張佳，黃昌林

中頻脈沖電流經(jīng)皮刺激肝區(qū)對(duì)運(yùn)動(dòng)性疲勞大鼠大腦皮質(zhì)自由基及尼氏體的影響

張佳，黃昌林

目的 研究中頻脈沖電流經(jīng)皮刺激肝區(qū)對(duì)大鼠抗運(yùn)動(dòng)性疲勞能力及大腦皮質(zhì)自由基和尼氏體的影響。方法 8周齡Wistar雄性大鼠72只，隨機(jī)分為安靜對(duì)照組(CG組)、疲勞訓(xùn)練組(FG組)、運(yùn)動(dòng)前刺激組(SBF組)、運(yùn)動(dòng)后刺激組(SAF組)，每組18只。除CG組外各組均進(jìn)行游泳訓(xùn)練，建立運(yùn)動(dòng)疲勞模型，SBF組和SAF組大鼠分別在游泳前和力竭后進(jìn)行肝區(qū)中頻脈沖電流刺激(頻率1024Hz，電流強(qiáng)度10mA，間動(dòng)周期1s，時(shí)間20min)。于第1、3、5周末測(cè)定各組大鼠的游泳力竭時(shí)間，檢測(cè)大腦皮質(zhì)中自由基脂質(zhì)過(guò)氧化相關(guān)指標(biāo)，包括總超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽過(guò)氧化物酶(GSH-Px)、SOD/MDA比值，并觀察神經(jīng)元尼氏體的病理改變。結(jié)果 第1周末各組各指標(biāo)比較差異均無(wú)統(tǒng)計(jì)學(xué)意義。第3周末SAF組大鼠游泳力竭時(shí)間明顯長(zhǎng)于FG組，第5周末SAF組大鼠游泳力竭時(shí)間明顯長(zhǎng)于FG組和SBF組(P<0.05)。第5周末FG組、SBF組SOD、GSH-Px、SOD/MDA明顯低于CG組和SAF組，MDA明顯高于CG組和SAF組(P<0.05)。神經(jīng)元尼氏體染色顯示，第5周末SAF組大鼠尼氏體數(shù)目/相應(yīng)面積的比值明顯高于FG組和SBF組(P<0.01)。結(jié)論 中頻脈沖電流經(jīng)皮刺激肝區(qū)可有效降低疲勞大鼠大腦皮質(zhì)的自由基脂質(zhì)過(guò)氧化損傷，減少尼氏體溶解、消失，提高游泳力竭時(shí)間，延緩疲勞的發(fā)生。

中頻脈沖電流；運(yùn)動(dòng)性疲勞；大腦皮質(zhì)；自由基；虎斑小體

延緩疲勞的發(fā)生和促進(jìn)疲勞恢復(fù)一直是軍事訓(xùn)練醫(yī)學(xué)、運(yùn)動(dòng)醫(yī)學(xué)及航天航海醫(yī)學(xué)的研究重點(diǎn)。目前，抗疲勞多采用中藥治療、針灸、艾灸等，在效果上各有不盡如人意之處。本課題組前期研究發(fā)現(xiàn)，中頻脈沖電流經(jīng)皮刺激肝區(qū)可緩解外周疲勞[1]，本研究在此基礎(chǔ)上探討了脈沖電流經(jīng)皮刺激肝區(qū)對(duì)大腦皮質(zhì)自由基和尼氏體的影響，旨在進(jìn)一步深入了解脈沖電流經(jīng)皮刺激肝區(qū)的抗疲勞作用機(jī)制。

1 材料與方法

1.1 實(shí)驗(yàn)動(dòng)物 清潔級(jí)8周齡雄性Wistar大鼠72只，體重204±15g，由河南省實(shí)驗(yàn)動(dòng)物中心提供，飼養(yǎng)室溫度23±2℃，濕度41%±15%，自然光照，分籠飼養(yǎng)，自由進(jìn)食水。

1.2 實(shí)驗(yàn)方法

1.2.1 動(dòng)物模型建立及分組 將實(shí)驗(yàn)動(dòng)物隨機(jī)分為4組：安靜對(duì)照組(CG組)、疲勞訓(xùn)練組(FG組)、運(yùn)動(dòng)前刺激組(SBF組)、運(yùn)動(dòng)后刺激組(SAF組)，每組18只。CG組不進(jìn)行任何訓(xùn)練。FG組、SBF組及SAF組大鼠連續(xù)5周進(jìn)行游泳訓(xùn)練，水深60cm，水溫31±2℃，每周訓(xùn)練6d，休息1d，游泳2次/d，每次均達(dá)到力竭，當(dāng)大鼠浮在水面不運(yùn)動(dòng)時(shí)用玻璃棒驅(qū)趕，維持其運(yùn)動(dòng)狀態(tài)，力竭標(biāo)準(zhǔn)為大鼠下沉后10s不能游回水面[2]。SBF組大鼠在游泳前、SAF組大鼠在游泳力竭后腹腔注射鹽酸氯胺酮0.25g/kg麻醉，然后行經(jīng)皮肝區(qū)中頻脈沖電流刺激，脈沖電流刺激頻率為1024Hz，電流強(qiáng)度為10mA，間動(dòng)周期為1s，時(shí)間為20min，2次/d。

1.2.2 標(biāo)本制備及指標(biāo)檢測(cè) 分別在第1、3、5周訓(xùn)練的最后1d測(cè)定FG組、SBF組和SAF組大鼠的游泳力竭時(shí)間。在第1、3、5周的休息日各組大鼠采取氯胺酮0.25g/kg腹腔注射麻醉后分批斷頭處死，立即開(kāi)顱，在冰盤上迅速剝?nèi)〈竽X皮質(zhì)，用冰冷的生理鹽水漂洗，濾紙吸干，一部分–80℃冰箱中保存，一部分用甲醛溶液固定，石蠟包埋。測(cè)試前用剪刀剪下0.6～0.9g大腦皮質(zhì)組織，按1:9(質(zhì)量分?jǐn)?shù))加入4℃生理鹽水，眼科小剪剪碎組織塊，超聲勻漿，制成質(zhì)量分?jǐn)?shù)為10%的腦組織勻漿液，3000r/min低溫離心10min，取上清液于樣品管中，用于測(cè)定相關(guān)指標(biāo)。總超氧化物歧化酶(SOD)采用黃嘌呤氧化酶法測(cè)定，丙二醛(MDA)采用硫代巴比妥酸(TBA)法測(cè)定，谷胱甘肽過(guò)氧化物酶(GSH-Px)采用化學(xué)比色法測(cè)定，所用試劑盒均由南京建成生物工程研究所提供，具體操作嚴(yán)格按說(shuō)明書(shū)進(jìn)行。

1.2.3 尼氏體焦油紫染色 取大鼠大腦皮質(zhì)組織，常規(guī)石蠟包埋、切片、脫蠟，雙蒸水水化3min，焦油紫室溫避光染色30min，水洗，95%乙醇分化，二甲苯透明，中性樹(shù)膠封固，光鏡下觀察，并采用Image-Pro Plus圖像分析軟件對(duì)尼氏體數(shù)目/相應(yīng)面積的比值進(jìn)行分析。

1.3 統(tǒng)計(jì)學(xué)處理 采用SPSS 18.0進(jìn)行統(tǒng)計(jì)分析，數(shù)據(jù)結(jié)果以±s表示，組間比較采用單因素方差分析，進(jìn)一步兩兩比較采用LSD-t檢驗(yàn)。P<0.05為差異有統(tǒng)計(jì)學(xué)意義。

2 結(jié) 果

表1 各組大鼠游泳力竭時(shí)間的比較(min，±s，n=6)Tab. 1 Exhausted swimming time of rat in every group (min,±s, n=6)

表1 各組大鼠游泳力竭時(shí)間的比較(min，±s，n=6)Tab. 1 Exhausted swimming time of rat in every group (min,±s, n=6)

(1)P<0.05 compared with FG group; (2)P<0.05 compared with SBF group

?

2.2 中頻脈沖電流經(jīng)皮刺激肝區(qū)對(duì)大鼠大腦皮質(zhì)自由基脂質(zhì)過(guò)氧化的影響 第1周末各組SOD、MDA、GSH-Px及SOD/MDA比值差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)。第3周末FG組、SBF組、SAF組SOD 及SOD/MDA比值明顯低于CG組，F(xiàn)G組MDA明顯高于CG組，F(xiàn)G組和SBF組GSH-Px明顯低于CG組(P<0.05，P<0.01)，其余各組間比較差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)。第5周末FG組和SBF組的SOD、GSH-Px及SOD/MDA比值明顯低于CG組和SAF組(P<0.01)，而FG組與SBF組比較、CG組與SAF組比較差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)，F(xiàn)G組和SBF組的MDA明顯高于CG組(P<0.05，P<0.01)，且SAF組的MDA明顯低于FG組(P<0.05)，其余各組間比較差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05，表2)。

2.3 尼氏體染色后光鏡下觀察結(jié)果及定量分析CG組、SAF組可見(jiàn)許多形態(tài)結(jié)構(gòu)較規(guī)則的塊狀(形如虎斑)或顆粒狀尼氏小體；FG組、SBF組神經(jīng)元胞質(zhì)內(nèi)尼氏體逐漸溶解或消失，數(shù)目減少，細(xì)胞排列紊亂、極不規(guī)則，部分神經(jīng)元缺失，胞核和胞質(zhì)分界不明顯，以第5周末較為明顯(圖1)。

表2 各組大鼠SOD、MDA、GSH-Px、SOD/MDA比較(±s，n=6)Tab. 2 Comparison of SOD, MDA, GSH-Px and SOD/MDA of rats in each group (±s, n=6)

表2 各組大鼠SOD、MDA、GSH-Px、SOD/MDA比較(±s，n=6)Tab. 2 Comparison of SOD, MDA, GSH-Px and SOD/MDA of rats in each group (±s, n=6)

(1)P<0.05, (2)P<0.01 compared with CG group; (3)P<0.05, (4)P<0.01 compared with FG group; (5)P<0.01 compared with SBF group

圖1 第5周末各組大鼠大腦皮質(zhì)神經(jīng)元尼氏體焦油紫染色觀察(×400)Fig. 1 The cortical neuron Nissl body at the fifth weekend (Cresyl viollet stainning ×400)

采用Image-Pro Plus軟件進(jìn)行分析顯示，F(xiàn)G組、SBF組尼氏體數(shù)目/相應(yīng)面積的比值于第3周末開(kāi)始減少，到第5周末更為明顯，與CG組及SAF組比較差異有統(tǒng)計(jì)學(xué)意義(P<0.01，圖2)。

3 討 論

長(zhǎng)期或劇烈運(yùn)動(dòng)可導(dǎo)致中樞神經(jīng)系統(tǒng)穩(wěn)態(tài)失調(diào)，損傷腦動(dòng)力，引發(fā)中樞性疲勞[3]。中樞性疲勞不能僅用肌肉本身的功能紊亂來(lái)解釋，同時(shí)還與中樞神經(jīng)系統(tǒng)特異性的功能改變有關(guān)[4]。

力竭時(shí)間是機(jī)體抗應(yīng)激、抗疲勞等多種能力的綜合體現(xiàn)，是衡量機(jī)體運(yùn)動(dòng)能力的重要直接指標(biāo)，目前研究中多用大鼠開(kāi)始游泳至力竭所用時(shí)間反映大鼠的力竭運(yùn)動(dòng)能力[5]。楊東升等[6]研究發(fā)現(xiàn)力竭運(yùn)動(dòng)所致外周持續(xù)低血糖可能是中樞能量代謝紊亂的原因之一。McKonna等[7]發(fā)現(xiàn)中樞神經(jīng)系統(tǒng)電生理功能的實(shí)現(xiàn)依賴于腦的能量代謝，中樞能量物質(zhì)葡萄糖和乳酸是保證神經(jīng)元正常電生理活動(dòng)的物質(zhì)基礎(chǔ)，對(duì)于維持神經(jīng)元的膜電位、復(fù)合動(dòng)作電位及突觸功能的完整性均起重要作用。此外在運(yùn)動(dòng)時(shí)血液的重新分布會(huì)導(dǎo)致肝臟等內(nèi)臟器官血供減少，影響肝臟組織的結(jié)構(gòu)和功能，導(dǎo)致運(yùn)動(dòng)性疲勞的發(fā)生。本研究結(jié)果表明，疲勞后中頻脈沖電刺激肝區(qū)有助于延長(zhǎng)大鼠的力竭時(shí)間，延緩疲勞的發(fā)生，其作用機(jī)制可能為：①脈沖電流刺激肝區(qū)促進(jìn)肝臟糖異生，使外周血糖升高；②脈沖電流刺激肝區(qū)導(dǎo)致肝血流量相對(duì)增加，延緩了疲勞的發(fā)生。

圖2 各組大鼠大腦皮質(zhì)神經(jīng)元尼氏體數(shù)目/相應(yīng)面積比值分析Fig. 2 A ratio of number/corresponding area of the cortical neuron Nissl body of rats

在正常情況下體內(nèi)自由基的產(chǎn)生和清除處于一個(gè)動(dòng)態(tài)平衡狀態(tài)[8]。SOD、GSH-Px是機(jī)體清除氧自由基的重要抗氧化酶，對(duì)機(jī)體的氧化與抗氧化平衡起著至關(guān)重要的作用，其活力的高低間接反映了機(jī)體清除氧自由基的能力。MDA是細(xì)胞脂質(zhì)過(guò)氧化的一種主要產(chǎn)物，其濃度是膜脂質(zhì)過(guò)氧化損害程度的標(biāo)志，大量MDA可使神經(jīng)元變性壞死，對(duì)腦組織有直接的損害作用，測(cè)定MDA濃度可間接反映氧自由基的水平及氧自由基對(duì)細(xì)胞的損傷程度[9-10]。SOD/MDA比值是反映機(jī)體組織細(xì)胞潛在抗氧化能力的重要參數(shù)，該比值升高表示組織細(xì)胞抗氧化能力相對(duì)增強(qiáng)或MDA生成量相對(duì)減少，降低則表示組織細(xì)胞抗氧化能力相對(duì)減弱或MDA生成量相對(duì)增多。力竭運(yùn)動(dòng)時(shí)，氧自由基大量產(chǎn)生，同時(shí)機(jī)體內(nèi)的自由基防御系統(tǒng)如SOD、GSH-Px等酶活力下降[11]，不足以清除過(guò)量的自由基，大量的氧自由基廣泛攻擊富含不飽和脂肪酸的神經(jīng)元膜和微血管，引起脂質(zhì)過(guò)氧化“瀑布狀”的連鎖反應(yīng)和微循環(huán)障礙，致使大量神經(jīng)元受損[12]。腦是機(jī)體氧消耗最多的器官之一，氧代謝過(guò)程中可產(chǎn)生少量的氧自由基，同時(shí)腦組織富含脂質(zhì)，氧自由基對(duì)不飽和共價(jià)鍵有一種特殊的親和力，最容易攻擊生物膜磷脂中的不飽和脂肪酸，引發(fā)生物膜的脂質(zhì)過(guò)氧化反應(yīng)[13-14]，破壞生物膜的完整性和流動(dòng)性，導(dǎo)致胞內(nèi)Ca2+嚴(yán)重超負(fù)荷，線粒體和三磷腺苷含量明顯減少，進(jìn)而使運(yùn)動(dòng)沖動(dòng)發(fā)放減弱，大腦分析、綜合能力下降，并產(chǎn)生各種感覺(jué)障礙，還可導(dǎo)致心理應(yīng)激增強(qiáng)、不良情緒增多，阻礙運(yùn)動(dòng)成績(jī)的發(fā)揮。Metin等[15]研究發(fā)現(xiàn)遞增負(fù)荷運(yùn)動(dòng)可使脂質(zhì)過(guò)氧化產(chǎn)物大量增加，進(jìn)而使膜的流動(dòng)性、通透性和興奮性降低，引起細(xì)胞腫脹和組織炎癥，從而導(dǎo)致疲勞。本研究結(jié)果表明，中頻脈沖電流經(jīng)皮刺激肝區(qū)可提高疲勞大鼠大腦皮質(zhì)的SOD、GSH-Px酶活力及SOD/MDA比值，同時(shí)降低MDA含量。其作用機(jī)制可能為：①激活機(jī)體內(nèi)源性的抗氧化防御系統(tǒng)；②加速體內(nèi)不飽和脂肪酸的氧化；③提高肝臟氧化呼吸鏈酶復(fù)合物活性水平；④脈沖電流刺激具有興奮中樞神經(jīng)元細(xì)胞的作用[16]。

尼氏體特異性地分布于神經(jīng)元胞體和樹(shù)突，電鏡觀察顯示其由粗面內(nèi)質(zhì)網(wǎng)、游離核糖體和多核糖體構(gòu)成，是神經(jīng)元合成蛋白質(zhì)最活躍的部位，尼氏體溶解或消失是神經(jīng)元受損的表現(xiàn)[17]。本研究結(jié)果顯示，力竭運(yùn)動(dòng)大鼠大腦皮質(zhì)尼氏體溶解或消失，提示尼氏體是對(duì)疲勞所致自由基損傷較為敏感的細(xì)胞器，而疲勞后中頻脈沖電流經(jīng)皮刺激肝區(qū)可以減輕大鼠大腦皮質(zhì)尼氏體的減少，對(duì)中樞神經(jīng)細(xì)胞具有保護(hù)作用。

小任務(wù)的實(shí)施隨課文講解的進(jìn)度進(jìn)行，教師不會(huì)專門留出時(shí)間進(jìn)行。如在進(jìn)行課文導(dǎo)入時(shí)，領(lǐng)取了導(dǎo)入任務(wù)的兩組學(xué)生分別進(jìn)行展示，負(fù)責(zé)資料查詢的兩位學(xué)生分別將搜集好的錢學(xué)森和喬布斯的生平、成就、貢獻(xiàn)等進(jìn)行匯報(bào)，另一組同學(xué)分別提出一些與主題相關(guān)的問(wèn)題并組織全班進(jìn)行討論，如他們是如何實(shí)現(xiàn)夢(mèng)想的？經(jīng)歷了哪些困難？給我們帶來(lái)哪些啟發(fā)？

綜上所述，中頻脈沖電流經(jīng)皮刺激肝區(qū)可提高疲勞大鼠的力竭時(shí)間，促進(jìn)自由基清除，減少自由基及其引發(fā)的脂質(zhì)過(guò)氧化對(duì)大腦皮質(zhì)的氧化損傷和對(duì)神經(jīng)元尼氏體的破壞，具有抗中樞性疲勞的作用。

[1]Huang CL, Zhu LG. Anti-fatigue effect of percutaneous stimulation with different frequency pulse current on hepatic region: an experimental study with rats[J]. Med J Chin PLA, 2009, 34(6): 740-742.[黃昌林, 朱履剛. 不同頻率脈沖電流經(jīng)皮刺激大鼠肝區(qū)增強(qiáng)抗疲勞能力的實(shí)驗(yàn)研究[J]. 解放軍醫(yī)學(xué)雜志, 2009, 34(6): 740-742.]

[2]Kanter MM. Free radicals exercise and antioxidant supplementation[J]. Int J Sport Nutr, 1994, 4(3): 205-206.

[3]Nybo L, Secher NH. Cerebtal perturbations provoked by prolonged exercise[J]. Prog Neurobiol, 2004, 72(4): 223-261.

[4]Davis JM, Bailey SP. Possible mechanism of central nervous system fatigue during exercise[J]. Med Sci Sports Exerc, 1997, 29(1): 45-57.

[5]Voces J, Alvarez AI, Vila L, et al. Effects of administration of the standardized Panax ginseng extract G115 on hepatie antioxidant function after exhaustive exercise[J]. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol, 1999, 123(2): 175-184.

[6]Yang DS, Liu XL, Qiao DC. Exhaustion movement process of glucose/lactic acid metabolism in rat striatum real-time observation[J]. Chin J Sports Med, 2009, 28(4): 384-387.[楊東升, 劉曉莉, 喬德才. 力竭運(yùn)動(dòng)過(guò)程中大鼠紋狀體葡萄糖/乳酸代謝的實(shí)時(shí)觀察[J]. 中國(guó)運(yùn)動(dòng)醫(yī)學(xué)雜志, 2009, 28(4): 384-387.]

[7]McKenna MC, Hopkins IB, Carey A. Alpha-cyano-4-hydroxycionamate decreasesboth glucose and lactate metabolism in neurons and astrocytes: implication for lactate as all energysubstrate for neurons[J]. J Neurosci Res, 2001, 66(5): 747-754.

[8]Husain K, Somani SM. Response of cardiac antioxidant system to alcohol and exercise training in the rat[J]. Alcohol, 1997, 14(3): 301-307.

[9]Fan LH, Wang KZ, Cheng B, et al. Anti-apoptotic and neuroprotective effects of Tetramethylpyrazine following spinal cord ischemia in rabbits[J]. BMC Neurosci, 2006, 7: 48.

[10] Abd-Elghaffar SKh, El-Sokkary GH, Sharkawy AA. Aluminuminduced neurotoxicity and oxidative damage in rabbits:protective effect of melatonin[J]. Neuro Endocrinol Lett, 2005, 26(5): 609-616.

[11] Dai PY, Huang CL. Influence of percutaneous stimulation of hepatic region with mid-frequency pulse current on the activity of serum GSH-PX, SOD, T-AOC and the content of malondialdehyde in exercise-induced fatigued soldiers[J]. Med J Chin PLA, 2014, 39(3): 245-248. [代朋乙, 黃昌林. 中頻脈沖電流經(jīng)皮刺激運(yùn)動(dòng)性疲勞士兵肝區(qū)對(duì)血清GSH-PX、SOD、T-AOC活性及MDA含量的影響[J]. 解放軍醫(yī)學(xué)雜志, 2014, 39(3): 245-248.]

[12] Yoshiha S, Abe K, Basto R, et al. Influence of transient ischemia on lipidsoluble antioxidants, free fatty acid and energy metabolites in rat brain[J]. Brain Res,1982, 2(5): 245-307.

[13] Selamoglu Talas Z, Ozdemir I, Yilmaz I, et al. The investigation of the antioxidative properties of the novel synthetic organoselenium compounds in some rat tissues[J]. Exp Biol Med (Maywood), 2008, 233(5): 575-579.

[14] Devrim E, Cetin M, Namuslu M, et al. Oxidant stress due to non ionic low osmolar contrast medium in rat kidney[J]. Indian Med Res, 2009, 130(4): 433-436.

[15] Metin G, Atukeren P, Alturfan AA, et al. Lipid peroxidation, erythrocyte superoxide-dismutase activity and trace metals in young male footballers[J]. Yonsei Med J, 2003, 44(6): 979-986.

[16] Zheng Yu, Cai D, Wang JH, et al. Effect of pulse magnetic field on distribution of neuronal action potential[J]. Acta Physiologica Sinica, 2014, 66(4): 438-448.[鄭羽, 蔡迪, 王金海, 等. 脈沖磁場(chǎng)對(duì)神經(jīng)元?jiǎng)幼麟娢话l(fā)放的影響[J]. 生理學(xué)報(bào), 2014, 66(4): 438-448.]

[17] Paul CA, Beltz B, Berger-Sweeney J. The nissl stain: a stain for cell bodies in brain sections[J]. CSH Protoc, 2008, 2008: pdb. prot4805.

Effects of percutaneous midband pulse current stimulation in hepatic region on free radical and nissl bodies in cerebral cortex of rats with exercise-induced fatigue

ZHANG Jia1, HUANG Chang-lin2*1Institute of Traumatic Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China
2Institute of Military Training Related Medical Sciences, 150 Hospital of PLA, Henan, Luoyang 471031, China
*

, E-mail: huangchanglin1945@263.net
This work was supported by the Health and Disease Prevention and Control Applied Research Program of Military Program (13BJYZ14)

ObjectiveTo investigate the effects of percutaneous midband pulse current stimulation in hepatic region on anti-exercise fatigue ability and the free radicals and nissl bodies in cerebral cortex tissue of rats with exercise-induced fatigue.MethodsSeventy-two 8-week old male Wistar rats were randomly divided into 4 groups (18 each): control group (CG), fatigue group (FG), stimulation before fatigue group (SBF) and stimulation after fatigue group (SAF). Animals in FG, SBF and SAF group were used to reproduce the swimming-exhaustion models. Midband current stimulation (1024Hz, 10mA, current cycle 1sec) for 20 minutes was given to the rats of group SBF before swimming, and to those in group SAF after exhaustion. At the weekend of the 1st, 3rd and 5th week after modeling, the exhaustive swimming time of rats in all but CG group was observed. Cerebral cortex tissue was harvested for the estimation of the level of lipid peroxidation, including SOD, MDA, GSH-Px and SOD/MDA, and the histopathological changes in nissl bodies in neurons were observed.ResultsAt the 1st weekend after modeling, no significant difference was found in all the indexes among the 4 groups, while at the 3rd weekend, the exhaustive time was obviously longer in SAF group than in FG group, and also in SAF group than in FG and SBF group at the 5th weekend (P<0.05). At the 5th weekend, the SOD and GSH-Px levels and SOD/MDA contents were obviously lower in FG and SBF group than in CG and SAF group, andthe MDA content was obviously higher in FG and SBF group than in CG and SAF group (P<0.05). As regarding the nissl bodies in neurons, it is observed that the ratio of number/area was obviously higher in SAF group than in FG and SBF group at the 5th weekend (P<0.01).ConclusionPercutaneous stimulation of hepatic region with midband pulse current can effectively reduce the lipid peroxidation damage of cerebral cortex tissue and decrease the dissolution and loss of nissl bodies in fatigued rats, prolong the exhausting exercise time, and postpone the development of fatigue.

mid-frequency pulse current; exercise-induced fatigue; cerebral cortex; free radicals; Nissl bodies

R333.4；R972.7

A

0577-7402(2015)04-0331-05

10.11855/j.issn.0577-7402.2015.04.16

2014-09-22；

2015-03-05)

(責(zé)任編輯：胡全兵)

2013年度部隊(duì)衛(wèi)生和疾病防控應(yīng)用性研究課題計(jì)劃(13BJYZ14)

張佳，碩士研究生。主要從事骨科及軍事訓(xùn)練損傷的基礎(chǔ)與臨床研究

710032 西安 第四軍醫(yī)大學(xué)西京醫(yī)院全軍創(chuàng)傷骨科研究所(張佳)；471031 河南洛陽(yáng) 解放軍150醫(yī)院全軍軍事訓(xùn)練醫(yī)學(xué)研究所(黃昌林)

黃昌林，E-mail：huangchanglin1945@263.net