劉義鑫,潘靈輝,林 飛,葛萬(wàn)運(yùn),楊 建

(廣西醫(yī)科大學(xué)附屬腫瘤醫(yī)院麻醉科,南寧 530021)

肺組織低氧代謝中葡萄糖轉(zhuǎn)運(yùn)蛋白1的表達(dá)及其作用*

劉義鑫,潘靈輝△,林 飛,葛萬(wàn)運(yùn),楊 建

(廣西醫(yī)科大學(xué)附屬腫瘤醫(yī)院麻醉科,南寧 530021)

目的探討單肺通氣對(duì)大鼠肺組織葡萄糖轉(zhuǎn)運(yùn)蛋白1(GLUT1)表達(dá)的影響?方法 30只Sprague Dawley大鼠經(jīng)10%水合氯醛4.5mL/kg腹腔注射麻醉后行氣管插管術(shù),建立單肺通氣模型,將建模后大鼠隨機(jī)分為對(duì)照組(n=6)與實(shí)驗(yàn)組(n=24),對(duì)照組大鼠采用主支氣管插管雙肺通氣;實(shí)驗(yàn)組大鼠均為右主支氣管插管通氣,左側(cè)肺不通氣,按左側(cè)肺不通氣時(shí)間隨機(jī)分為實(shí)驗(yàn)0.5h組?實(shí)驗(yàn)1.0h組?實(shí)驗(yàn)2.0h組及實(shí)驗(yàn)4.0h組,每組6只?采用透射電子顯微鏡觀察大鼠Ⅱ型肺泡上皮細(xì)胞(AECⅡ)超微結(jié)構(gòu),半定量逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(RT-PCR)檢測(cè)大鼠肺組織GLUT1mRNA的表達(dá)情況?結(jié)果對(duì)照組AECⅡ細(xì)胞核內(nèi)染色質(zhì)分布均勻,細(xì)胞質(zhì)內(nèi)板層小體圓形且密度均勻,微絨毛清晰?各實(shí)驗(yàn)組AECⅡ的細(xì)胞核染色質(zhì)?細(xì)胞質(zhì)內(nèi)板層小體?細(xì)胞膜及微絨毛等有不同程度的改變?與對(duì)照組比較,實(shí)驗(yàn)0.5h組?實(shí)驗(yàn)1.0h組大鼠肺組織GLUT1mRNA表達(dá)量顯著降低(P0.05);實(shí)驗(yàn)2.0h組大鼠肺組織GLUT1mRNA表達(dá)量略有降低,但差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05);實(shí)驗(yàn)4.0h組大鼠肺組織GLUT1mRNA表達(dá)量明顯增加(P0.05)?除實(shí)驗(yàn)1.0h組與實(shí)驗(yàn)0.5h組大鼠肺組織GLUT1mRNA的表達(dá)差異無(wú)統(tǒng)計(jì)學(xué)意義外(P0.05),其余各實(shí)驗(yàn)組兩兩比較,差異均有統(tǒng)計(jì)學(xué)意義(P0.05)?結(jié)論低氧條件下,肺組織GLUT1mRNA的上調(diào)對(duì)AECⅡ具有保護(hù)作用?

肺通氣;細(xì)胞低氧;肺泡上皮細(xì)胞;葡萄糖轉(zhuǎn)運(yùn)蛋白;大鼠

單肺通氣麻醉目前已廣泛應(yīng)用于臨床?單肺麻醉時(shí)一側(cè)肺完全萎陷,萎陷肺的血流灌注明顯下降,肺組織缺氧[1]?肺泡細(xì)胞在缺氧時(shí),依靠無(wú)氧酵解獲取能量,這意味著肺泡細(xì)胞需要攝取大量葡萄糖以滿足機(jī)體的正常代謝?葡萄糖轉(zhuǎn)運(yùn)蛋白1(glucose transporter 1,GLUT1)是GLUT家族成員之一,主要負(fù)責(zé)細(xì)胞內(nèi)?外葡萄糖的跨膜轉(zhuǎn)運(yùn),對(duì)調(diào)節(jié)機(jī)體糖代謝發(fā)揮關(guān)鍵作用?目前國(guó)內(nèi)?外尚未見(jiàn)在低氧環(huán)境下肺泡細(xì)胞GLUT1表達(dá)的相關(guān)報(bào)道?本研究通過(guò)分析不同時(shí)間低氧對(duì)肺泡細(xì)胞中GLUT1mRNA表達(dá)的影響,探討在低氧環(huán)境下肺泡細(xì)胞GLUT1mRNA的表達(dá)及其作用?

1 材料與方法

1.1 動(dòng)物 健康Sprague Dawley大鼠30只,不分雌雄,體質(zhì)量(240.0±20.0)g,由廣西醫(yī)科大學(xué)實(shí)驗(yàn)動(dòng)物中心提供?

1.2 動(dòng)物單肺通氣模型的建立及分組 實(shí)驗(yàn)前大鼠禁食8h,不限制飲水?用10%水合氯醛4.5mL/kg腹腔注射麻醉,氣管切開(kāi)后行氣管插管術(shù),通氣設(shè)置:潮氣量5mL/kg?呼吸頻率80次/min?吸呼比(inspiratory expiratory ratio,I:E)為1∶2,呼氣末正壓通氣(postive end-expiratory pressure,PEEP)6cm H2O?吸入氧體積分?jǐn)?shù)(fraction of inspire O2,FiO2)為1.0?將建模后大鼠隨機(jī)分為對(duì)照組(n=6)與實(shí)驗(yàn)組(n=24),對(duì)照組大鼠采用主支氣管插管雙肺通氣;實(shí)驗(yàn)組大鼠均為右主支氣管插管通氣,左側(cè)肺不通氣,按左側(cè)肺不通氣時(shí)間隨機(jī)分為實(shí)驗(yàn)0.5h組?實(shí)驗(yàn)1.0h組?實(shí)驗(yàn)2.0h組及實(shí)驗(yàn)4.0h組,每組6只?

1.3 透射電鏡檢測(cè) 取各組大鼠左肺下葉組織(1mm3)置于4℃?2%戊二醛液(pH 7.4)中固定,磷酸鹽緩沖溶液(phosphate buffered solution,PBS)沖洗?鋨酸固定?乙醇脫水?丙酮脫水?環(huán)氧樹(shù)脂Epon812包埋?100%丙酮浸透,采用LKB-Ⅴ電鏡切片機(jī)(瑞典LKB公司)制成超薄切片,醋酸雙氧鈾-檸檬酸鉛雙重染色后,H-500型透射電子顯微鏡(日本Hitachi公司)觀察組織?細(xì)胞超微結(jié)構(gòu)?

1.4 半定量逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(reverse transcriptase-polymerase chain reaction,RT-PCR) Trizol法提取大鼠左?右肺下葉組織總RNA,按逆轉(zhuǎn)錄試劑盒(美國(guó)Fermentas公司)說(shuō)明進(jìn)行逆轉(zhuǎn)錄獲取cDNA,自動(dòng)PCR儀(Light Cycle,美國(guó)Roche公司)擴(kuò)增?GLUT1及內(nèi)參β-actin引物由上海生物工程技術(shù)服務(wù)有限公司合成?GLUT1上游引物:5′-GGA GAC GCA TAG TCA CAG AAC G-3′,下 游 引 物:5′-GCC AAA GCG ATT AAC AAA GAG-3′,擴(kuò)增產(chǎn)物長(zhǎng)度為348bp;內(nèi)參β-actin上游引物:5′-AGA TGT ACG TAG CCA TCC-3′,下游引物:5′-CTC TCA GCT GTG GTG GTG AA-3′,擴(kuò)增產(chǎn)物長(zhǎng)度為228bp?GLUT1循環(huán)條件:95℃預(yù)變性5min;94℃變性30s,58℃退火30s,72℃延伸90s,共33個(gè)循環(huán);最后72℃延伸10min,4℃保存?擴(kuò)增結(jié)束后取8μL PCR產(chǎn)物經(jīng)2%非變性瓊脂糖凝膠電泳檢測(cè),凝膠成像獲取的圖片經(jīng)Quantity One v462軟件(美國(guó)Biorad公司)進(jìn)行分析,以目的條帶與內(nèi)參灰度值的比值反映GLUT1mRNA的表達(dá)?

1.5 統(tǒng)計(jì)學(xué)處理 采用SPSS13.0軟件進(jìn)行統(tǒng)計(jì)學(xué)分析,計(jì)量數(shù)據(jù)用±s表示,組間比較采用方差分析和SNK(Student-Newman-Keuls)法檢驗(yàn)(方差齊)及矯正t檢驗(yàn)(方差不齊),以P0.05為差異有統(tǒng)計(jì)學(xué)意義?

2 結(jié) 果

2.1 大鼠Ⅱ型肺泡上皮細(xì)胞(alveolar epithelial cell typeⅡ,AECⅡ)的透射電鏡觀察 對(duì)照組大鼠AECⅡ:細(xì)胞核及其邊界清晰,細(xì)胞核內(nèi)染色質(zhì)分布均勻;細(xì)胞質(zhì)內(nèi)板層小體圓形且密度均勻正常;細(xì)胞膜連續(xù)完整,微絨毛清晰,見(jiàn)圖1?實(shí)驗(yàn)0.5h組大鼠AECⅡ:細(xì)胞核及其邊界清楚,細(xì)胞核內(nèi)染色質(zhì)分布均勻;細(xì)胞質(zhì)內(nèi)板層小體數(shù)目減少,體積增大,呈環(huán)狀排列;微絨毛排列較整齊,見(jiàn)圖2?實(shí)驗(yàn)1.0h組大鼠AECⅡ:細(xì)胞核及其邊界清楚,核仁偏移,細(xì)胞核內(nèi)染色質(zhì)不清;細(xì)胞質(zhì)內(nèi)板層小體體積增大,密度減小;微絨毛排列紊亂,見(jiàn)圖3?實(shí)驗(yàn)2.0h組大鼠AECⅡ:細(xì)胞核及其邊界清楚,細(xì)胞核變形,核仁碎裂,染色質(zhì)分布不均勻;細(xì)胞質(zhì)內(nèi)板層小體相對(duì)密度降低,數(shù)目減少,體積增大,伴有空泡樣變,微絨毛消失,見(jiàn)圖4?實(shí)驗(yàn)4.0h組大鼠AECⅡ:細(xì)胞核?核仁碎裂呈2個(gè),細(xì)胞核內(nèi)染色質(zhì)不清;細(xì)胞質(zhì)內(nèi)板層小體空泡樣變,并向細(xì)胞外排出;細(xì)胞膜結(jié)構(gòu)不完整,見(jiàn)圖5?

2.2 大 鼠 肺 組 織 中GLUT1mRNA的 表 達(dá) RT-PCR結(jié) 果 分析表明,與對(duì)照組比較,實(shí)驗(yàn)0.5h組?1大鼠肺織GLUT1mRNA表達(dá)量顯著降低(P0.05);實(shí)驗(yàn)2.0h組大鼠肺組織GLUT1mRNA表達(dá)量略有降低,但差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05);實(shí)驗(yàn)4.0h組大鼠肺組織GLUT1mRNA表達(dá)量明顯增加(P0.05)?除實(shí)驗(yàn)1.0h組與實(shí)驗(yàn)0.5h組大鼠肺組織GLUT1mRNA的表達(dá)差異無(wú)統(tǒng)計(jì)學(xué)意義外(P0.05),其余各實(shí)驗(yàn)組兩兩比較,差異均有統(tǒng)計(jì)學(xué)意義(P0.05),見(jiàn)圖6?與對(duì)照組比較,實(shí)驗(yàn)1.0h組右肺下葉組織GLUT1mRNA的表達(dá)量降低(P0.05)?見(jiàn)表1?圖6?

圖1 對(duì)照組大鼠AECⅡ的超微結(jié)構(gòu)(×2 800)?

圖2 實(shí)驗(yàn)0.5h組大鼠AECⅡ的超微結(jié)構(gòu)(×4 800)

圖3 實(shí)驗(yàn)1.0h組大鼠AECⅡ的超微結(jié)構(gòu)(×4 800)

表1 對(duì)照組大鼠肺組織與實(shí)驗(yàn)1.0h組右肺下葉組織GLUT1mRNA表達(dá)的比較(±s,n=6)

表1 對(duì)照組大鼠肺組織與實(shí)驗(yàn)1.0h組右肺下葉組織GLUT1mRNA表達(dá)的比較(±s,n=6)

*:P0.05,與對(duì)照組比較?

組別GLUT1mRNA對(duì)照組0.36±0.07實(shí)驗(yàn)1.0h組右肺下葉組織 0.13±0.05*

圖4 實(shí)驗(yàn)2.0h組大鼠AECⅡ的超微結(jié)構(gòu)(×7 700)

圖5 實(shí)驗(yàn)4.0h組大鼠AECⅡ的超微結(jié)構(gòu)(×5 900)

圖6 各組大鼠肺組織GLUT1mRNA表達(dá)的電泳圖

3 討 論

單肺通氣技術(shù)已廣泛應(yīng)用于胸外科手術(shù),單肺通氣技術(shù)使一側(cè)肺通氣,一側(cè)肺萎陷停止呼吸,為手術(shù)提供良好的視野,由于大部分手術(shù)都能在4.0h內(nèi)完成,因此,本研究選擇單肺通氣時(shí)間為0.5～4.0h?

單肺通氣期間,非通氣側(cè)肺的血液沒(méi)有得到氧合,其動(dòng)脈血與靜脈血摻雜,肺組織缺氧,導(dǎo)致肺組織細(xì)胞損傷及功能損害[1-2]?葡萄糖是肺泡細(xì)胞主要的能源物質(zhì)?正常情況下,肺泡細(xì)胞主要靠葡萄糖的有氧代謝獲取能量;而缺氧時(shí),肺泡細(xì)胞主要靠葡萄糖的無(wú)氧酵解獲取能量?1分子葡萄糖無(wú)氧酵解可凈生成2分子ATP,而有氧氧化可凈生成38分子ATP?因此,為了維持肺泡細(xì)胞所需的能量,細(xì)胞需要攝取大量葡萄糖?細(xì)胞攝取葡萄糖主要通過(guò)GLUT,GLUT家族中GLUT1是哺乳動(dòng)物細(xì)胞內(nèi)參與葡萄糖跨膜轉(zhuǎn)運(yùn)的主要載體,GLUT主要功能是跨膜將葡萄糖分子轉(zhuǎn)運(yùn)入細(xì)胞內(nèi)?目前發(fā)現(xiàn)GLUT共有13個(gè)成員,分別命名為GLUT 1～12和H+-肌醇轉(zhuǎn) 運(yùn) 體 (H+myo-inositol transporter,HMIT)[3]? 其 中,GLUT1是介導(dǎo)細(xì)胞葡萄糖攝取的主要載體,在人體各組織?細(xì)胞中廣泛存在,與代謝密切相關(guān),主要介導(dǎo)細(xì)胞內(nèi)外的跨膜轉(zhuǎn)運(yùn),調(diào)節(jié)葡萄糖攝取,對(duì)糖代謝的調(diào)節(jié)功能發(fā)揮關(guān)鍵作用[4]?GLUT1的 表 達(dá) 受 多 種 因 素 的 影 響 ,缺 氧 誘 導(dǎo) 因 子1?降 糖 藥 ?腫瘤壞死因子?葡萄糖生長(zhǎng)激素轉(zhuǎn)化β成纖維細(xì)胞生長(zhǎng)因子1和癌基因等均可上調(diào)GLUT1mRNA的表達(dá)[5]?本研究結(jié)果表明,隨著低氧時(shí)間延長(zhǎng),尤其是單肺通氣達(dá)到4h時(shí),大鼠AECⅡ超微結(jié)構(gòu)破壞越嚴(yán)重,細(xì)胞結(jié)構(gòu)受破壞的程度與缺氧時(shí)間成正比?GLUT1是慢性缺氧的標(biāo)記物[6],低氧時(shí),GLUT1基因表達(dá)和轉(zhuǎn)運(yùn)能力增強(qiáng),同時(shí)低親和力的GLUT1被激活向細(xì)胞膜轉(zhuǎn)位,使組織細(xì)胞攝取葡萄糖的能力增強(qiáng)?在缺氧的情況下,低氧誘導(dǎo)因子-1α(hypoxia induced factor 1α,HIF1α)表達(dá)急劇升高,激活 GLUT1 5′端的增強(qiáng)子序列,從而引起GLUT1mRNA的大量表達(dá)[7]?本研究表明實(shí)驗(yàn)0.5h組及實(shí)驗(yàn)1.0h組的大鼠肺組織GLUT1mRNA的表達(dá)量下調(diào),由此,本研究增加了檢測(cè)通氣右肺下葉組織,結(jié)果右下肺組織通氣1.0h后的GLUT1mRNA的表達(dá)量同樣出現(xiàn)下調(diào),說(shuō)明在單肺通氣0.5～1.0h時(shí),肺血管缺氧性收縮產(chǎn)生肺內(nèi)分流,代償性保證了非通氣左肺組織的氧供給,兩側(cè)肺泡細(xì)胞攝氧是平衡均等并能滿足肺泡細(xì)胞能量代謝的需要,因此,出現(xiàn)GLUT1mRNA表達(dá)量下調(diào)?實(shí)驗(yàn)研究表明,在單肺通氣超過(guò)2h后,肺泡細(xì)胞處于低氧代謝環(huán)境,AECⅡ的形態(tài)?結(jié)構(gòu)和功能受到影響,AECⅡ凋亡?裂解?壞死,導(dǎo)致AECⅡ的數(shù)量減少,而其在短時(shí)間內(nèi)不能得到補(bǔ)充和代償,從而啟動(dòng)了GLUT1調(diào)控?因此,本實(shí)驗(yàn)中,大鼠肺組織GLUT1mRNA從低氧2.0h開(kāi)始上調(diào),低氧4.0h時(shí)GLUT1mRNA的表達(dá)量顯著增加?Stein等[8]發(fā)現(xiàn)低氧時(shí)GLUT1mRNA的半衰期從0.52h增加到8.00h?Ouiddir等[9]報(bào)道,AECⅡ的GLUT1在低氧誘導(dǎo)下活性明顯提高,在復(fù)氧后GLUT1的活性迅速降低?由此可見(jiàn),低氧刺激誘導(dǎo)了GLUT1的表達(dá)及其活性增加,從而保證糖代謝的速率?

單肺通氣可以使通氣/血流比例失衡,增加肺內(nèi)分流導(dǎo)致低氧血癥[10]?有研究發(fā)現(xiàn),單肺通氣超過(guò)2.0h,氧合指數(shù)小于300;超過(guò)3.0h,氧合指數(shù)為216,達(dá)到急性肺損傷的診斷標(biāo)準(zhǔn)[11]?單肺通氣可引起缺氧性肺損傷,甚至發(fā)展成為急性呼吸窘迫綜合征 (acute respiratory distress syndrome,ARDS)?缺氧時(shí),肺泡細(xì)胞無(wú)氧代謝增加,能量匱乏,GLUT1基因表達(dá)和轉(zhuǎn)運(yùn)能力增強(qiáng)使肺泡細(xì)胞攝取葡萄糖能力增強(qiáng)[12],這有助于恢復(fù)肺泡細(xì)胞的能量代謝,減少組織?細(xì)胞的損害[13],對(duì)AECⅡ具有保護(hù)作用?有研究發(fā)現(xiàn)GLUT1表達(dá)的增加可修復(fù)缺氧對(duì)組織?細(xì)胞的損害,它可通過(guò)激活c-Jun氨基末端激酶 (c-Jun N-terminal kinases,JNK)信號(hào)途徑阻止缺氧誘導(dǎo)的細(xì)胞凋亡[14]?進(jìn)一步研究缺氧條件下肺組織GLUT1的調(diào)控機(jī)制可能對(duì)防治缺氧性肺損傷,甚至ARDS,均有重要意義?

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Expression of glucose transporter 1 and its effects in lung tissue of hypoxic metabolism*

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ObjectiveTo explore the effect of one-lung ventilation on the expression of glucose transporter 1(GLUT1)in lung tissue of rats.Methods30Sprague Dawley rats were subjected to anesthesia by intraperitoneal injection of 10%chloral hydrate 4.5mL/kg,followed by endotracheal intubation to establish rat models of one-lung ventilation.Rats after modeling were randomly divided into control group(n=6)and experimental group(n=24).Lung ventilation using main-stem bronchial intubation was conducted in rats in the control group,and in the experimental group,lung ventilation was performed through right main-stem bronchial intubation with no ventilation in the left lung.Rats in the experimental group were subdivided into experimental 0.5hgroup,experimental 1.0hgroup,experimental 2.0hgroup and experimental 4.0hgroup,according to the duration of non-ventilation in the left lung.Transmission electron microscopy was employed to observe the ultrastructure of alveolar epithelial cell typeⅡ(AECⅡ)of rats and semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR)was adopted to detect the expression ofGLUT1 mRNA in lung tissue of rats.ResultsAECⅡin control group showed nuclear chromatin with well-distribution,cytoplasmic lamellar bodies with round shape and uniform density,and clear microvilli.AECⅡin each experimental group were found different degrees of changes in nuclear chromatin,cytoplasmic lamellar bodies and microvilli.Compared with the control group,expression ofGLUT1mRNA was significantly decreased in lung tissue of rats in experimental 0.5hgroup and experimental 1.0hgroup(P0.05),it was slightly reduced in experimental 2.0hgroup with no statistically significance,and it was markedly increase in experimental 4.0hgroup(P0.05).Paired comparison among experimental groups,except the comparison between experimental 1.0h group and experimental 0.5hgroup,differences were statistically significant(P0.05).ConclusionIn the condition of hypoxia,the up-regulation ofGLUT1mRNA in lung tissue possesses the protective effect on AECⅡ.

pulmonary ventilation;cell hypoxia;alveolar epithelial cells;glucose transporters;rats

10.3969/j.issn.1671-8348.2012.09.015

A

1671-8348(2012)09-0872-03

廣 西 壯族自 治 區(qū) 科 學(xué) 技術(shù)自 然 基 金 資 助項(xiàng)目(桂 科 自0991235);廣 西醫(yī) 療 衛(wèi) 生 重 點(diǎn) 科研 課 題 資 助 項(xiàng) 目 (重2010070)?△

,Tel:(0771)5320919;E-mail:plinghui@yahoo.com

2011-11-21

2012-01-08)

?臨床研究?