(nèi)脂肪異位化以及肌纖維橫截面積減少,并且健側(cè)肢體及患側(cè)肢體均會發(fā)生上述改變[12-15]。

        2.2 泛素蛋白酶體通路與肌萎縮

        2.2.1 肌肉生長抑制素(myostatin)和轉(zhuǎn)化生長因子β

        關(guān)于肌萎縮的發(fā)生機制,目前認為與幾個主要的信號通路有關(guān),而其中最受關(guān)注的是泛素蛋白酶體通路,其中包括2個比較重要的細胞因子(肌肉生長抑制素和轉(zhuǎn)化生長因子β)。一項動物實驗研究[16]的結(jié)果顯示,缺乏肌肉生長抑制素的大鼠,其肌容量是正常大鼠的2倍;而轉(zhuǎn)化生長因子β也是肌萎縮的誘發(fā)因子,可導致顯著的肌肉萎縮和肌肉力量的下降[17]。RYAN等[18]的研究表明,癱瘓側(cè)的肌肉生長抑制素mRNA水平明顯高于非癱瘓的肌肉,由此認為肌肉生長抑制素基因在肌萎縮的發(fā)生機制中起著重要的作用。SPTINGER等[19]通過建立大鼠缺血性腦卒中模型,探討營養(yǎng)攝入、感染、肌肉生長抑制素和caspase蛋白等與腦卒中后肌萎縮之間的關(guān)系,結(jié)果發(fā)現(xiàn)相關(guān)代謝通路在腦卒中后會被激活,但對具體機制仍不清楚。

        2.2.2 肌 肉 環(huán) 指 蛋 白1(muscle ring finger protein 1,MURF-1)和atrogin-1

        MURF-1和atrogin-1是2種泛素蛋白連接酶E3s,常被肌肉生長抑制素和轉(zhuǎn)化生長因子β信號所誘導,在肌萎縮的發(fā)生中具有重要意義。BODINE等[20]的研究發(fā)現(xiàn),缺乏atrogin-1的大鼠表現(xiàn)出可以抵抗失神經(jīng)支配所致肌萎縮的能力,同時也發(fā)現(xiàn)隨著肌肉的萎縮,伴有atrogin-1和MURF-1的一過性升高。SACHECK等[21]的研究也支持這一結(jié)果。

        2.3 CAF22(C-terminal agrin fragment 22)與肌萎縮

        最近,CAF被假設為老年人群神經(jīng)肌肉接頭退化所致肌萎縮的生物學標志物[22],其中agrin是神經(jīng)肌肉接頭處后突觸的重要組成部分,而CAF22是從人類血清中分離出的agrin片段之一[23]。2013年有研究報道,在因神經(jīng)肌肉接頭處退化而導致肌萎縮的老年人群中,發(fā)現(xiàn)血漿CAF22水平明顯升高[24]。SCHERBAKOV等[25]研究了123例處于腦卒中恢復期的患者,并將年齡及體型與之匹配的健康人作為對照,評估血漿CAF22水平以及癱瘓側(cè)肌力及肌圍度,結(jié)果顯示腦卒中患者的血漿CAF22水平顯著高于對照者;且在康復過程中,CAF22水平逐漸下降,而癱瘓側(cè)肌力及肌圍度則逐漸增加。由此認為,CAF22可能參與了腦卒中后肌萎縮的發(fā)生。

        3 小結(jié)

        綜上所述,卒中相關(guān)性肌萎縮是近年來提出的新概念,有關(guān)其發(fā)生機制的研究還較少,國內(nèi)更鮮見相關(guān)研究報道。探索卒中相關(guān)性肌萎縮的發(fā)生機制及其預防措施,有助于對腦卒中后肌萎縮的預防和治療新思路提供循證依據(jù)。今后國內(nèi)應著手開展旨在探索卒中相關(guān)性肌萎縮發(fā)生機制的研究,可從肌肉生長抑制素、atrogin-1和MURF-1水平的檢測及分析入手,以期更好地指導卒中相關(guān)性肌萎縮的預防和治療。

        [1]GO A S, MOZAFFARlAN D, ROGER V L, et al. Heart disease and stroke statistics_2013 update: a report from the American Heart Association[J]. Circulation, 2013, 127(1):e6-e245.

        [2]SCHERBAKOV N, DOEHNER W. Sarcopenia in stroke-facts and numbers on muscles loss accounting for disability after stroke[J]. J Cachexia Sarcopnenia Muscle, 2011,2(1):5-8.

        [3]CARDA S, ClSARl C, lNVERNlZZl M. Sarcopenia or muscle modifications in neurologic disease: a lexical or pathophysiological difference?[J]. Eur J Phys Rehabil Med, 2013, 49(1):119-130.

        [4]ARASAKl K, lGARASHl O, lCHlKAWA Y, et al.

        Reduction in the motor unit number estimate (MUNE) after cerebral infarction[J]. J NeurolSci, 2006, 250(1-2):27-32.

        [5]Ll X, SHlN H, ZHOU P, et al. Power spectral analysis of surface electromyography (EMG) at matched contraction levels of the first dorsal interosseous muscle in stroke survivors[J]. Clin Neurophysiol, 2014,125(5):988-994.

        [6]HARRlS M L, POLKEY M l, BATH P M, et al. Quadriceps muscle weakness following acute hemiplegic stroke[J]. Clin Rehabil,2001, 15(3):274-281.

        [7]KOSTKA T. Quadriceps maximal power and optimal shortening velocity in 335 men aged 23-88 years[J]. Eur J Appl Physiol,2005,95(2-3):140-145.

        [8]DE DEYNE P G, HAFER-MACKO C E, lVEY F M, et al. Muscle molecular phenotype after stroke is associated with gait speed[J]. Muscle Nerve,2004, 30(2):209-215.

        [9]SCHERBAKOV N, VON HAEHLlNG S, ANKER S D, et al. Stroke induced Sarcopenia:muscle wasting and siability after stroke[J]. lnt J Cardiol, 2013, 170(2):89-94.

        [10]SCHERBAKOV N, SANDEK A, DOEHNER W. Stroke-related Sarcopenia: specific characteristics[J]. J Am Med Dir Assoc,2015, 16(4):272-276.

        [11]KORTEBElN P, FERRANDO A, LOMBElDA J, et al. Effect of 10 days of bed rest on skeletal muscle in healthy older adults[J]. JAMA,2007, 297(16):1772-1774.

        [12]CARlN-LEVY G, GRElG C, YOUNG A, et al. Longitudinal changes in muscle strength and mass after acute stroke[J]. Cerebrovasc Dis,2006, 21(3):201-207.

        [13]J?RGENSEN L, JACOBSEN B K. Changes in muscle mass, fat mass, and bone mineral content in the legs after stroke: a 1 year prospective study[J]. Bone, 2001,28(6):655-659.

        [14]HUGHES V A, FRONTERA W R, ROUBENOFF R, et al. Longitudinal changes in body composition in older men and women: role of body weight change and physical activity[J]. Am J Clin Nutr, 2002, 76(2):473-481.

        [15]RYAN A S, BUSCEMl A, FORRESTER L, et al. Atrophy and intramuscular fat in specific muslces of the thigh: associated weakness and hyperinsulinemia in stroke survirors[J]. Neurorehabil Neural Repair, 2011,25(9):865-872.

        [16]MCPHERRON A C, LAWLER A M, LEE S J. Regulation of skeletal muscle mass in mice by a new TGFbeta superfamily member[J]. Nature, 1997, 387(6628):83-90.

        [17]MENDlAS C L, GUMUClO J P, DAVlS M E, et al. Transforming growth factor-beta induces skeletal muscle atrophy and fibrosis through the induction of atrogin-1 and scleraxis[J]. Muscle Nerve, 2012, 45(1):55-59.

        [18]RYAN A S, lVEY F M, PRlOR S, et al. Skeletal muscle hypertrophy and muscle myostatin reduction after resistive training in stroke survivors[J]. Stroke, 2011, 42(2):416-420.

        [19]SPRlNGER J, SCHUST S, PESKE K, et al. Catabolic signaling and muscle wasting after acute ischemic stroke in mice[J]. Stroke,2014, 45(12):3675-3683.

        [20]BODlNE S C, LATRES E, BAUMHUETER S, et al. ldentification of ubiquitin ligases required for skeletal muscle atrophy[J]. Science,2001, 294(5547):1704-1708.

        [21]SACHECK J M, HYATT J P, RAFFAELLO A,et al. Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases[J]. FASEB J, 2007, 21(1):140-155.

        [22]HETTWER S, DAHlNDEN P, KUCSERA S,et al. Elevated levels of a C-terminal agrin fragment identifies a new subset of sarcopenia patients[J]. Exp Gerontol, 2013,48(1):69-75.

        [23]BEZAKOVA G, RUEGG M A. New insights into the roles of agrin[J]. Nat Rev Mol Cell Biol,2003, 4(4):295-308.

        [24]DREY M, SlEBER C C, BAUER J M,et al. C-terminal Agrin Fragment as a potential marker for sarcopenia caused by degeneration of the neuromuscular junction[J]. Exp Gerontol, 2013,48(1):76-80.

        [25]SCHERBAKOV N, KNOPS M, EBNER N, et al. Evaluation of C-terminal Agrin Fragment as a marker of muscle wasting in patients after acute stroke during early rehabilitation[J]. J Cachexia Sarcopenia Muscle, 2016,7(1):60-67.

        Research progress in pathogenesis of stroke-related sarcopenia

        WANG Lijing1, 2, ZHAN Qing1, 2
        1. Department of Neurology, Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China
        2. Department of Neurorehabilitation, Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine,Shanghai 200137, China

        ABSTRACT

        Physical disability is common in stroke survivors. Sarcopenia after stroke has a strong impact on the decision and efficiency of rehabilitation and it may lead to the delayed recovery of patients. The pathogenesis of sarcopenia has not been investigated in details. “Stroke-related sarcopenia” was proposed in 2013 and several factors have been well known to contribute to sarcopenia, such as immobilization, impaired feeding and the activation of ubiquitin proteasome pathway. This paper reviews the recent studies on pathogenesis of stroke-related sarcopenia and distinguishes it from sarcopenia induced by other diseases,providing a basis for the prevention and therapy of sarcopenia after stroke.

        Stroke; Muscular atrophy; Pathogenesis

        ZHAN Qing

        10.12022/jnnr.2016-0045

        上海市殘疾人聯(lián)合會基金項目(編號:K2014015);上海市進一步加快中醫(yī)藥事業(yè)發(fā)展三年行動計劃(編號:ZY3-FWMS-2-1012);上海中醫(yī)藥大學附屬第七人民醫(yī)院“七院新星”基金項目(編號:XX2016-03)FUNDlNG/SUPPORT: Foundation of Shanghai Disabled Persons’ Federation (No. K2014015); Shanghai Three-year Action Planning for Further Accelerating Development of Chinese Medicine (No. ZY3-FWMS-2-1012); “New Star” Project ofSeventh People’s Hospital of Shanghai University of Traditional Chinese Medicine (No. XX2016-03)

        CONFLlCT OF lNTEREST: The authors have no conflicts of interest to disclose. Received May 5, 2016; accepted for publication Jun. 5, 2016

        Copyright ? 2016 by Journal of Neurology and Neurorehabilitation

        腦卒中后殘障發(fā)生率較高。卒中后出現(xiàn)的肌萎縮嚴重影響著康復治療方法的選擇與療效,一定程度上制約了患者的有效康復。目前有關(guān)卒中后肌萎縮的發(fā)生機制尚無統(tǒng)一結(jié)論。有學者提出卒中相關(guān)性肌萎縮的概念,但對于其發(fā)生機制尚不完全明確。目前認為,卒中相關(guān)性肌萎縮可能與發(fā)病后活動減少、攝入不足以及泛素蛋白酶體通路激活有關(guān)。本文通過結(jié)合近年來肌萎縮的相關(guān)研究,對卒中相關(guān)性肌萎縮發(fā)生機制進行綜述,同時與其他疾病所致的肌萎縮進行鑒別,以期為卒中后肌萎縮的預防和治療提供參考依據(jù)。

        To cite: WANG L J, ZHAN Q. Research progress in pathogenesis of stroke-related sarcopenia. J Neurol and Neurorehabil, 2016,12(2):102-105.

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