肠三叶因子对小鼠炎症性肠病肠道病变的保护作用

目的 探讨肠三叶因子(ITF)对小鼠炎症性肠病(IBD)肠道病变的影响,分析ITF对小鼠IBD肠道先天性免疫功能的调节作用.方法 48只小鼠随机分为3组,每组16只.三硝基苯磺酸(TNBS)组:用TNBS建立IBD模型后每只小鼠给予9g.L-1盐水0.1 mL腹腔注射;基因重组肠三叶因子(rITF)组:建立IBD模型后每只小鼠给予rITF0.1 mL腹腔注射;乙醇对照组:未造模型小鼠每只小鼠给予9g.L-1盐水0.1 mL腹腔注射.各组均连续5d注射,第14天评估小鼠临床表现,麻醉处死小鼠后取其结肠组织作组织学评分,HE染色行肠组织病理学检查,并采用免疫组织化学法及实时定量PCR法检测其肠道TNF-α及Toll样受体(TLR4)和核因子( NF-κBp65)基因、蛋白表达水平.结果 与TNBS组小鼠比较,r-ITF组小鼠死亡只数、大便性状、血便情况、体质量下降情况等临床表现及肠道局部炎症均明显减轻,肠道病理大体观及组织学评分均明显下降(Pa＜0.05),TNF-α蛋白表达水平明显下降(Pa＜0.05),TLR4、NF-κBp65基因及蛋白表达明显下调(Pa＜0.01).乙醇对照组无死亡,临床症状及肠道局部炎症轻微,TNBS组TNF-α、TLR4、NF-κBp65基因及蛋白表达明显高于乙醇对照组(Pa＜0.01).结论 ITF对IBD小鼠肠道病变具有保护作用,可能与调节肠道先天免疫有关.     

肠三叶因子对肠组织核因子-κB及肿瘤坏死因子-α的调节及与肠损伤保护作用的关系

目的 探讨肠三叶因子(ITF)对肠组织NF-KB及TNF-α的调节及与肠损伤保护作用的关系.方法 24只10日龄的Wistar幼鼠随机分为正常对照组(NS组),脂多糖(LPS)组,ITF组,每组8只.NS组予9 g/L盐水1 mL/kg腹腔注射;LPS组予LPS(5 g/L)5 mg/kg腹腔注射;ITF组予重组ITF(5 g/L)0.1 mL/只+LPS 5 mg/kg腹腔注射.于腹腔注射后3h处死幼鼠,留取远端回肠组织,HE染色,光镜下行肠组织病理学检查.RT-PCR检测肠组织NF-κB mRNA表达水平.免疫组织化学检测肠组织NF-κB蛋白定位表达.ELISA法检测肠组织TNF-α分泌水平.结果 光镜下NS组肠组织结构正常,ITF组和LPS组均可见肠黏膜间质和上皮细胞水肿,ITF组较LPS组明显减轻;ITF组肠组织NF-KB mRNA和NF-κB蛋白表达均较LPS组明显下降(P均＜0.01);ITF组肠组织TNF-α分泌较LPS组明显减少(P＜0.01).结论 ITF减轻肠组织损伤的保护作用可能与其下调NF-KB mRNA和蛋白的表达及降低炎性介质TNF-α的分泌相关.     

肠三叶因子对内毒素血症幼鼠肠组织Toll样受体2和4表达的影响

目的：探讨肠三叶因子对内毒素血症幼鼠肠组织Toll样受体（TLR）2、4表达的调节及对肠组织损伤的影响。方法：24只10日龄Wistar幼鼠随机分为正常对照组（NS组,n=8,生理盐水1 mL/kg腹腔注射）;内毒素血症组（LPS组,n=8,LPS 5 mg/kg 腹腔注射）;肠三叶因子组（ITF组,n=8,重组肠三叶因子 0.1 mL/只＋LPS 5 mg/kg腹腔注射）。于腹腔注射后3 h处死,留取远端回肠组织观察肠组织病理改变,RT-PCR检测肠组织TLR2、4-mRNA的表达。结果：光镜下NS组肠组织结构正常,ITF组和LPS组均可见间质和上皮细胞水肿,ITF组较LPS组病变明显减轻。ITF组肠组织TLR2 mRNA 表达较NS组、LPS组明显增高（P＜0.01）; 而TLR4 mRNA表达较NS组和LPS组明显下降（P＜0.01）。结论：肠三叶因子可减轻内毒素血症幼鼠肠组织损伤,这种保护作用可能与其下调TLR4 mRNA的表达相关。     

肠三叶因子对新生鼠坏死性小肠结肠炎Bim和Bcl-xl基因表达的影响及意义

目的 分析肠三叶因子(ITF)对坏死性小肠结肠炎(NEC)新生鼠肠黏膜组织Bim基因与Bcl-xl基因表达水平的影响,探讨ITF对NEC的保护作用机制.方法 采用简单随机法将30只新生鼠分为对照组、NEC组及ITF组,每组10只,对照组不作处理,NEC组建立NEC模型后予以腹腔注射生理盐水0.2ml;ITF组为NEC模型后予以腹腔注射ITF 0.2 mg.对切片行HE染色并作组织病理学检查及免疫组织化学法检测Bim基因与Bcl-xl基因表达,并进行图像分析.结果 病理切片显示NEC组肠壁损伤轻重不一,可见全肠黏膜绒毛坏死,病理组织学改变中位积分为3分;ITF组肠上皮细胞少量脱落,顶端绒毛坏死,病理组织学改变中位积分为1分;图像分析结果显示NEC组Bim基因表达(7.87±0.14)高于对照组(2.15±0.28)及ITF组(3.27±0.34),三组比较差异均有统计学意义(P<0.05);ITF组Bcl-xl基因表达(11.23±0.22)高于对照组(1.89±0.28)及NEC组(2.51±0.13),三组比较差异均有统计学意义(P<0.05).结论 通过腹腔注射ITF可减轻NEC大鼠的肠道损伤,而ITF可能通过改变Bim基因与Bcl-xl基因表达水平保护NEC大鼠肠道损伤.     

姜黄素对急性心肌梗死小鼠心肌细胞凋亡相关基因表达的影响

目的 探讨姜黄素对急性心肌梗死小鼠心肌细胞凋亡相关基因表达的影响.方法 30只健康昆明种小鼠随机分为假手术组、模型组和姜黄素组.假手术组腹腔注射9 g·L-1盐水10 Ml·kg-1,每隔30 min注射1次,共2次;模型组腹腔注射9 g·L-1盐水10 Ml·kg-1,30 min后腹腔注射垂体后叶素(Pit) 10 Ml·kg-1;姜黄素组腹腔注射姜黄素100 mg·kg-1,30 min后腹腔注射Pit 10 Ml·kg-1.ELISA法检测各组小鼠血清乳酸脱氢酶(LDH)和心肌肌钙蛋白I(cTnI)水平.采用RT-PCR法检测各组小鼠心肌组织Fas Mrna及FasL Mrna的表达水平.结果 与假手术组相比,模型组血清LDH、cTnI和心肌组织Fas Mrna及FasL Mrna表达水平显著升高(Pa＜0.01);与模型组相比,姜黄素组血清LDH、cTnI和心肌组织Fas Mrna及FasL Mrna的表达水平显著降低(Pa＜0.01).结论 姜黄素对急性心肌梗死小鼠有较好的保护作用,其机制可能与下调Fas Mrna及FasL Mrna的表达有关.     

肠三叶因子对坏死性小肠结肠炎新生大鼠白细胞介素-1β的影响

目的 探讨肠三叶因子(ITF)对坏死性小肠结肠炎(NEC)新生大鼠肠黏膜组织IL-1β水平的影响,分析ITF对NEC的保护作用.方法 50只新生鼠随机分为5组,每组10只:A组为正常对照组,未进行缺氧、低温处理和注射药物;B组为正常ITF组,予皮下注射ITF0.2 mg(0.2 mL);C组为NEC模型组,建立NEC模型后未予药物注射;D组为NEC加9 g/L盐水(NS)组,建立NEC模型后予皮下注射NS 0.2 mL;E组为NEC加ITF组,建立NEC模型后予皮下注射ITF0.2 mg(0.2 mL).第4天断头处死动物后取其回盲部肠组织1～2 cm固定、包埋,HE染色行病理学检查,其他肠道组织制备组织匀浆取上清液应用ELISA试剂盒榆测IL-1β水平.结果 病理切片示C、D组HE染色切片见肠壁损伤轻重不一,可见全肠黏膜绒毛坏死,病理组织学积分为2～4分,E组肠上皮细胞有少量脱落,顶端绒毛坏死,病理组织学积分为0～2分.C、D组组织匀浆IL-1β水平均较E组显著增高(Pa＜0.01);E组与A、B组比较均无显著性差异(Pa ＞0.05).结论 ITF下可通过降低IL-1β的水平减轻NEC模型的肠道炎性反应,ITF有可能为NEC的治疗提供新方法.     

肠三叶因子在新生鼠坏死性小肠结肠炎模型中对Bax和Bcl-2及Caspase-3表达的影响及意义

目的 通过研究肠三叶因子(ITF)对新生大鼠坏死性小肠结肠炎(NEC)模型肠组织病理学改变及肠道组织中蛋白酶Caspase-3、蛋白Bax和Bcl-2的含量变化,探讨ITF对NEC保护作用的可能机制.方法 30只新生1日龄Wistar大鼠随机分为3组,正常对照组、实验组、干预组,每组10只.实验组为NEC模型后加生理盐水0.2 ml腹腔注射;干预组为NEC模型后予以腹腔注射TTF 0.2 mg(0.2 ml);正常对照组未予处理.第4天处死所有大鼠,取肠组织待检,取近回盲部1～2 cm肠道组织,采用分光光度法检查Caspase-3的表达、采用免疫组化法检测肠道组织中Bax及Bcl-2的含量变化并做病理学检查.结果 实验组Caspase-3表达高于正常对照组和干预组(P均＜0.05),干预组与正常对照组比较差异无统计学意义(P＞0.05);实验组Bax表达高于正常对照组和干预组(P均＜0.05),干预组与正常对照组相近(P＞0.05);干预组Bcl-2表达高于正常对照组和干预组(P均＜0.05),实验组高于正常对照组(P＜0.05).正常对照组的肠组织病理学未见异常,病理评分为0分;实验组HE染色切片见肠壁损伤轻重不一,可见全肠黏膜绒毛坏死,病理评分的中位积分为3分;干预组肠上皮细胞少量脱落,顶端绒毛坏死,病理评分的中位积分为1分.与实验组比较,ITF治疗后NEC导致的组织病理学改变明显减轻.结论 注射ITF可通过减少Caspase-3、Bax表达和增加Bcl-2表达减轻NEC肠道损伤.     

DC-SIGN在炎症性肠病肠黏膜上皮细胞表达及与肠黏膜损伤的关系

目的探讨树突状细胞(DC)表型分子DC-SIGN在炎症性肠病(IBD)肠黏膜上皮细胞的表达及临床意义。方法选取2006年1月至2010年6月收治的IBD患儿32例,其中克罗恩病18例,溃疡性结肠炎14例;10例正常对照儿童。免疫组织化学方法检测肠黏膜组织DC-SIGN表达;人肠上皮细胞株NCM460经LPS(50 ng/ml)刺激,Western-Blot印迹、流式细胞术分别检测肠上皮细胞DC-SIGN以及共刺激分子CD80、CD86表达,分析肠黏膜上皮细胞DC-SIGN表达与IBD及其肠黏膜损伤的关系。结果 DC-SIGN在正常对照儿童肠黏膜组织中基本不表达或低表达,而IBD患儿肠黏膜组织中表达增强,并以肠黏膜上皮细胞为主,其中克罗恩病为61.11%(11/18),溃疡性结肠炎为50.00%(7/14),与正常对照儿童比较,差异均有统计学意义(P<0.05);DC-SIGN表达与IBD患儿的疾病活动度呈正相关(r=0.475,P<0.01)。体外培养肠上皮细胞经LPS刺激后DC-SIGN表达增强,且CD80、CD86表达相应上调。结论 IBD患儿肠上皮细胞表达DC-SIGN,与细胞转分化有关;DC-SIGN可能介导肠上皮细胞在IBD及肠黏膜损伤中发挥DC样的免疫调节作用。     

坏死性小肠结肠炎新生大鼠核因子-κB活性变化及肠三叶因子的干预作用

目的 研究肠三叶因子(ITF)对坏死性小肠结肠炎(NEC)新生大鼠肠黏膜组织核因子-κB(NF-κB)表达的影响,探讨ITF是否对NEC具有保护作用及其在NEC发病机制中的作用.方法 新生鼠50只随机分为5组,每组10只,A组(正常对照组)不做处理;B组(ITF组)皮下注射ITF 0.2 mg;C组为NEC模型组;D组[NEC加9g/L盐水(NS)组]制备NEC模型后皮下注射NS;E组(NEC加ITF组)制备NEC模型后皮下注射ITF 0.2 mg,连续3 d.大鼠均于实验第4天处死.分别于其十二指肠、小肠近中远端及结肠近端和远端处取1～2 cm肠道组织固定、包埋、切片、HE染色行病理学检查及免疫组织化学染色观察NF-κB表达.结果 C、D组组织中NF-κB(p65)阳性表达较A、B及E组显著升高(Pa ＜0.01),E组与A、B组比较也有升高(Pa ＜0.01),且随NF-κB(p165)的激活有明显的核转移;病理切片示C、D组HE染色见肠肇损伤轻重不一,可见全肠黏膜绒毛坏死,病理评分2～4分;E组轻度肠上皮细胞脱落,顶端绒毛坏死,肠组织病理评分0～2分.结论 通过皮下注射ITF可减轻NEC新生大鼠肠道炎性反应,NF-κB通路参与了NEC的发病过程,ITF可能通过抑制NF-κB的活化保护NEC模型新生大鼠的肠黏膜.     

Fas/Fas-L在幼鼠肠缺血再灌注损伤下免疫器官凋亡中的作用

目的 探讨幼鼠肠缺血再灌注下免疫器官凋亡的发生机制，加深认识临床上免疫抑制状态的病理生理机制。方法 免疫组化检测Fas、Fas—L蛋白的表达。结果 免疫组化结果；胸腺内存在Fas／Fas—L蛋白的表达，但蛋白量少；脾脏Fas蛋白明显高于Fas—L,Fas在脾脏主要在脾窦内巨噬细胞、淋巴小结周围淋巴细胞膜和细胞浆内表达，且以巨噬细胞为主；淋巴结Fas—L蛋白表达高于Fas，Fas—L在淋巴结主要在髓窦内巨噬细胞、淋巴小结周围淋巴细胞膜和细胞浆内表达，且以巨噬细胞为主。结论 (1)在幼鼠肠缺血再灌注早期，脾主要以增加Fas的表达引发凋亡。(2)在幼鼠肠缺血再灌注早期，肠系膜淋巴结主要以增加Fas—L的表达引发凋亡。(3)在幼鼠肠缺血再灌注早期，可能通过影响外周免疫器官巨噬细胞及淋巴细胞的凋亡，影响免疫功能状态。     

葡聚糖硫酸钠诱导炎症性肠病大鼠结肠黏膜紧密连接蛋白表达及其通透性的改变

目的：建立葡聚糖硫酸钠（DSS）诱导的大鼠炎症性肠病（IBD）模型,观察其肠上皮紧密连接蛋白表达以及结肠黏膜通透性的变化。方法：将雄性Sprague-Dawley（SD）大鼠随机分为对照组和IBD模型组,每组27只,通过使用3% DSS持续经饮水途径饲养大鼠6 d后恢复正常饮水14 d建立IBD模型,对照组自由饮水。分别于DSS处理后第7天、第14天和第21天观察结肠黏膜病理变化,第21天取结肠组织标本检测髓过氧化物酶活性;采用Ussing chamber检测结肠上皮通透性;通过real-time PCR和Western blot从转录水平和翻译水平分析肠上皮紧密连接蛋白表达。结果：IBD模型组大鼠出现腹泻、便血、体重下降,炎症集中在远端结肠,表现为隐窝脓肿,炎症细胞浸润。与对照组比较,IBD模型组大鼠结肠髓过氧化物酶活性显著增加（P<0.01）,肠上皮跨膜电阻抗值和跨膜电势差显著降低（P<0.01）,短路电流值明显增加（P<0.01）;Real-time PCR和Western blot的结果均提示正常大鼠尚未检测出claudin2的表达,IBD模型组 claudin2 mRNA及蛋白表达阳性;IBD模型组 occludin、claudin3、ZO-1 mRNA及蛋白表达水平均显著低于对照组（P<0.01）。结论：IBD大鼠结肠黏膜屏障功能受损,多种紧密蛋白表达改变,其中紧密连接蛋白表达变化可能在慢性修复期IBD屏障受损发病机制中起到重要作用。     

Plain abdominal radiographs in children with inflammatory bowel disease

The value of plain abdominal radiography in children with inflammatory bowel disease (IBD) has not been ascertained. We reviewed the scout radiographys prior to first barium examination in 100 children with IBD [53 Crohn, 47 ulcerative colitis (UC) and scout films prior to excretory urography in 50 patients who had no clinical evidence of intestinal disease (controls)]. The films were reviewed without clinical information, and the abnormalities on each film scored according to severity and location. Criteria included: mural thickening, dilatation and mucosal abnormalities of the small bowel and colon, as well as abnormal quantity and/or distribution of feces in the colon. Eighty percent (40/50) of the films in the control group were interpreted as normal. Abnormalities suggestive of IBD were present in 73% of the IBD group (76% Crohn and 72% UC). Thirty-one percent of the films in the IBD group had a moderately abnormal score (>=3) or markedly abnormal score (>=5) at presentation. The most reliable radiographic findings were: mucosal abnormality in the colon and small bowel and an abnormal stool pattern (feces completely absent or only present in one colonic segment). The clinical presentation of IBD in childhood is often vague and nonspecific. Abnormalities in plain films of the abdomen are common in these patients and may be helpful in suggesting the presence and, to a great degree, the severity of disease in these children.     

Turner Syndrome with Ulcerative Colitis

Turner syndrome is a chromosomal disease frequently associated with autoimmune disorders including diabetes mellitus, thyroid disease and inflammatory bowel disease (IBD). Although the etiology of IBD has not been fully elucidated, genetic analysis has recently revealed several susceptibility genes. Recently, cases with Turner syndrome associated with IBD have been reported. We report here a 13-yr-old girl with Turner syndrome associated with ulcerative colitis. The patient was undergoing growth hormone treatment and presented with abdominal discomfort and bloody diarrhea. Her karyotype pattern was 46,X,i(Xq). Barium enema revealed punctate collections of barium suggesting microulcerations in the descending and sigmoid colon with loss of haustra. Flexible sigmoidoscopy showed that the mucosa was erythematous and friable upon touch and that the wall had frank hemorrhage and inflammatory polyp formation from the anal verge through the splenic flexure. Histologically, mucosal and submucosal inflammation was prominent, suggesting cryptitis and crypt abscess formation. Based on these findings, she was diagnosed as having ulcerative colitis, and 5-aminosalicylic acid, prednisolone and dietary therapy were initiated. Our observations in this patient suggest that X chromosome abnormality may influence the development of IBD and that screening for gastrointestinal disease in patients with Turner syndrome may help lengthen life expectancy in these patients.     

幼鼠实验性结肠炎模型特点

目的建立幼鼠结肠炎模型,研究其自然病程的特点,为临床研究儿童炎症性肠病(IBD)提供动物模型。方法采用三硝基苯磺酸(TNBS)/乙醇法制作幼鼠结肠炎模型,对照组给予生理盐水灌肠,0时组作为基础值不予任何刺激。应用统一评分标准对结肠粘膜损伤进行评估。结果模型组于造模后24h粘膜损伤最重,有明显溃疡形成,1周溃疡基本愈合,2周起粘膜大体评分与对照组差异无显著性,4周时镜下评分与对照组差异无显著性;模型组体重增长缓慢。结论幼鼠实验性结肠炎模型不同于成年鼠模型,可有生长发育迟缓的表现,更适合于对儿童IBD的研究。     

Dextran sulfate sodium-induced inflammation is enhanced by intestinal epithelial cell chemokine expression in mice

Dextran sulfate sodium (DSS) induces an inflammatory bowel disease-like colitis in animals. To determine the contribution of epithelium to inflammation in the intestine, we examined the effects of DSS in transgenic mice that specifically secrete macrophage inflammatory protein-2 (MIP-2) from the intestinal epithelium. We first confirmed the production of MIP-2 from intestinal epithelial cells by Western blots in transgenic mice. MIP-2 transgenic mice were therefore an appropriate model to examine the role of epithelial cell chemokines in an inflammatory state induced by DSS. We then examined the neutrophil migration into the intestine and the effect of DSS on this migration by myeloperoxidase staining. There was an increase of myeloperoxidase-positive neutrophils in the intestine from wild-type and transgenic mice after the DSS treatment. Furthermore, the increase of neutrophils under stimulation with DSS was confirmed quantitatively by measuring specific tissue myeloperoxidase activities. It was significantly greater in DSS-treated MIP-2 transgenic mice than in wild-type mice in both the small intestine and colon. These results suggest that the inflammatory effects of DSS on both small intestine and colon are enhanced by MIP-2 secreted by epithelial cells in the transgenic mice. In conclusion, intestinal epithelial cells can act in concert with other inflammatory stimuli in maintaining inflammation.     

Interleukin-6 changes tight junction permeability and intracellular phospholipid content in a human enterocyte cell culture model

Proinflammatory cytokines and secretory phospholipase A(2) (sPLA(2)) are elevated in patients with inflammatory bowel disease (IBD). We previously reported that the proinflammatory cytokine IL-6 increased the expression of sPLA(2) (a hydrolyzer of phosphatidylcholine) and decreased membrane integrity in an intestinal epithelial cell culture model. To determine the physiological effects of the IL-6 mediated increase in sPLA(2) on decreased epithelial layer integrity, we investigated alterations of intracellular/secretory phospholipid (PL) composition in a cell culture model. In addition, since other PLs may also mediate epithelial membrane activity, we investigated the effect of IL-6 on PL activity in a Caco-2 enterocyte culture model. Caco-2 cells were incubated for 72 h with IL-6 or media alone (control). Both media and cell lysate were analyzed for PL composition using thin-layer chromatography. The PL composition in the media did not show any differences between the two groups ( p>0.1). Total intracellular PL contents were also unchanged; however, IL-6 led to significant changes in PL composition including an increase in phosphatidylethanolamine (PE) and sphingomyelin (SM) and a decrease in phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) ( p<0.05). Both PE and SM are known as inflammatory signaling factors involved in human IBD. Our study suggests that the decreased membrane integrity seen with IL-6 application may occur via intracellular PL alterations, rather than through the direct effects of sPLA(2).     

Cancer and pediatric inflammatory bowel disease

Cancer in children may be mistakenly diagnosed as inflammatory bowel disease (IBD), and specific cancers may develop in patients who truly have IBD. Ulcerative colitis patients historically carry an increased risk of colorectal adenocarcinoma, but current practices of surveillance and early surgery may have an impact on this. Crohn's disease patients require surveillance for colon cancer, but are also likely to be at increased risk for small bowel tumors and lymphoma. Some malignancies affecting IBD patients are sequelae of immunomanipulation, performed in the interest of IBD therapy itself. Knowing the cancer risks associated with IBD and those associated with agents used for IBD treatment, and practicing long-term surveillance for these tumors, are central components of caring for patients with IBD. Lessons learned from the fields of oncology and bone marrow transplantation may provide future directions and potential cures in IBD.     

肠三叶因子在内毒素致幼鼠肠损伤中的作用及意义

目的：探讨内毒素(LPS)致幼鼠肠损伤中二胺氧化酶(DAO)及肿瘤坏死因子(TNF-α)的变化及基因重组肠三叶因子(rITF)的保护作用,为临床治疗提供实验依据。方法：Wistar幼鼠10日龄96只分为3组,A组:生理盐水对照组;B组:LPS组;C组:LPS+rITF组,每组32只。以生理盐水(1mL/kg),EcoliO55:B5(1mL/kg)、rITF(0.1mL/只、配制浓度5g/L)腹腔注射后2,6,24,72h断头处死动物,取动静脉混合血,测血DAO活性。留取肠组织,免疫组化法检测TNF-α蛋白含量,PCR法检测TNF-αmRNA表达。同时作电镜观测肠组织超微结构变化。结果：B组血浆DAO活性自LPS作用后2h即开始升高,至6h达到最高值,较A组差异有显著性(1.519±0.13U/Lvs1.081±0.04U/L,P<0.01),72h仍持续高值;C组血浆DAO活性较B组明显下降(P<0.01或P<0.05);与A组6h比较差异有显著性(P<0.01),其余各时间点差异无显著性(P>0.05);B组TNF-α积分光密度含量明显高于A组,以LPS作用后6h达高峰(37247.64±3387.59vs6191.02±482.32,P<0.01),C组TNF-α含量较B组明显降低,但仍高于A组(P<0.01);TNF-αmRNA在A组各时间点有微弱的表达,在B组各时间点表达明显增强,较A组差异显著(P<0.01);而C组各时间点表达明显减少,较B组差异显著(P<0.01或P<0.05)。电镜下肠组织超微结构:A组正常,B组变化明显,C组变化较B组减轻。结论：ITF可降低血浆DAO活性,抑制肠组织TNF-αmRNA及蛋白表达,减轻LPS所致幼鼠肠损伤,发挥保护作用。