有氧運(yùn)動(dòng)對(duì)酒精性肝損傷小鼠ALT、AST、IL-10和IL-6等的影響

蔡文麗,張 慧,唐 選,牛英鵬

有氧運(yùn)動(dòng)對(duì)酒精性肝損傷小鼠ALT、AST、IL-10和IL-6等的影響

蔡文麗,張 慧,唐 選,牛英鵬

(河南大學(xué)體育學(xué)院,河南開(kāi)封475001)

目的:建立小鼠酒精性肝損傷模型,探討有氧運(yùn)動(dòng)對(duì)小鼠酒精性肝損傷后肝功能的影響以及血液白細(xì)胞介素-10(IL-10)、白細(xì)胞介素-6(IL-6)和總抗氧化能力(T-AOC)等的變化。方法:40只8周齡小鼠隨機(jī)分為N組(對(duì)照組)、E組(運(yùn)動(dòng)組)、AL組(酒精灌胃組)和E+AL組(運(yùn)動(dòng)+酒精灌胃組),分別施加有氧運(yùn)動(dòng)、酒精灌胃干預(yù)。10周后處死取脾臟、肝臟和血清,分別檢測(cè)IL-10、T-AOC、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷草轉(zhuǎn)氨酶(ALT)、谷丙轉(zhuǎn)氨酶(AST)和IL-6。結(jié)果:(1)血清ALT和AST含量,AL組和E+AL組非常顯著高于N組(P＜0.01),AL組高于E+AL組(P＜0.05);(2)脾臟IL-10含量,AL和E+AL組明顯高于N組,E組低于N組,E+AL組高于A(yíng)L組;AL組和E+AL組血清IL-6含量高于N組(P＜0.01),E+AL低于A(yíng)L組(P＜0.05);(3)肝臟TAOC,AL組、E+AL組低于(P＜0.01、P＜0.05)、E組高于(P＜0.05)N組,AL組低于E+AL組(P＜0.05);肝臟SOD,與N組比較,AL組(P＜0.05)、E+AL組降低、E組升高,E+AL組高于A(yíng)L組(P＜0.05),MDA含量,與N組相比,E組降低(P＜0.05),AL組升高(P＜0.01);E+AL組顯著性低于A(yíng)L組(P＜0.05)。結(jié)論:乙醇在肝臟內(nèi)代謝過(guò)程中會(huì)引起機(jī)體免疫反應(yīng)和炎癥反應(yīng),同時(shí)導(dǎo)致肝臟的脂質(zhì)過(guò)氧化損傷;適度的有氧運(yùn)動(dòng)干預(yù)可提高各實(shí)驗(yàn)對(duì)象抗氧化能力和抗炎能力,促進(jìn)機(jī)體免疫穩(wěn)定,減輕肝臟脂質(zhì)過(guò)氧化損傷和炎癥損傷,對(duì)酒精灌胃所致肝細(xì)胞損傷、炎癥反應(yīng)具有一定的緩解作用,提高機(jī)體免疫穩(wěn)定能力,但并不能阻止酒精性肝損傷的發(fā)生。

有氧運(yùn)動(dòng);酒精性肝損傷;ALT;AST;IL-10;IL-6;抗氧化能力

目前,酒精已成為繼病毒性肝炎后致肝損傷的第二大病因。乙醇在肝臟進(jìn)行代謝的過(guò)程中可生成多種活性氧自由基,包括超氧陰離子、羥自由基、過(guò)氧化氫等,進(jìn)而造成肝細(xì)胞廣泛的損傷。酒精誘發(fā)肝細(xì)胞損傷的機(jī)制較復(fù)雜,酒精對(duì)肝細(xì)胞的氧化損傷是其早期改變[1]。同時(shí),代謝紊亂、細(xì)胞因子、內(nèi)毒素等因素共同導(dǎo)致了酒精性肝損傷的發(fā)生[2-4]。近年來(lái),細(xì)胞因子與酒精性肝損傷發(fā)生機(jī)制的聯(lián)系成為研究熱點(diǎn)[5-8]。

長(zhǎng)期進(jìn)行中低強(qiáng)度的有氧運(yùn)動(dòng)可增強(qiáng)免疫功能,能有效改善非酒精性脂肪肝患者肝損傷、儲(chǔ)備功能及血脂代謝紊亂[9-11],但目前關(guān)于有氧運(yùn)動(dòng)對(duì)酒精性肝病影響的研究較少,且主要探討其提高肝臟抗氧化能力、改善肝臟脂質(zhì)過(guò)氧化等方面。本研究擬通過(guò)有氧運(yùn)動(dòng)干預(yù),分析其對(duì)小鼠肝功能、炎癥細(xì)胞因子、抗氧化等指標(biāo)的影響,探討有氧運(yùn)動(dòng)預(yù)防酒精性肝損傷的可能性,為運(yùn)動(dòng)干預(yù)改善酒精性肝損傷所致炎癥反應(yīng)、免疫抑制、抗氧化能力下降等提供理論依據(jù)。

1 實(shí)驗(yàn)對(duì)象和方法

1.1 實(shí)驗(yàn)對(duì)象

健康雌性清潔級(jí)C57BL/6小鼠40只,8周齡,分籠飼養(yǎng),每籠5只,國(guó)家標(biāo)準(zhǔn)嚙齒動(dòng)物飼料喂養(yǎng),自由飲食。飼養(yǎng)環(huán)境為室溫18±2℃,光照時(shí)間12小時(shí),相對(duì)濕度為40%～50%。實(shí)驗(yàn)動(dòng)物和飼料均由河南省實(shí)驗(yàn)動(dòng)物中心提供(許可證號(hào)SCXK(豫)2005-0001)。

1.2 實(shí)驗(yàn)方法

1.2.1 實(shí)驗(yàn)分組及處理 正式實(shí)驗(yàn)前,對(duì)所有實(shí)驗(yàn)對(duì)象進(jìn)行3天跑臺(tái)適應(yīng)性訓(xùn)練,然后隨機(jī)分為4組:N(對(duì)照)組、E(運(yùn)動(dòng))組、AL(酒精灌胃)組、E+AL(運(yùn)動(dòng)+酒精灌胃)組。參照加拿大學(xué)者femando[12]的研究方法,確定E組和E+AL組有氧運(yùn)動(dòng)干預(yù)方案如下:正式實(shí)驗(yàn)開(kāi)始后,第1周運(yùn)動(dòng)強(qiáng)度由6m/min逐漸遞增到9m/min,運(yùn)動(dòng)時(shí)間由10min/day遞增至50min/day;第2-10周按照12m/min、60min/day、0%坡度強(qiáng)度進(jìn)行運(yùn)動(dòng),每周訓(xùn)練5天。N組和AL組正常喂養(yǎng)。

1.2.2 酒精性肝損傷模型的建立 E+AL組和AL組建立慢性酒精性肝損傷小鼠模型。參照《小鼠酒精性肝損傷模型的動(dòng)態(tài)研究》[13]確定AL組和E+AL組酒精性肝損傷模型的灌胃方案:灌胃材料,56%的二鍋頭;灌胃劑量,每千克體重每天灌胃15ml;灌胃時(shí)間,第7-10周,每周6天。N組和E組實(shí)驗(yàn)對(duì)象按照相同方案灌胃安慰劑(生理鹽水)。

1.2.3 測(cè)試樣品的采集、處理及指標(biāo)測(cè)試 10周后,麻醉后股動(dòng)脈取血,離心處理分離血清待測(cè);取血后,將小鼠頸椎脫臼處死,取出脾臟、肝臟待測(cè)。谷草轉(zhuǎn)氨酶(ALT)和谷丙轉(zhuǎn)氨酶(AST)含量測(cè)定,賴(lài)氏法;脾臟細(xì)胞中白細(xì)胞介素-10(IL-10)表達(dá)的測(cè)定,制備懸液、染色、流式細(xì)胞儀測(cè)定分析;血清白細(xì)胞介素-6(IL-6),酶聯(lián)免疫(ELISA)法;肝組織總抗氧化能力(T-AOC),鐵還原法;肝組織丙二醛(MDA)含量測(cè)定,硫代巴比妥酸法;肝組織超氧化物歧化酶(SOD)活力測(cè)定,黃嘌呤氧化酶法。主要測(cè)試儀器:紫外可見(jiàn)光分光光度儀(北京普析通用儀器有限公司),流式細(xì)胞儀(FACSCalibur型,BD公司,USA);主要試劑盒:AST/GOT、ALT/GPT、MDA、SOD、T-AOC、IL-6試劑盒購(gòu)于南京建成科技有限公司;熒光標(biāo)記抗體購(gòu)于Biolegend公司。

1.3 數(shù)據(jù)處理

所有數(shù)據(jù)以平均數(shù)±標(biāo)準(zhǔn)差(M±SD)表示,采用SPSS 13.0軟件分析處理。組間進(jìn)行方差分析(ANOVA),方差不齊時(shí)采用多個(gè)獨(dú)立樣本非參數(shù)檢驗(yàn)。P＜0.05為顯著性差異,P＜0.01為非常顯著性差異。

2 實(shí)驗(yàn)結(jié)果

2.1 血清指標(biāo)變化情況

各組實(shí)驗(yàn)對(duì)象血清ALT、AST和IL-6變化情況見(jiàn)表1。

表1 各實(shí)驗(yàn)組血清ALT、AST、IL-6變化情況

如表1所示,與N組相比,AL組和E+AL組小鼠ALT和AST含量明顯升高(P＜0.01);E+AL組顯著性低于A(yíng)L組(P＜0.05)。血清IL-6含量測(cè)定結(jié)果顯示,AL組和E+AL組明顯高于N組(P＜0.01),E組低于N組(P＜0.05);與AL組相比,E+AL組出現(xiàn)下降,具有顯著性差異(P＜0.05)。表明酒精灌胃導(dǎo)致小鼠血清ALT、AST和IL-6含量升高,提示其引起肝細(xì)胞損傷和炎癥反應(yīng),運(yùn)動(dòng)干預(yù)具有一定的緩解作用。

2.2 脾淋巴細(xì)胞CD4+T cell IL-10變化情況

如圖1所示,IL-10的檢測(cè)結(jié)果,與N組相比,AL和E+AL組脾淋巴細(xì)胞中IL-10的含量明顯增高,E組降低;E+AL相對(duì)于A(yíng)L組含量增高。

圖1 各組小鼠CD4+T淋巴細(xì)胞亞群IL-10表達(dá)情況

2.3 肝組織T-AOC、SOD、MDA變化情況

肝組織T-AOC水平,與N組比較,AL組非常顯著性(P＜0.01)、E+AL組顯著性降低(P＜0.05),E組顯著性升高(P＜0.05);E+AL組顯著性高于A(yíng)L組(P＜0.05)。SOD水平,AL組顯著性低于(P＜0.05)、E+AL組低于N組,E組顯著性(P＜0.05)高于N組;與AL組比較,E+AL組升高,差異具有顯著性(P＜0.05)。MDA含量,與N組相比,E組顯著性降低(P＜0.05),AL組非常顯著性(P＜0.01)升高,E+AL組也升高,但沒(méi)有統(tǒng)計(jì)學(xué)意義;E+AL組顯著性低于A(yíng)L組(P＜0.05)。

表2 各實(shí)驗(yàn)組肝組織T-AOC、SOD、MDA變化情況

3 分析與討論

3.1 小鼠酒精性肝損傷造模情況分析

乙醇及其代謝產(chǎn)物乙醛對(duì)肝細(xì)胞有毒性作用,若長(zhǎng)期過(guò)量飲酒而不能及時(shí)代謝可導(dǎo)致不同程度的肝損傷;從生化指標(biāo)的變化看,可有標(biāo)志肝細(xì)胞線(xiàn)粒體損傷的谷草轉(zhuǎn)氨酶(AST)升高、標(biāo)志肝細(xì)胞膜損傷的谷丙轉(zhuǎn)氨酶(ALT)升高、標(biāo)志肝臟脂肪代謝紊亂的甘油三脂(TG)水平升高等[14]。本實(shí)驗(yàn)小鼠酒精性肝損傷造模參考趙敏等的《小鼠酒精性肝損傷模型的動(dòng)態(tài)研究》。實(shí)驗(yàn)結(jié)果顯示:AL組和E+AL組實(shí)驗(yàn)對(duì)象血清ALT、AST以及炎性因子IL-6和肝臟MDA含量顯著性升高,酒精灌胃導(dǎo)致血清轉(zhuǎn)氨酶含量升高、出現(xiàn)明顯的炎性和脂質(zhì)過(guò)氧化損傷,表明本實(shí)驗(yàn)酒精性肝損傷模型建模成功[13,14]。

3.2 血清ALT、AST的變化與分析

ALT、AST是人體內(nèi)兩種十分重要的轉(zhuǎn)氨酶,存在于細(xì)胞核及線(xiàn)粒體中。正常情況下兩種轉(zhuǎn)氨酶在血清中含量極低,ALT在肝臟中活性最強(qiáng),AST主要存在于心肌細(xì)胞和肝臟中。當(dāng)肝細(xì)胞受到損傷或發(fā)生病變時(shí),導(dǎo)致細(xì)胞的結(jié)構(gòu)和功能完整性遭到破壞,其內(nèi)部的ALT、AST大量釋放近入血液,引起血清ALT、AST含量升高同時(shí)導(dǎo)致肝臟組織中兩種酶的活性下降,因此血清中ALT、AST升高可作為肝臟功能受損或病變的敏感指標(biāo)標(biāo)[15,16]。本研究結(jié)果顯示,酒精灌胃致小鼠血清ALT、AST含量顯著升高。酒精攝入后引起的血清酶如AST、ALT水平增高,可能是因?yàn)榫凭鸬母渭?xì)胞損傷、細(xì)胞膜通透性增強(qiáng)所致[17]。有氧運(yùn)動(dòng)能降低血清ALT、AST含量[18],提示通過(guò)合理的有氧運(yùn)動(dòng)能有效減輕肝細(xì)胞微損傷、維護(hù)肝臟細(xì)胞膜結(jié)構(gòu)功能的完整性,防治酒精灌胃導(dǎo)致的肝細(xì)胞損傷。

3.3 IL-10、IL-6的變化與分析

細(xì)胞因子具有多種生物學(xué)功能,是由細(xì)胞分泌的一種小分子蛋白質(zhì),其在生物體免疫細(xì)胞的分化、免疫調(diào)節(jié)、免疫應(yīng)答以及炎癥反應(yīng)和造血過(guò)程中起著非常重要的作用,并且參與機(jī)體某些疾病和損傷的發(fā)生和發(fā)展[19]。IL-10具有多種重要的生物學(xué)功能,如通過(guò)抑制Kupfffer細(xì)胞的激活和其他炎性介質(zhì)、自由基生成與釋放、細(xì)胞因子、NF-Kb活性等,參與肝細(xì)胞再生的調(diào)節(jié)和抗肝纖維化等;通過(guò)減少TH1細(xì)胞生成INF-γ和白細(xì)胞介素-2(IL-2)等,參與生物體炎癥反應(yīng)過(guò)程并起到抗炎的作用。IL-10主要由TH2細(xì)胞、肝臟細(xì)胞、肝臟星形細(xì)胞、肥大細(xì)胞和巨噬細(xì)胞等生成,參與某些病理、損傷和炎性反應(yīng)過(guò)程,是CD4+CD25+Treg重要的免疫抑制因子,誘導(dǎo)其轉(zhuǎn)化為具有調(diào)節(jié)性T細(xì)胞功能的CD4+CD25+T細(xì)胞等。在炎癥過(guò)程中發(fā)揮反調(diào)控效應(yīng),在肝臟病變或受到損傷時(shí)能起到一定的保護(hù)作用,減輕肝臟病變或損傷的程度[20-22]。因此IL-10在脾臟淋巴細(xì)胞中的表達(dá)可作為評(píng)價(jià)機(jī)體免疫能力和抗炎能力的敏感指標(biāo)。IL-6是一個(gè)多效型細(xì)胞因子,可由多種細(xì)胞分泌,包括單核/巨噬細(xì)胞、T細(xì)胞等,其受體廣泛表達(dá)于免疫細(xì)胞、肝細(xì)胞等多種組織細(xì)胞,在免疫和免疫調(diào)節(jié)中發(fā)揮著重要作用,但是濃度過(guò)高可引起病理?yè)p傷。大量研究表明IL-6與酒精性肝損傷的發(fā)生發(fā)展有密切聯(lián)系[23-25]。

本研究結(jié)果統(tǒng)計(jì)顯示,與N組相比,AL和E+AL組脾淋巴細(xì)胞中IL-10的含量明顯增高,E+AL相對(duì)于A(yíng)L組含量增高,酒精灌胃顯著提高了CD4+T細(xì)胞亞群IL-10的表達(dá)量。這些結(jié)果提示酒精灌胃可能通過(guò)增加CD4+T細(xì)胞IL-10的表達(dá)來(lái)抑制機(jī)體的免疫功能;而E+AL組CD4+IL-10相對(duì)增加,提示有氧運(yùn)動(dòng)可能通過(guò)上調(diào)抗炎癥性細(xì)胞因子IL-10的表達(dá),抑制促炎癥性細(xì)胞因子IL-6和TNF-α的產(chǎn)生,從而抑制細(xì)胞免疫反應(yīng),減輕炎癥對(duì)肝細(xì)胞造成的損傷,通過(guò)穩(wěn)定免疫系統(tǒng)炎癥因子表達(dá)提高機(jī)體免疫力。適度的有氧運(yùn)動(dòng)可以降低IL-6的含量,有利于提高機(jī)體的免疫功能和抗炎能力,減少疾病的發(fā)生[26,27]。本研究血清IL-6水平,與N組相比,AL組和E+AL組明顯升高;與AL組相比,E+AL組降低。表明酒精灌胃導(dǎo)致了肝臟的炎癥損傷,有氧運(yùn)動(dòng)干預(yù)能明顯抑制酒精性肝損傷小鼠血清IL-6水平增高和肝細(xì)胞的炎癥反應(yīng)。本實(shí)驗(yàn)酒精性肝損傷小鼠細(xì)胞因子IL-6、IL-10均明顯升高,表明酒精灌胃導(dǎo)致炎癥反應(yīng)和抗炎能力均增強(qiáng)。而有氧運(yùn)動(dòng)干預(yù)引起IL-6明顯降低、IL-10增高,說(shuō)明有氧運(yùn)動(dòng)干預(yù)對(duì)酒精灌胃造成的炎癥反應(yīng)有明顯抑制作用,小鼠免疫機(jī)能穩(wěn)定,可減輕酒精導(dǎo)致的肝臟炎癥性損傷。

3.4 抗氧化能力的變化與分析

機(jī)體總抗氧化能力(Total Anti Oxide Capacity T-AOC)由酶促和非酶促兩類(lèi)抗氧化體系組成,綜合反映了機(jī)體總抗氧化以及清除自由基的能力?？寡趸赶蛋⊿OD、CAT、GSH-PX等,其中SOD活性最強(qiáng),作用最廣泛。在生物體內(nèi),由于脂質(zhì)過(guò)氧化反應(yīng)的增強(qiáng)和機(jī)體抗氧化能力下降,導(dǎo)致大量自由基生成,并且反應(yīng)終產(chǎn)物MDA含量增加,誘發(fā)細(xì)胞內(nèi)蛋白質(zhì)、核酸等的交聯(lián)聚合,具有較大的細(xì)胞毒性作用,使細(xì)胞的結(jié)構(gòu)和功能完整性遭到破壞。大量研究表明,適度的有氧運(yùn)動(dòng)能增強(qiáng)肝組織清除氧自由基的能力,降低肝組織脂質(zhì)過(guò)氧化反應(yīng),從而減輕酒精對(duì)肝臟的損傷,促進(jìn)肝功能的恢復(fù)[28-30]。本實(shí)驗(yàn)結(jié)果肝組織T-AOC、SOD水平,與N組比較,AL組、E+AL組降低,E組升高,并且E+AL組顯著性高于A(yíng)L組;MDA含量,E組顯著性低于、AL組非常顯著性高于N組,E+AL組也升高,但顯著性低于A(yíng)L組。以上結(jié)果表明,酒精灌胃導(dǎo)致小鼠抗氧化能力下降,有氧運(yùn)動(dòng)可通過(guò)提高SOD等相關(guān)抗氧化酶的活性,增強(qiáng)肝臟總抗氧化能力,防止酒精灌胃導(dǎo)致的小鼠抗氧化能力的下降及肝臟脂質(zhì)過(guò)氧化損傷。

4 小 結(jié)

酒精灌胃導(dǎo)致小鼠肝臟脂質(zhì)過(guò)氧化損傷的同時(shí)引起免疫與炎癥性反應(yīng);有氧運(yùn)動(dòng)在一定程度上提高了小鼠抗氧化能力、免疫能力和抗炎能力,減輕肝臟脂質(zhì)過(guò)氧化損傷和炎癥損傷,對(duì)酒精灌胃所致肝細(xì)胞損傷、炎癥反應(yīng)具有一定的緩解作用,提高機(jī)體免疫能力,但并不能阻止酒精性肝損傷的發(fā)生。

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Effects of Aerobic Exercise on ALT,AST,IL-10 and IL-6 in Mice with Alcoholic Injury of Liver

CAI Wenli,ZHANG Hui,TANG Xuan,NIU Yingpeng
(Institute of Physical Education,Henan University,Kaifeng 475001,Henan,China)

Objective:To analyze the changes of liver function,IL-10,IL-6 and T-AOC in mice,intervene by alcoholic and aerobic exercise,to explore its effects on alcoholic liver injury and its mechanism.Methods:40 mice were randomly divided into control group(N),exercise group(E),alcohol group(AL),exercise plus alcohol group(E+AL),constructing a model of aerobic exercise and alcoholic liver injury.After 10 weeks,taking the serum,liver and spleen,the AST,ALT,IL-10,IL-6,T-AOC,SOD and MDA index were tested.Results:(1)the content of ALT and AST,compared with N group,AL and E+AL group were significantly increased(P＜0.01);group E+AL was significant lower than that in AL group(P＜0.05);(2)the content of IL-10 in spleen lymphocyte,compared with N group,AL and E+AL group are decreased significantly,but E+AL group are increased vs.AL group.The content of serum IL-6,AL and E+AL group were significantly higher than that in N group(P＜0.01),E group was lower,and E+AL was lower than that of AL group(P＜0.05);(3)the level of T-AOC in hepatic tissue,compared with group N,AL and E+AL group were decreased significantly(P＜0.01,P＜0.05),E+AL group was significantly higher than that of AL(P＜0.05);The level of SOD,AL and E+AL group were significantly lower than in group N;E+AL group was raised than AL group(P＜0.05).The content of MDA,compared with that of N group,E group decreased significantly(P＜0.05),AL group was increased significantly(P＜0.01);E+AL group was significantly lower than those in group AL(P＜0.05).Conclusion:Aerobic exercise can improve the ability of anti-oxidation,immunity and inflammation,reduce liver lipid per oxidation and inflammatory injury of liver caused by alcohol,and has a preventive effect on the damage,but can’t prevent the occurring of alcoholic liver injury.

aerobic exercise;alcoholic injury of liver;ALT;AST;IL-10;IL-6;antioxidant capacity

G804.7

A

1004-0560(2013)03-0089-04

2013-03-11;

2013-04-26

河南省科技發(fā)展(攻關(guān)重點(diǎn))計(jì)劃,項(xiàng)目編號(hào):112102310576。

蔡文麗(1981-),女,講師,碩士,主要研究方向?yàn)檫\(yùn)動(dòng)與健康促進(jìn)。

責(zé)任編輯:劉紅霞