HSP70基因转染对缺氧-再复氧肠上皮细胞生长能力影响的研究

目的 :研究重组腺病毒介导的热休克蛋白 70转染对缺氧再复氧损伤后肠上皮细胞生长能力的影响。方法 :将重组含人全长 HSP70基因的腺病毒转染体外培养的肠上皮细胞株 IEC 6 ,检测转染细胞 HSP70的 m RNA表达水平。 IEC 6细胞经缺氧再复氧处理后 ,对未转染组 ,转染 2 4 h、4 8h及 72 h组细胞的细胞活力、生长曲线、增殖能力进行检测分析。结果 :腺病毒转染组细胞 HSP70 m RNA表达呈阳性。经缺氧再复氧处理后 ,IEC 6转染细胞活力较未转染组活力明显增强 (P<0 .0 1) ,生长能力提高 (P<0 .0 5 ) ,分裂指数增高(P<0 .0 5 )。结论 :重组腺病毒介导的 HSP70转染可增强肠上皮细胞生长及增殖能力 ,从而保护其抵抗缺氧再复氧损伤。     

激光共聚焦显微镜观察前胡丙素对新生大鼠缺氧再灌注心肌细胞内游离钙的影响

目的 激光共聚焦显微镜观察缺氧再灌注损伤对心肌细胞内Ca^2＋浓度（[Ca^2＋]i）的影响，以及前胡丙素对模拟心肌缺氧再灌注过程中减轻钙超载的作用。方法 采用SD大鼠乳鼠进行心肌细胞培养，建立模拟缺氧再灌注模型。实验分4组：正常组：细胞正常培养；缺氧预适应组：预先缺氧2h，复氧1h，再缺氧12h后，复氧2h；前胡丙素预处理组：先予前胡丙素单体终浓度为100μmol／L 作用1h，再行缺氧12h，后复氧2h；模拟缺氧再灌注组缺氧12h，后复氧2h。细胞上清检测LDH值。心肌细胞以Fluo-3／AM荧光指示剂负载，应用激光共聚焦显微镜技术检测心肌细胞（[Ca^2＋]i）变化。结果 模拟缺氧再灌注组心肌细胞（[Ca^2＋]i）荧光强度值显著高于前胡丙素预处理组及缺氧预适应组（P〈0．01），前胡丙素预处理组与缺氧预适应组细胞内荧光强度无明显组间差异。结论 心肌细胞缺氧再灌注损伤导致Ca^2＋超载，而前胡丙素有明显减轻心肌细胞模拟缺氧再灌注时Ca^2＋超载的作用。应用激光扫描共聚焦显微镜技术可以直观地进行细胞内钙离子研究。     

参附注射液对心肌细胞缺氧及缺氧/复氧时Fas/FasL表达的影响

目的 探讨参附注射液（SF）对培养的乳鼠心肌细胞缺氧及缺氧／复氧时凋亡相关基因Fas／FasL蛋白表达的影响。方法 按常规培养新生4d乳鼠心肌细胞，于培养24h后进行缺氧及缺氧／复氧实验。以免疫组织化学方法检测心肌细胞Fas／FasL蛋白表达的变化。结果 缺氧4．5h及10．5h后，心肌细胞Fas／FasL蛋白的阳性表达指数（positive expression index，PEI）均显著高于对照。10．5h组与4．5h组无明显差异。参附注射液组PEI明显低于缺氧组（P〈0．05）。缺氧30min后再给氧4h与10h，心肌细胞Fas／FasL蛋白的PEI显著高于对照，复氧10h组与4h组无明显差异，参附注射液组PEI低于无SF组（P〈0．05）。结论 缺氧及缺氧／复氧时均有凋亡相关基因Fas及其配体FasL蛋白表达的增强，参附注射液可通过下调Fas／FasL蛋白表达，减少凋亡从而减轻缺氧损伤及缺氧／复氧损伤。     

龙胆苦甙对减轻乳鼠心肌缺血再灌注损伤的细胞研究

目的：观察龙胆苦甙（Gentiopicroside,GPS）后处理对离体心肌细胞缺血/再灌注损伤（ischemia and reperfusion injury,I/R）的拮抗作用及其可能的机制。方法采用SD大鼠乳鼠培养心肌原代细胞,用缺氧复氧模型模拟缺血再灌注（stimulated ischemia reperfusion,SI/R）。实验分为正常对照组（Control＋ScrambleRNA＋Veh）;缺氧复氧组（I/R＋ScrambleRNA＋Veh）;缺氧复氧＋龙胆苦甙后处理组（I/R＋ScrambleRNA＋GPS 组）以及缺氧复氧＋AktSiRNA＋龙胆苦甙后处理组（I/R＋AktSiRNA＋GPS）。采用化学法缺氧复氧模型,缺氧2 h,复氧4 h。复氧前给予GPS药物,检测心肌细胞乳酸脱氢酶（LDH）以及TUNEL染色确定心肌细胞的损伤程度以及抑制Akt表达后GPS的保护作用变化。结果与I/R＋ScrambleRNA＋Veh组相比,I/R＋ScrambleRNA＋GPS组LDH明显降低（P＜0.01）,TUNEL染色阳性率增加减少（P＜0.01）,Akt/Gsk3β信号通路磷酸化程度明显增加（P＜0.01）。与I/R＋ScrambleRNA＋GPS组相比,SI/R＋SiAktRNA＋GPS组,LDH活性显著增加（P＜0.01）,TUNEI染色阳性率增加（P＜0.01）,Gsk3β磷酸化程度减弱（P＜0.01）。结论 GPS后处理对I/R大鼠心肌具有保护作用,其作用机制与AKT/Gsk3β信号通路的活化有关。     

Uqcrc1的 RNA 干扰片段筛选及其对 H9C2心肌细胞耐受缺氧/复氧损伤的影响

目的：筛选泛醇-细胞色素c还原酶核心蛋白（Ubiquinol-cytochrome c reductase core protein 1, Uqcrc1）高效的 RNA 干扰片段,探讨 Uqcrc1基因沉默对大鼠 H9C2心肌细胞耐受缺氧/复氧（hypoxia/reoxygenation,H/R）损伤的影响。方法制备三种针对Uqcrc1的RNA干扰片段,采用RT-PCR和Western blot检测Uqcrc1 RNA干扰片段转染后Uqcrc1基因和蛋白的表达,从中筛选出最有效的RNA干扰片段及转染浓度,采用MTT法和LDH试剂盒分别检测H/R损伤后H9C2心肌细胞的存活率和LDH漏出率。结果靶序列为CCGUUGCUGUAGCUAACAAdTdT的siUqcrc1片段对Uqcrc1 mRNA的抑制作用最明显,在转染浓度为200 nmol/L时对Uqcrc1蛋白表达抑制最明显。靶向Uqcrc1的RNA干扰片段转染降低了H9C2心肌细胞耐受H/R损伤的能力。与阴性对照组相比,Uqcrc1基因沉默组H9C2心肌细胞H/R损伤后的存活率显著降低,LDH漏出率升高（P＜0.01）。结论 Uqcrc1在心肌细胞耐受H/R损伤中起了重要作用,它可能是心肌保护的又一个关键靶点。     

骨骼肌细胞缺氧复氧损伤的保护机制研究

目的 探讨碱性成纤维细胞生长肽（bFGF)对新生大鼠骨骼肌细胞缺氧复氧（A／R）损伤的保护作用。方法 应用培养的新生Wistar大鼠骨骼肌细胞制备A／R损伤模型，观察bFGF对A／R损伤后肌细胞存活率、胞浆乳酸脱氢酶（LDH）漏出的影响。并用免疫组化法检测bFGF对A／R损伤后肌细胞凋亡（apoptosis)相关基因蛋白bcl-2表达的影响。结果 bFGF预处理呈浓度依赖性地提高了A／R后肌细胞存活率，减少了胞浆LDH的漏出，明显上调bcl-2的表达。结论 bFGF对A／R损伤的骨骼肌细胞有明显保护作用。     

类泛素蛋白FAT10通过Nrf2/HO-1通路对心肌细胞缺血缺氧修复损伤的保护作用

目的 探讨类泛素蛋白人类白细胞抗原F介导转录因子10(FAT10)在心肌细胞缺氧修复损伤中的作用及机制。方法 采用H9C2大鼠心肌细胞构建缺氧复氧模型,将心肌细胞分为对照组、缺氧4 h组、复氧2 h组及复氧4 h组。采用细胞活力检测试剂盒（CCK-8）检测细胞活性,采用Annexin V-FITC/PI法检测心肌细胞凋亡,采用微量酶标法检测乳酸脱氢酶（LDH）。将阴性对照RNA序列（si-CON）和FAT10沉默序列转入心肌细胞,将细胞分为对照组、缺氧4 h+si-CON组、缺氧4 h+siRNA组、复氧4 h+si-CON组、复氧4 h+siRNA组。Western-blot检测细胞FAT10、Nrf2、HO-1蛋白表达水平。结果 随复氧时间延长,心肌细胞存活率下降,心肌细胞损伤加重,细胞凋亡率升高,在复氧4 h后最低。复氧4 h组细胞存活率低于对照组,而LDH水平及细胞凋亡率高于对照组,差异均有统计学意义（P<0.05）。FAT10蛋白表达水平：复氧4 h+siRNA组<缺氧4 h+siRNA组<缺氧4 h+si-CON组,差异均有统计学意义（P<0.05）...     

Ⅰ型磷酸酶抑制亚基1对大鼠心肌细胞缺氧/复氧损伤的保护作用

目的 探讨Ⅰ型磷酸酶抑制亚基1(PPI1)对大鼠乳鼠心肌细胞缺氧/复氧(H/R)损伤的保护作用及其机制.方法 用PPI1野生型和活化型突变体表达质粒分别转染乳鼠心肌细胞,并建立乳鼠心肌细胞缺氧/复氧H/R模型,测定各组心肌细胞的存活率、丙二醛(MDA)、乳酸脱氢酶(LDH)的含量、caspase-3活性及超氧化物歧化酶(SOD)活力,此外用流式细胞术测定各组心肌细胞凋亡率,Western blot分析PPI1对凋亡相关蛋白表达及PI3K/Akt信号通路的影响.结果 与正常组比较,模型组LDH、MDA含量、caspase-3活性及细胞凋亡率增高(P<0.05),细胞存活率和SOD活性降低(P<0.05);PPI1活化型突变体转染组细胞的LDH、MDA含量、caspase-3活性和细胞凋亡率则降低,细胞存活率和SOD活性升高,与缺氧/复氧组比较各实验指标差异均具有统计学意义(P<0.05).Western blot表明该组细胞P53、Bax 表达下调,pAkt表达上调.结论 PPI1活化型突变体对H/R造成的心肌细胞损伤具有保护作用,其机制与稳定心肌细胞膜、减轻氧自由基损伤及减少细胞凋亡有关.     

参附汤血中移行成分对缺氧复氧心肌细胞凋亡和自噬的影响

目的:观察参附汤血中移行成分对缺氧复氧心肌细胞凋亡和自噬的影响,探讨参附汤血中移行成分心肌保护作用机制。方法:建立缺氧复氧心肌细胞损伤模型,采用MTT法检测心肌细胞的存活率,TUNEL显色法检测细胞凋亡率,Western blotting法测定自噬相关基因Beclin-1表达量。结果:与正常对照组相比,缺氧复氧组细胞存活率降低,细胞凋亡率和Beclin-1表达量明显升高,参附汤血中移行成分组可明显提高缺氧复氧组心肌细胞的存活率,降低细胞凋亡率和抑制Beclin-1表达。结论:参附汤血中移行成分可保护缺氧复氧的心肌细胞,据有抑制细胞凋亡和自噬的作用。     

芬太尼对乳鼠心肌细胞缺氧复氧损伤的保护作用

目的 采用乳鼠心肌细胞缺氧复氧模型,观察芬太尼与缺氧预适应对心肌细胞缺氧复氧损伤的影响,探讨芬太尼能否直接作用于心肌细胞并模拟缺氧预透应(APC)样心肌保护作用,试图在细胞水平上为临床应用大剂量芬太尼减轻心肌缺血再灌注损伤提供理论依据.方法 以常规方法 制备与培养心肌细胞,分为4组:正常对照组(C组)不经任何处理;单纯缺氧复氧组(A/R组)、缺氧预适应组(AP组)及芬太尼组(F组)均经历2小时缺氧及1小时复氧.缺氧前,AP组预先经历20分钟缺氧及20分钟复氧;F组给予终浓度为50 ng/ml的芬太尼.分别以四甲基偶氮唑盐(MTT)快速比色法检测细胞存活情况、流式细胞仪检测细胞凋亡率及透射电子显微镜观察细胞超微结构改变.结果 F组和AP组OD值均显著高于A/R组,细胞凋亡率显著低于A/R组;F组OD值与细胞凋亡率与AP组比较差异无显著性意义;电镜显示A/R组细胞超微结构改变呈典型的凋亡细胞形态学改变,AP组及F组细胞形态大致正常,凋亡细胞少见.结论 芬太尼对乳鼠心肌细胞缺氧复氧损伤有保护作用,且其保护效应与APC的心肌保护作用相似.     

Transgenic mice expressing the human heat shock protein 70 have improved post-ischemic myocardial recovery.

Heat shock treatment induces expression of several heat shock proteins and subsequent post-ischemic myocardial protection. Correlations exist between the degree of stress used to induce the heat shock proteins, the amount of the inducible heat shock protein 70 (HSP70) and the level of myocardial protection. The inducible HSP70 has also been shown to be protective in transfected myogenic cells. Here we examined the role of human inducible HSP70 in transgenic mouse hearts. Overexpression of the human HSP70 does not appear to affect normal protein synthesis or the stress response in transgenic mice compared with nontransgenic mice. After 30 min of ischemia, upon reperfusion, transgenic hearts versus nontransgenic hearts showed significantly improved recovery of contractile force (0.35 +/- 0.08 versus 0.16 +/- 0.05 g, respectively, P < 0.05), rate of contraction, and rate of relaxation. Creatine kinase, an indicator of cellular injury, was released at a high level (67.7 +/- 23.0 U/ml) upon reperfusion from nontransgenic hearts, but not transgenic hearts (1.6 +/- 0.8 U/ml). We conclude that high level constitutive expression of the human inducible HSP70 plays a direct role in the protection of the myocardium from ischemia and reperfusion injury.     

Expression of inducible stress protein 70 in rat heart myogenic cells confers protection against simulated ischemia-induced injury.

Myocardial ischemia markedly increases the expression of several members of the stress/heat shock protein (HSP) family, especially the inducible HSP70 isoforms. Increased expression of HSP70 has been shown to exert a protective effect against a lethal heat shock. We have examined the possibility of using this resistance to a lethal heat shock as a protective effect against an ischemic-like stress in vitro using a rat embryonic heart-derived cell line H9c2 (2-1). Myogenic cells in which the heat shock proteins have been induced by a previous heat shock are found to become resistant to a subsequent simulated ischemic stress. In addition, to address the question of how much does the presence of the HSP70 contribute to this protective effect, we have generated stably transfected cell lines overexpressing the human-inducible HSP70. Embryonal rat heart-derived H9c2(2-1) cells were used for this purpose. This stably transfected cell line was found to be significantly more resistant to an ischemic-like stress than control myogenic cells only expressing the selectable marker (neomycin) or the parental cell line H9c2(2-1). This finding implicates the inducible HSP70 protein as playing a major role in protecting cardiac cells against ischemic injury.     

Protective role of heat stress in burn trauma

OBJECTIVE: This study was designed to determine whether cutaneous burn injury up-regulated expression of myocardial heat shock protein (HSP)70 and to determine a potential cardioprotective role of inducible HSP70 (iHSP70) in postburn myocardial contractile function. DESIGN: Experimental study. SETTING: Research laboratory. SUBJECTS: Adult Hartley guinea pigs. INTERVENTIONS: The first set of studies determined whether heat stress (increasing body temperature to 42 degrees C for 20 mins) in adult Hartley guinea pigs would increase expression of myocardial iHSP70. MEASUREMENTS AND MAIN RESULTS: Our model of heat stress increased expression of inducible HSP in the myocardium (Western blot), and this response persisted 1, 2, 4, and 24 hrs after the initial heat stress. We then determined whether burn trauma over 40% total body surface area (TBSA) increased myocardial expression of iHSP70. Time-matched sham and burned guinea pigs were killed 1, 2, 4, 12, 18, or 24 hrs postburn, and hearts were used either to examine myocardial iHSP70 expression by Western blot or to determine myocardial contractile function (Langendorff). Burn trauma produced a two-fold increase in myocardial iHSP70 that was evident as early as 1 hr postburn and persisted 24 hrs postburn; increased iHSP70 expression occurred despite only a modest and transient increase in body temperature after burn trauma. We then determined whether heat shock stress before burn trauma provided a protective or detrimental effect on cardiac function. Body temperature was increased to 42 degrees C for 20 mins, animals were allowed to recover, and body temperature returned to baseline; burn trauma was then produced (40% TBSA) either 1, 2, 4, or 24 hrs after the initial heat stress. Myocardial contraction and relaxation deficits were evident after burn trauma alone; however, heat stress 1 hr before burn trauma improved left ventricular developed pressure and positive or negative maximum change in pressure in time and shifted left ventricular function curves upward and leftward from those calculated for burn in the absence of heat stress, indicating improved ventricular performance. Increasing the time between the initial heat stress and burn injury decreased the cardioprotective effects of heat stress. Thus, organ protection was evident only when the time period between the initial heat stress and the second insult was brief (1 hr). CONCLUSIONS: Our finding that the amount of myocardial iHSP70 remained constantly elevated after heat stress while the cardio-protective effect afforded by a prior heat stress declined with time suggested that the initial heat stress evoked several compensatory/adaptive mechanisms that may include modulation of autonomic nervous system responses, changes in metabolic function, modulation of pro/anti-inflammatory cytokine responses, and heat stress-related alterations in antioxidant capacity.     

In vivo gene transfection with heat shock protein 70 enhances myocardial tolerance to ischemia-reperfusion injury in rat.

Heat shock protein 70 (HSP70) has been reported to be involved in the myocardial self-preservation system. To obtain the evidence that HSP70 plays a direct role in the protection from myocardial ischemia-reperfusion injury, rat hearts were transfected with human HSP70 gene by intracoronary infusion of hemagglutinating virus of Japan (HVJ)-liposome containing human HSP70 gene. The control hearts were infused with HVJ-liposome without the HSP70 gene. The hearts from whole-body heat-stressed or nontreated rats were also examined. Western blot and immunohistochemical analysis showed that apparent overexpression of HSP70 occurred in the gene transfected hearts and that gene transfection might be more effective for HSP70 induction than heat stress. In Langendorff perfusion, better functional recovery as well as less creatine phosphokinase leakage after ischemia were obtained in the gene transfected hearts with HSP70 than in the control or nontreated hearts. Furthermore, the gene transfected hearts showed better functional recovery than the heat-stressed hearts. These results indicated that overexpressed HSP70 plays a protective role in myocardial injury, suggesting the possibility that gene transfection with HSP70 may become a novel method for myocardial protection through enforcing the self-preservation systems.     

大黄多糖对脑损伤后大鼠脑皮层热休克蛋白70表达的影响

目的观察大黄多糖(TanguticumMaximpolysaccharides,TMP)对大鼠脑损伤后不同时间热休克蛋白(heatshockprotein,HSP)70表达的影响,探讨大黄多糖的脑保护作用机制,为其用于临床治疗脑损伤寻求依据。方法复制大鼠脑挫裂伤模型,分别在伤后6,24,48h以免疫组织化学方法检测大脑皮层表达HSP70的神经细胞,以Western-blot蛋白印迹方法检测脑皮层HSP70表达变化。结果大黄多糖治疗组6hHSP70表达高于损伤组,24,48h均低于治疗组。结论大黄多糖能促进HSP70的表达,这可能是其脑保护作用的机制之一。     

热休克预处理对严重烫伤大鼠胃黏膜氧自由基的作用

目的:观察热休克预处理对严重烫伤大鼠胃黏膜氧自由基及热休克蛋白(HSP)70表达的影响,探讨氧自由基在大鼠烫伤后急性胃黏膜损伤中的作用及热休克预处理对严重烫伤大鼠胃黏膜的保护作用机制。方法:将96只Wistar大鼠随机分为烫伤组(B组,n=48,其中8只大鼠作为正常对照)及热休克预处理后烫伤组(HB组,n=48,其中8只大鼠作为实验对照),观察各时相点两组大鼠胃黏膜损伤指数(UI)、胃黏膜丙二醛(MDA)及胃黏膜细胞SOD活性变化。应用免疫组化染色分析胃黏膜细胞中HSP 70表达变化。结果:大鼠严重烫伤后胃黏膜细胞SOD大量消耗,MDA显著增加,胃黏膜损害明显;热休克预处理能显著减轻大鼠严重烫伤后急性胃黏膜损害。HB组较B组大鼠胃黏膜HSP 70表达水平显著升高(P<0.05),热休克预处理能显著降低胃黏膜细胞SOD的消耗,减少MDA的产生。胃黏膜损伤指数(UI)与MDA呈显著正相关(r=0.695,P<0.01),与HSP 70呈显著负相关(r=-0.794,P<0.01);胃黏膜SOD与MDA呈显著负相关(r=-0.823,P<0.01),而与HSP 70呈显著正相关(r=0.527,P<0.05)。结论:严重烫伤大鼠胃黏膜存在氧自由基损伤;热休克预处理可显著减轻烫伤大鼠胃黏膜氧自由基损伤,保护机制与HSP 70保护抗氧化酶SOD活性密切相关。     

Glutamine attenuates lung injury and improves survival after sepsis: role of enhanced heat shock protein expression

OBJECTIVE: Heat shock protein (HSP) expression is vital to cellular and tissue protection after stress or injury. However, application of this powerful tool in human disease has been limited, as known enhancers of HSPs are toxic and not clinically relevant. Glutamine (GLN) can enhance HSP expression in non-clinically relevant animal injury models. The aim of this study was to assess the ability of GLN to enhance pulmonary HSP expression, attenuate lung injury, and improve survival after sepsis in the rat. DESIGN: Prospective, randomized, controlled animal trial. SETTING: University research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: We utilized a rat model of cecal ligation and puncture to induce sepsis. GLN or saline was administered 1 hr after initiation of sepsis via single tail-vein injection. We analyzed heat shock factor-1 phosphorylation, HSP-70, and HSP-25 via Western blot. Tissue metabolism was assayed by magnetic resonance spectroscopy. Occurrence of lung injury was determined via histopathologic examination. An inhibitor of HSP expression, quercetin, was utilized to assess role of HSP expression in prevention of sepsis-related mortality. MEASUREMENTS AND MAIN RESULTS: GLN, given after initiation of sepsis, enhanced pulmonary heat shock factor-1 phosphorylation, HSP-70, HSP-25, and attenuated lung injury after sepsis. Further, GLN improved indices of lung tissue metabolic function (adenosine 5-triphosphate/adenosine 5-diphosphate ratio, nicotinamide adenine dinucleotide) after sepsis. No significant effect of GLN on lung tissue-reduced glutathione was observed. GLN treatment led to a significant decrease in mortality (33% [6 of 18] GLN-treated rats vs. 78% [14 of 17] saline-treated rats). Administration of the HSP inhibitor quercetin blocked GLN-mediated enhancement of HSP expression and abrogated GLN's survival benefit. CONCLUSIONS: GLN has been safely administered to critically ill patients and shown to improve outcome without clear understanding of the protective mechanism. Our results indicate GLN may prevent the occurrence of lung injury, lung tissue metabolic dysfunction, and mortality after sepsis via enhancement of deficient lung heat shock factor-1 phosphorylation/activation and HSP expression.     

银杏叶提取物对大鼠肾脏缺血-再灌注损伤热休克蛋白表达的影响

目的　探讨银杏叶提取物通过诱导热休克蛋白的合成 ,保护大鼠肾脏缺血 再灌注损伤作用与机理。方法　 34只SD大鼠随机分为假手术组 (n =10 )、单纯缺血 再灌注组 (n =12 )、缺血再灌注 +银杏叶提取物处理组 (n=12 )。通过免疫组织化学方法观察诱导型HSP70的表达情况。结果　与假手术组相比 ,单纯缺血 再灌注组肾小管上皮细胞呈明显的缺血性改变 ,HSP70表达明显增强 ,两组差异有显著性(P <0 0 1) ;缺血再灌注 +银杏叶提取物处理组与单纯缺血 再灌注组相比 ,肾小管上皮细胞缺血性改变减轻 ,HSP70表达增强 (P <0 0 5 )。结论　银杏叶提取物诱导大鼠肾缺血 再灌注组织中HSP70表达 ,减轻大鼠肾脏缺血再灌注损伤     

严重烧伤早期肠黏膜组织热休克蛋白70的表达规律

目的探讨大鼠烧伤后早期肠黏膜组织热休克蛋白70(HSP70)的表达变化规律及其意义。方法采用大鼠烫伤模型,通过逆转录-聚合酶链反应(RT-PCR)、蛋白质免疫印迹(Westernblot)及免疫组化等方法,检测伤后3、6、12、24和48h不同时间点肠黏膜组织内HSP70及热休克因子1(HSF1)的表达分布情况。结果烫伤后3h肠黏膜组织内HSP70mRNA及蛋白表达均显著增加,分别在伤后6h和12h达高峰,伤后48h仍高于正常对照组(P均<0.01);伤后3h大鼠肠黏膜组织HSF1出现一过性降低,伤后6h其表达显著高于正常对照组,并呈逐渐增加的趋势直至持续到伤后48h(P均<0.01)。结论严重烧伤早期肠黏膜组织HSP70及HSF1表达均显著增加,提示严重烧伤早期即可引起肠黏膜组织细胞的应激反应,可能与细胞的自我保护机制启动有关。