联合应用生长激素和谷氨酰胺对短肠大鼠小肠粘膜上皮细胞凋亡发生分布的影响

目的 :探讨联合应用生长激素和谷氨酰胺对短肠大鼠小肠粘膜上皮细胞凋亡发生分布的影响。材料和方法 :选用 4 0只手术成功的SD短肠大鼠 ,按 2× 2析因实验设计随机分为四组 ,分别给予常规全肠外营养 (STD组 ,n=1 0 )、附加谷氨酰胺 (Gln组 ,n =1 0 )、附加生长激素 (GH组 ,n =1 0 )及附加谷氨酰胺和生长激素全肠外营养 (GG组 ,n =1 0 ) ,持续 6天 ,取 8只正常大鼠模拟手术后第一天处死 ,作为基础对照组 (Control组 ,n =8)。应用原位末端标记方法对比观察残留小肠粘膜上皮细胞凋亡的发生和分布。结果 :凋亡细胞主要位于肠绒毛的顶部。STD组小肠粘膜上皮细胞凋亡指数较对照组明显高增高 (P <0 .0 1 ) ;GH组和Gln组凋亡指数明显低于STD组 (P <0 .0 1 ) ;而GG组凋亡指数又显著低于GH组和GLN组 (P <0 .0 1 )。结论 :联合应用生长激素和谷氨酰胺能够减少小肠粘膜上皮细胞的凋亡 ,从而防止小肠粘膜萎缩的发生。     

金葡菌肠毒素B在烫伤脓毒症大鼠早期肠损害中的作用及意义

目的：探讨金黄色葡萄球菌肠毒素B(SEB)在烫伤脓毒症大鼠早期肠损害中的作用。方法：雄性Wistar大鼠86只，随机分为正常对照组（n=10）、烫伤对照组（n=10）、烫伤后金葡菌感染组（n=50）和SEB单克隆抗体（单抗）拮抗组（n=16）。留取血样品测定SEB、内毒素、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）水平；同时测定组织内毒素水平及小肠组织二胺氧化酶（DAO）活性。结果：烫伤后金葡菌感染动物血浆SEB、TNF-α和IFN-γ水平均显著高于正常对照组，并于2 h、6 h达峰值（P<0.05或P<0.01），此后降低；而小肠组织DAO活性则持续低于对照组（P<0.05）。相关分析显示，小肠组织DAO活性与血浆SEB水平呈显著负相关（r=-0.4398，P<0.05）。此外，金葡菌攻击后动物血浆及心、肝、肺、肾等组织中内毒素含量亦明显高于正常和烫伤对照组水平（P<0.05）；SEB单抗干预可不同程度抑制血浆及组织内毒素水平的变化，其中伤后2 h肾脏改变显著（P<0.05）。结论：在严重烫伤后金葡菌感染时，金葡菌的重要致病因子－SEB可加重动物小肠粘膜屏障功能损害，促进肠源性内毒素移位并蓄积于局部组织，后者可能与金葡菌致病因子协同作用导致脓毒症的病理生理过程进一步恶化。     

选择性肠道清洁法对重症烫伤大鼠肠源性内毒素血症的影响

本实验采用大鼠４０％Ⅲ°烫伤模型，初步观察了选择性肠道清洁法（ＳＤＤ）对肠源性内毒素血症的防治效果。结果发现，防治组动物门、体循环内毒素水平伤后均显著降低（Ｐ＜０．０５～０．０１），各段肠腔内游离内毒素含量较烫伤对照组下降９９．５％以上。且肠道细菌易位率致伤１～５天都明显减少，回肠粘膜二胺氧化酶活性逐渐恢复。防治组大鼠严重烫伤５天存活率提高２６．７％（Ｐ＜０．０５）。本结果提示，该方法对于重症烫伤大鼠肠源性内毒素血症具有显著防护效应，并能抑制肠道细菌的移居与减轻肠粘膜的进一步损害。因此，及早进行ＳＤＤ可能有助于烧伤后肠源性感染及其它并发症的防治。     

联合应用GH和Gln对短肠大鼠小肠粘膜上皮细胞谷氨酰胺酶和鸟氨酸脱羧酶活性的影响

目的 :探讨生长激素和谷氨酰胺促进小肠粘膜上皮细胞分裂增殖的作用途径及它们发挥协同作用的可能机制。方法 :选用 4 0只手术成功的SD短肠大鼠 ,按 2× 2析因实验设计随机分为四组 ,分别给予常规全肠外营养(STD组 ,n =1 0 )、附加谷氨酰胺 (Gln组 ,n =1 0 )、附加生长激素 (GH组 ,n =1 0 )及附加谷氨酰胺和生长激素全肠外营养 (GG组 ,n =1 0 ) ,持续 6天 ,取 8只正常大鼠模拟手术后第一天处死 ,作为基础对照组 (Gontrol组 ,n =8)。分别应用分光光度法和荧光分光光度法测定各组大鼠小肠粘膜上皮鸟氨酸脱羧酶和谷氨酰胺酶活性。结果 :谷氨酰胺能够显著增强小肠粘膜鸟氨酸脱羧酶和谷氨酰胺酶的活性 (P <0 .0 1 ) ,生长激素对这两种酶活性无明显影响 ,而联合应用谷氨酰胺和生长激素可明显增强此两种酶的活性 ,效果优于Gln的单独应用 (P <0 .0 1 )。结论 :研究表明联合应用生长激素和谷氨酰胺能显著增强短肠大鼠小肠粘膜上皮谷氨酰胺酶和鸟氨酸脱羧酶活性 ,促进小肠粘膜细胞对谷氨酰胺的代谢和多胺的生成 ,从而发挥其促进小肠粘膜细胞分裂增殖 ,防止小肠粘膜萎缩的发生的作用。     

TOLL样受体-4和髓样分化蛋白-2在血吸虫病小鼠肝脏的表达及意义

目的:探讨血吸虫病小鼠肝脏TOLL样受体-4(TLR-4)和髓样分化蛋白-2(MD-2)的表达及其在肝脏损害中的作用。方法:将40只健康小鼠随机分成正常对照组(N组,20只)与模型组(M组,20只),M组采用腹部敷贴法制作血吸虫病模型,造模150天后处死动物,鲎试验法测定血清内毒素水平;免疫组化和RT-PCR方法检测肝脏中TLR-4和MD-2的表达。结果:M组血清内毒素水平高于N组(P<0.01);M组小鼠肝脏TLR-4/MD-2表达水平高于N组(P<0.01);M组小鼠肝脏TLR-4/MD-2高表达主要位于肝窦内皮细胞及肝窦区周围细胞。结论:血吸虫病肝硬化可发生肠源性内毒素易位、内毒素血症;脂多糖通过其信号转导蛋白TLR-4和MD-2在肝脏的高表达,激活一系列促炎基因的转录,可能是引起血吸虫病肝脏损害的原因之一。     

急性肝功能衰竭时肠粘膜屏障损伤的研究

目的：探讨急性肝功能衰竭（简称肝衰）时肠粘膜屏障损伤及其机制,并观察中药大黄对它的防治作用。方法：采用鲨试剂法作血浆内毒素定量,酚一次氨酸法测定谷氨酰胺浓度及荧光法测定谷氨酰胺酶活性和组胺含量,Dans蓝染色法测定肠粘膜通透性。结果：硫代乙酰胺（thioacetamide,TAA)引发大鼠急性肝衰,并伴有严重的肠源性内毒素血症（intestinalendotoxemiaIETM)：肠谷氨酸肢酶活性降低,肠粘膜对谷氨酸胺利用减少,肠粘膜通透性增加。组织细胞学显示,TAA组动物肝细胞发生严重变性坏死;肠粘膜淤血、水肿、糜烂,肠肥大细胞脱颗粒。电镜示肠微绒毛倒伏、脱落,细胞间紧密连接破坏。大黄组动物IETM与肝组织损伤明显减轻。结论：急性肝袁伟有肠粘膜屏障损伤,其发生机制与IETM及其介导的组腹增多有关。大黄对急性肝衰时肠粘膜屏障损伤有一定防治作用。     

谷氨酰胺二肽肠外营养对大鼠移植小肠的营养作用——小肠粘膜的形态学观察

研究采用18只接受纯种近段空肠异体移植的Wistar大鼠,随机分组,分别给于常规全肠外营养(n=8)和含3%丙氨酰-谷氨酰胺二肽的全肠外营养(n=10),持续10天.应用光镜、电镜和组织化学等技术对两组大鼠的移植小肠进行形态学的对比研究.结果显示:谷氨酰胺组移植小肠的粘膜厚度、隐窝深度、绒毛高度和绒毛表面积均明显大于常规组(P相似文献   

急性肝衰竭时肠源性内毒素血症对肝脏能量代谢的影响

目的:研究急性肝衰竭时肠源性内毒素血症对肝脏能量代谢的影响。方法:以硫代乙酰胺(TAA)染毒建立急性肝损伤大鼠模型;应用酶荧光法测定动脉血酮体(乙酰乙酸、β-羟基丁酸)浓度及肝细胞线粒体ATP含量;采用结肠切除术并观察血浆内毒素水平与血清丙氨酸氨基移换酶(ALT)活性的变化。结果:TAA组大鼠血浆内毒素水平与血清ALT活性均显著高于正常对照组(P＜0.01),动脉血酮体比(AKBR)降至0.4以下,动脉血中总酮体浓度显著低于正常对照组(P＜0.01)。切除结肠的TAA染毒组大鼠未发生内毒素血症,肝细胞线粒体ATP含量显著高于TAA组(P＜0.01),血清ALT活性虽高于正常对照组(P＜0.05),但显著低于TAA组(P＜0.01)。结论:肠源性内毒素血症可损伤肝脏能量代谢,使肝脏代谢和功能发生严重障碍,在急性肝衰竭的发生过程中具有关键性作用。     

肠源性内毒素血症对肝组织细胞间粘附分子-1表达的影响

目的:探讨肠源性内毒素血症对肝组织细胞间粘附分子-1(ICAM-1)表达的影响。方法:采用Western blot 的方法检测硫代乙酰胺(TAA)诱导的肠源性内毒素血症大鼠肝组织中ICAM-1表达的变化。结果:ICAM-1的分子量为95 kD,正常对照组与注射TAA 6 h组ICAM-1的表达很弱,而在注射TAA 12 h以后的表达有增强,且与血浆内毒素水平及反映肝损伤程度的ALT活性变化相一致。结论:肠源性内毒素血症可诱导肝组织中ICAM-1表达的上调,后者与肝损伤程度相一致。     

重症急性胰腺炎大鼠肠黏膜ICAM-1表达与黏膜损伤的关系

为探讨重症急性胰腺炎 (SAP)时肠黏膜细胞黏附分子ICAM 1表达的变化 ,以及与肠粘膜损伤、细菌移位、内毒素血症的关系。经胰胆管逆行注射 5 %牛黄胆酸钠制备大鼠SAP模型 ,检测血浆淀粉酶 (AMY)、脂肪酶 (LIP)及内毒素 (LPS)水平 ,小肠黏膜细胞ICAM 1的表达 ,胰、肝、肺、脾及肠系膜细菌培养 ,观察胰腺、小肠病理形态、肠黏膜超微结构的改变。与假手术组相比 ,SAP组AMY、LIP、LPS及肠黏膜组织ICAM 1的表达量随时限延长逐渐增高 ,且SAP6、12及 18h均明显升高 (P <0 0 1)。假手术组各脏器细菌培养均为阴性 ,SAP组脏器细菌培养呈现不同程度的阳性。SAP组肠绒毛呈不同程度的排列稀疏、脱落、紊乱、倒伏 ,伴中性粒细胞浸润 ,尤以SAP12h组为甚。结果显示 ,SAP时肠黏膜细胞ICAM 1表达明显增高 ,由此介导的中性粒细胞在局部聚集活化 ,可能是造成肠黏膜损伤 ,引发细菌移位和内毒素血症的原因之一     

TNFα在酒精性诱导肠黏膜损伤中的表达和作用

目的制备酒精灌胃诱导急性酒精性肠黏膜损伤模型,探讨TNFα在急性酒精摄入导致肠黏膜损伤的作用。方法雄性Wistar大鼠32只,随机分成4组,每组8只。正常组,酒精模型组,TNFα组,抗TNFα-Ig G抗体组。ELISA方法检测血清TNFα水平,Western blot方法检测小肠标本occludin的表达。结果酒精组与对照组比,TNFα明显升高(0.05),同时occludin的相对表达量明显下降(0.05);外源性TNFα预处理后,TNFα表达进一步升高,而occludin的相对表达量进一步下降;TNFα-Ig G抗体可抑制occludin表达量下降。结论酒精诱导大鼠肠黏膜损伤时TNFα过表达,TNFα可能成为治疗酒精诱导的肠黏膜损伤的新靶点。     

Lipopolysaccharide-Induced Bacterial Translocation Is Intestine Site-Specific and Associates with Intestinal Mucosal Inflammation

The present study aimed to determine whether any specific intestinal site or intestinal mucosal inflammation is highly correlated with bacterial translocation (BT). Enterostomy tubes were surgically placed in adult male Sprague?CDawley rats 5?days before induction of experimental model. After surgery, sterile water containing kanamycin (25?mg/L) was injected into each intestinal segment through the tubes for 3?days. Green fluorescent protein (GFP)-transfected Escherichia coli (n?=?30 for lipopolysaccharide (LPS) group, and n?=?30 for control group) or 0.9?% saline (n?=?30 for blank group) were injected into each intestinal segment through the tubes for two consecutive days. Rats were then subjected to LPS-induced endotoxemia; lactulose and mannitol were injected into each intestinal segment through the tubes simultaneously. At 6?h after LPS injection, BT to distant organs and integrity of tight junctions (TJ) were examined by fluorescence and electron microscopy, respectively. The urinary excretion ratio of lactulose/mannitol (L/M) and intestinal mucosal cytokine levels were assessed. We found that the intestinal permeability, reflected by translocation rates of GFP-labeled E. coli, the levels of open TJ, the excretion ratio of L/M, and the inflammatory cytokine levels were higher in the LPS group than in the control and blank groups. The endotoxemia ileum showed the highest levels of both intestinal permeability and inflammatory cytokine, while the colon showed the lowest. The present study of endotoxemia rats suggests that LPS increases gut paracellular permeability and induces BT. The ileum is the site of greatest BT risk, while the colon is the lowest, and the difference in risk between these sites is correlated with intestinal mucosal inflammation.     

乌司他丁联合ghrelin对内毒素血症大鼠肠功能障碍的影响

目的观察乌司他丁(UTI)联合ghrelin(GHL)对内毒素血症大鼠肠功能障碍的影响,探讨UTI联合GHL改善内毒素血症大鼠肠功能的作用及其可能机制。方法以内毒素(LPS)15 mg/kg腹腔注射大鼠作为内毒素血症动物模型。将60只雄性SD大鼠随机等分为对照组(CON组)、LPS组、UTI组、GHL组、UTI+GHL组,采用HE染色、RealTime-PCR、小肠葡聚糖蓝-2000(BD-2000)推进率和ELISA等方法在12 h及24 h观察各组大鼠小肠屏障功能、小肠运动功能以及炎症介质TNF-α、IL-6、HMGB1等变化。结果 HE染色结果显示UTI+GHL组、UTI组与LPS组相比能不同程度减轻回肠结构损伤,且UTI+GHL组更明显(P0.05)。UTI组和UTI+GHL组在RD-5和TFF3 mRNA表达水平方面较LPS组有显著提高(P0.05),且UTI+GHL组升高明显(P0.05)。GHL组和UTI+GHL组较LPS组小肠运动功能均显著升高,且UTI+GHL组更为明显(P0.05)。UTI+GHL组、UTI组、GHL组与LPS组相比均能显著降低TNF-α、IL-6、HMGB1等炎症因子表达(P0.05),且在肠黏膜组织中发现了类似结果。结论 UTI联合GHL可通过抑制内毒素血症时全身炎症反应及肠组织局部炎症反应,明显改善肠屏障及提高肠运动功能。     

真人养脏汤对溃疡性结肠炎大鼠肠道黏膜屏障功能的保护作用

目的:观察真人养脏汤(ZRYZ)对三硝基苯磺酸(TNBS)诱导的溃疡性结肠炎(UC)大鼠肠道黏膜屏障功能的保护作用以及紧密连接相关蛋白闭锁小带蛋白1(zonula occludens-1,ZO-1)和闭锁蛋白(occludin)的表达变化,探讨其可能作用机制。方法:将Wistar雄性大鼠随机分为正常组、模型组、柳氮磺吡啶(SASP)阳性对照组、ZRYZ高剂量组和ZRYZ低剂量组。除正常组外,其它各组用TNBS/50%乙醇混合溶液局部灌肠法复制溃疡性结肠炎大鼠模型。造模成功后阳性对照组给予SASP混悬液灌胃;ZRYZ高剂量组和ZRYZ低剂量组分别按生药30.4 g/kg和15.2 g/kg剂量灌胃;正常组与模型组等量生理盐水灌胃,共21 d。给药结束后,考察大鼠疾病活动指数(DAI)变化,进行大体损伤评分,测定肠道黏膜通透性(以尿中乳果糖/甘露醇的比值表示,即L/M值),测定结肠组织髓过氧化物酶(MPO)活性,计数结肠组织杯状细胞数量,测定血清二胺氧化酶(DAO)及D-乳酸(D-LA)水平,检测ZO-1和occludin的表达。结果:与正常组相比,模型组DAI、大体损伤评分、L/M值、结肠组织MPO活性以及血清D-LA和DAO水平明显升高(P0.05),结肠组织杯状细胞数量以及ZO-1和occludin表达明显降低(P0.05);与模型组相比,ZRYZ高剂量组和ZRYZ低剂量组DAI、大体损伤评分、L/M值、结肠组织MPO活性以及血清DAO和D-LA水平明显降低(P0.05),结肠组织杯状细胞数量以及ZO-1和occludin表达明显升高(P0.05)。结论:真人养脏汤可通过降低肠道黏膜通透性,保护溃疡性结肠炎大鼠肠道上皮细胞黏膜屏障功能,其机制可能与升高ZO-1和occludin表达有关。     

紫杉醇联合顺铂化疗对人卵巢浆液性囊腺癌组织occludin和ZO-1表达以及线粒体超微结构的影响

 目的：观察紫杉醇联合顺铂化疗对人卵巢浆液性囊腺癌（serous cystadenocarcinoma, SC）组织紧密连接蛋白occludin和zonula occludens-1(ZO-1)表达以及线粒体超微结构的影响。方法：取紫杉醇联合顺铂化疗和未化疗的卵巢癌患者SC组织,用电镜观察其线粒体超微结构,用免疫组织化学法观察癌组织occludin和ZO-1蛋白的表达,并以子宫肌瘤患者的正常卵巢组织为正常对照。结果：SC细胞线粒体明显肿胀,呈现巨线粒体,且嵴断裂十分显著;化疗后的SC细胞线粒体肿胀减轻,形态接近正常。SC细胞较正常卵巢上皮细胞occludin和ZO-1蛋白表达明显降低（P<005或P<001）;化疗组较未化疗组SC细胞occludin和ZO-1蛋白表达明显增多（P<001）。结论: 紧密连接蛋白occludin 和 ZO-1的低表达可能是SC浆液生成增多和细胞代谢异常的关键所在,而化疗可促进紧密连接蛋白表达,从而减轻线粒体结构肿胀并改善细胞功能。     

脂多糖在肝肺综合症发生中的作用

目的：探讨肠源性内毒素血症在肝肺综合征发生中的作用。 方法： 用复合因素复制大鼠肝硬化模型。腹腔内一次性注射小剂量内毒素以加重肝硬化动物的内毒素血症。另设正常动物注射内毒素组和甘氨酸拮抗内毒素组加以对照。 结果： 实验第8周末的肝硬化大鼠发生了肝肺综合征。小剂量内毒素一次性腹腔内注射后肝硬化动物肺脏的病理变化加剧；甘氨酸在在体和离体实验中均可明显拮抗内毒素的生物学效应，减轻肝肺综合征的各种病理变化。 结论： 肝硬化动物所伴之肠源性内毒素血症很可能在肝肺综合征发病机制中起重要作用；内毒素直接和其诱导产生的TNF-α等细胞因子在肝肺综合征发病机制中起作用。     

Alteration of intestinal intraepithelial lymphocytes and increased bacterial translocation in a murine model of cirrhosis

Alterations in immunological defense in the gut may lead to the bacterial infection that is frequently associated with cirrhosis of the liver. The aim of this study was to investigate the changes in distribution and function of intestinal intraepithelial lymphocytes (IELs) in relation to intestinal barrier dysfunction in experimental cirrhosis. Cirrhosis was induced in mice by treatment with carbon tetrachloride (CCl4) intraperitoneally with 5% alcohol in drinking water for 12 weeks. Bacterial translocation was assessed in mesenteric lymph nodes (MLNs) by the transport of fluorescence-labeled latex beads and by bacteriological cultures. The lymphocyte subpopulation was compared in three groups (cirrhosis, alcohol alone and controls). IFN-gamma production from isolated IELs was determined by ELISA after stimulation with anti-CD3 or IL-12/IL-18. The total number of IELs significantly increased in the cirrhosis and alcohol groups. There was a preferential increase in TCRgammadelta+CD8+ population in the alcohol group, but no change in cirrhosis. Bacterial translocation was negative in the control group, and a small number was noted in the alcohol group, whereas it was significantly noted in the cirrhosis group. Although the number of IEL was significantly increased in the cirrhosis group, their proliferative response was decreased, and IFN-gamma production from each IEL was markedly diminished in either stimulation by anti-CD3 or IL-12/IL-18. These changes were more remarkable in the cirrhosis group than in the alcohol group. In conclusion, bacterial translocation due to intestinal barrier dysfunction in cirrhosis may be closely correlated with the alteration of the immune function in IELs.     

细胞色素P450ⅡE1在肠道血吸虫病并结直肠癌患者肠黏膜中的表达

目的 探讨细胞色素P450ⅡE1（CYPⅡE1）的蛋白表达与肠道血吸虫病并结直肠癌之间的相关性及其可能的作用机制。方法 采用免疫组织化学SP法,检测60例肠道血吸虫并结直肠癌癌组织、60例单纯结直肠癌癌组织（无肠道血吸虫感染）、60例单纯肠道血吸虫感染组、50例无血吸虫感染的正常肠道组织中的CYPⅡE1蛋白的表达情况;分析肠道血吸虫病并结直肠癌癌组织中CYPⅡE1的表达与患者的性别、年龄、病理分型、淋巴结转移等临床病理参数的关系。 结果 肠道血吸虫病并结直肠癌组织中CYPⅡE1的表达阳性为73.33%,单纯肠道血吸虫感染组表达阳性为46.67%,60例单纯结直肠癌癌组织（无肠道血吸虫感染）表达阳性为31.67%,而正常组织中的表达为16%。在黏液腺癌中CYPⅡE1蛋白表达明显增高（P＜0.01）。血吸虫并结直肠癌组CYPⅡE1蛋白表达阳性与性别、年龄、肿瘤部位、淋巴结转移无关,与组织分化程度和病理分型有关。逐步回归法进行 Logistic多因素分析结果显示,组织学分型是CYPⅡE1表达阳性的唯一危险因素（OR=11.4,P=0.024）。 结论 CYPⅡE1可能在肠道血吸虫病并结直肠癌的发病机制中有一定的作用。CYPⅡE1的表达与结直肠癌组织的病理分型有关。     

Protective effect of salvianolic acid B on NASH rat liver through restoring intestinal mucosal barrier function

Aim: To investigate the effect of Salvianolic acid B (Sal B) on the disease progress of NASH and change of intestinal barrier function. Methods: Sixty Sprague-Dawley (SD) rats were randomly divided into control group, model group and treated group, with the former given normal diet and the latter 2 groups rats fed high-fat diet. In treated group, rats were infused through the stomach with 1 mg/ml Sal B every day at a dose of 20 mL/kg body weight. All animals were killed at the 24th week and plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC), endotoxin (ET) and diamine oxdase (DAO) were analyzed using the blood samples. The histopathology of liver was observed by H&E staining. The expression changes of tight junction protein occludin and ZO-1 were analyzed by immunocytochemistry. Ultrastructural morphology of small intestinal tissues was investigated by transmission electron microscopy. Results: Plasma levels of ALT, AST, TG, TC, ET and DAO were significantly higher in model group than those in both control group and group treated with Sal B. In model group, vacuolated swelling of the cytoplasm with aggregates of chronic inflammatory cells was observed in the liver tissue but not in Sal B-treated group. NAFLD Activity Score in the treated group was significantly lower than that in model group. Immunohistochemical staining showed that Sal B administration recovered the expression of occludin and ZO-1, which was downregulated in the model group. Transmission electron microscopy analysis demonstrated that cell surface microvilli and major intercellular junctional complex including tight junction, gap junction and adherens junction were restored in Sal B-treated group. Conclusion: Sal B exerted protective function against high-fat diet-induced liver damage by restoring healthy barrier function of intestine in NASH rat model.