肠炎清对湿热内蕴型肠黏膜受损时菌群失调的影响

[目的]研究肠炎清对湿热内蕴型肠黏膜受损时菌群失调的影响.[方法]将60例符合纳入标准的门诊及住院患者随机分为2组,各30例,其中2组菌群失调者各17例.治疗组口服中药肠炎清,50 ml/次,2次/d,并用肠炎清直肠滴注100ml,1次/d,连续治疗6周;对照组口服美沙拉嗪,0.5 g/次,3次/d,连续治疗6周.观察患者大便中细菌总数变化,革兰氏阳性、阴性杆菌及球菌的比率改变和大便培养情况,结肠镜下观察黏膜变化,并对治疗前后进行统计学分析.[结果]治疗组与对照组均有效修复肠黏膜,治疗组在改善菌群失调方面明显优于对照组(P＜0.05);当肠黏膜修复明显时,对应的菌群失调也明显改善;而肠黏膜无修复时,对应的菌群失调改善也不明显.[结论]通过口服及灌肠的方法,肠炎清能够抑制肠黏膜损伤,修复受损肠黏膜,明显改善肠道菌群失调.     

醒脑静注射液对重型颅脑损伤患者肠黏膜通透性及血浆二胺氧化酶的影响

目的探讨醒脑静注射液对重型颅脑损伤患者肠黏膜通透性及血浆二胺氧化酶的影响。方法在该院接受治疗的重型颅脑患者86例,随机分成对照组和观察组各43例。对照组患者入院后接受常规治疗,观察组患者在对照组治疗方式的基础上,应用醒脑静注射液静脉滴注治疗。采用格拉斯哥昏迷评分(GCS评分)评价重型颅脑损伤患者病情的改善情况,并测定治疗前后重型颅脑损伤患者血浆二胺氧化酶和乳果糖排泄率水平。结果观察组患者总有效率高于对照组(P<0.05)。治疗后,观察组GCS评分高于对照组(P<0.01)。治疗后5、10 d,观察组患者血浆二胺氧化酶和乳果糖排泄率低于对照组(P<0.01)。结论醒脑静注射液治疗重型颅脑损伤疗效显著,能够缓解患者的病情,改善患者的肠黏膜通透性,保护患者肠道黏膜屏障功能。     

益生菌对肝硬化患者肠黏膜通透性的影响

目的:探讨肝硬化门脉高压患者肠黏膜屏障功能及双歧杆菌等三联活菌胶囊(培菲康)对肝硬化患者肠黏膜通透性的影响.方法:选择我院肝硬化门脉高压、肝功能Child-pugh分级为B级的患者34例,随机分为对照组和双歧杆菌等三联活菌胶囊(培菲康)治疗组,两组均给予常规对症治疗,治疗组加用培菲康,每次420 mg,每日3次,口服2 wk.所有患者均于治疗前后测定血清二胺氧化酶(DAO)及内毒素(ETX)含量.另选12例健康体检者作为正常对照组.结果:肝硬化患者治疗组及对照组血清DAO及ETX含量均高于正常对照组,差异有统计学意义(0.2502±0.0969 kU/L,0.2263±0.1145kU/L vs 0.1145±0.0680 kU/L,P<0.01;0.3801±0.1929 EU/mL,0.3283±0.1251 EU/mL vs0.2338±0.0843 EU/mL,均P<0.05);血清DAO及ETX两指标呈线性相关(r=0.800,P<0.01);培菲康组治疗后血清DAO及ETX水平较治疗前下降,差异均有统计学意义(0.1635±0.0592kU/L vs 0.2502±0.0969 kU/L,0.2445±0.1219EU/mL vs 0.3801±0.1929 EU/mL,P<0.05);对照组治疗后血清DAO及ETX水平较治疗前下降,但差异无统计学意义.结论:血清DAO及ETX水平可作为肝硬化Child-pugh分级B级患者肠黏膜屏障功能的监测指标;补充肠道益生菌可帮助改善肠黏膜屏障功能.     

谷氨酰胺对COPD患者肠黏膜屏障功能的影响

将40例慢性阻塞性肺疾病(COPD)患者随机分为两组,A组行常规治疗,B组加用谷氨酰胺(Gln)治疗;另选20例健康者作为对照组(C组).治疗前及治疗后7 d检测三组血浆二胺氧化酶(DAO)、D-乳酸、内毒素(LPS),比较A、B组肠功能恢复时间及呼衰发生率.结果 显示,治疗前A、B组血浆DAO、D-乳酸、LPS显著高于C组(P均<0.01),A、B组间无统计学差异;治疗后B组上述指标显著低于A组(P<0.01).与B组比较,A组肠功能恢复时间长,呼衰发生率高(P均<0.05).提示Gln有助于增加COPD患者的肠黏膜上皮细胞能量供给,缩短肠功能恢复时间,降低呼衰发生率.     

重症急性胰腺炎大鼠并发肠黏膜屏障功能障碍

目的探讨重症急性胰腺炎(SAP)大鼠肠黏膜屏障功能的状况。方法 48只SD大鼠,随机分两组:假手术组(A组,n=24)、SAP模型组(B组,n=24)。用3%牛磺胆酸钠制备SAP大鼠模型。麻醉苏醒,即开始灌胃,6h/次,A、B组用灌胃器按1 mL/100 g/次生理盐水灌胃。制模后各组在6、12、24 h 3个时间点取材;开腹后观察腹水量及其颜色,观察胃肠道大体情况;取血用酶联免疫吸附双抗夹心法检测血清二胺氧化酶(DAO)及D-乳酸浓度;取胰腺及回肠末段组织做病理检查,并进行胰腺病理组织评分;取回肠末段部分组织做扫描电镜检查。结果A组无腹水;B组腹水多,肠道明显扩张,积液积气,部分肠管发黑。B组血清DAO、D-乳酸的浓度较A组升高(P<0.01)。B组胰腺及回肠病理损害重,胰腺病理组织评分较A组高(P<0.05);扫描电镜检查A组基本正常,B组损伤重。结论 SAP大鼠并发肠黏膜屏障功能障碍。     

复合膳食纤维对实验性溃疡性结肠炎大鼠肠黏膜屏障功能的影响

目的 观察添加复合膳食纤维(DFC)的肠内营养(EN)对实验性结肠炎大鼠肠黏膜屏障功能的影响.方法 将96只SD大鼠用乙酸灌肠法制成结肠炎模型后随机分成3组,C组给予不含DFC的整蛋白型肠内营养粉剂(商品名:能全素);T1组和T2组分别给予含整蛋白型肠内营养 粉剂和DFC的EN.DFC由可溶性膳食纤维(SDF)和不溶性膳食纤维(IDF)按一定比例配制,T1组和T2组中,SDF和IDF的比例分别为1:2和1:3.检测EN后第1、3、5、7天大鼠血浆D-乳酸浓度和血浆二胺氧化酶(DAO)活性并取肠道标本观察肠黏膜变化情况.结果 第3、5、7天的T1组与T2 组血浆D-乳酸浓度和DAO活性较C组下降(P<0.05),T1组与T2组间差异无统计学意义(P>0.05).各时间点T1组与T2组结肠损伤组织学评分均较C组下降(P<0.05),第5、7天T2组较T1组评分下降幅度大(P<0.05).结论 结肠炎大鼠用含有DFC的EN可降低肠道通透性,对肠黏膜屏障有一定的保护作用,不同比例的SDF和IDF 对肠黏膜保护效果不同,适量增加IDF的比例可以增加这种保护效果.     

脑干出血患者肠黏膜屏障功能变化

<正>脑出血占急性脑血管病的20%~30%,年发病率(60~80)人/10万人口,其中脑干出血占脑出血的10%以上〔1〕。创伤、休克可致肠道黏膜损伤,脑干出血作为一种应激反应是否同样对患者肠黏膜造成损伤,国内外尚未见报道。本研究对脑干出血患者不同病程血清D-乳酸(LAC)、二胺氧化酶(DAO)进行检测,探讨其是否存在肠道屏障功能损伤及损伤程度、持续时间。1资料和方法     

梗阻性黄疸对肠黏膜屏障的影响

肠黏膜屏障包括机械屏障、免疫屏障、生物屏障和化学屏障,四者共同维持肠黏膜的正常防御功能。梗阻性黄疸患者引起肠黏膜屏障损伤,导致细菌移位及内毒素血症,后者又加重屏障功能障碍。本文主要就梗阻性黄疸对肠黏膜屏障损伤的机制作一综述。     

心肺复苏后肠黏膜屏障功能受损机制的研究进展

心脏骤停后进行心肺复苏已得到广泛应用,但其生存率仍然不高.肠黏膜屏障损伤是心肺复苏后导致患者死亡的重要原因之一.心肺复苏后,肠道对缺血缺氧极其敏感,可能引起缺血再灌注损伤,导致细菌移位、炎症反应以及肠道菌群紊乱等,进而引起肠黏膜屏障功能受损,最终发展为多器官功能障碍综合征,但其受损机制尚未完全清楚.因此,明确心肺复苏后...     

益生菌对溃疡性结肠炎患者肠黏膜屏障的修复作用

目的探讨益生菌对溃疡性结肠炎患者肠黏膜屏障的修复作用。方法将54例溃疡性结肠炎患者随机分为研究组和对照组。观察双歧杆菌、乳杆菌、嗜热链球菌治疗前1天、治疗后14天患者乳果糖、甘露醇尿液排泄率比值（LAC／MAN）以及血浆内毒素水平。结果益生菌治疗后患者肠黏膜通透性显著下降（P〈0．01），血浆内毒素水平也明显下降（P〈0．05）。结论益生菌可能对溃疡性结肠炎患者肠黏膜屏障有一定修复作用。     

Protection effect of Emodin pretreatment on intestinal I-RI damage of intestinal mucosa in ratsa

Objective:To linvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.Methods:A total of 50SD rats were randomly divided into control group,model group,emodin groups of low,medium and high dose,with 10 in each group.Ischemia-reperfusion injury(I-RI)mode was established by using noninvasive clamp on superior mesentericartery(SMA).Control group and model group were pretreated with 0.5%sodium carboxymethyl cellulose solution lavage 2 h before operation,emodin groups of low,medium and high dose were given emodin lavage with 20,40,60 mg/kg pretreatment,femoral venous blood before the lavage pretreatment(TO)and 1 h ischemia(Tl),and inferior vena venous blood after 1 h of reperfusion(T2)were extracted from each group of rats for detection of serun level of intestinal fatty acid binding protein(I-FABP),tumor necrosis factor(TNF-α),endotoxin,interleukin 6(IL-6),and die content of diamine oxidase(DAO);Mter model establishment,the rats were sacrificed,intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase(MPO],malondialdehyde(MDA)and superoxide dismutase(SOD)levels.And upper small intestine tissue was retrieved,followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy.Results:In emodin groups of low,medium and high dose at T1 and T2,I-FABP,TNF-α,endotoxin.IL,-6 and DAO level were significandy lower than that of model group(P0.05);in emodin group of low,medium and high dose,MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group(P0.05),SOD level was significantly higher than that of model group(P0.05).Intestinal damage of emodin low,medium and high dose groups were significandy lighter than model group.Conclusions:Emodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury.     

Effects of intestinal mucosal blood flow and motility on intestinal mucosa

AIM:To investigate the role of intestinal mucosal blood flow(IMBF) and motility in the damage of intestinal mucosal barrier in rats with traumatic brain injury.METHODS:Sixty-four healthy male Wistar rats were divided randomly into two groups:traumatic brain injury(TBI) group(n = 32),rats with traumatic brain injury;and control group(n = 32),rats with sham-operation.Each group was divided into four subgroups(n = 8) as 6,12,24 and 48 h after operation.Intestinal motility was measured by the propulsion ratio o...     

Increased intestinal permeability in pathogenesis and progress of nonalcoholic steatohepatitis in rats

AIM: To investigate whether increased intestinal permeability contributes to the pathogenesis and progress of nonalcoholic steatohepatitis by observing its dynamic change in rat models. METHODS: Rat models of nonalcoholic steatohepatitis were established by giving a fat-rich diet. The rats were sacrificed at wk 8, 12 and 16 during the study. Rats fed with normal diet were taken as control. Plasma D-lactate, plasma diamine oxidase, serum lipids and liver transaminases were measured in blood of the femoral artery. Hepatic steatosis and inflammation were assessed by haematoxylin-eosin staining. RESULTS: A rat model of nonalcoholic steatohepatitis was established successfully. Plasma D-lactate level in model group at wk 8, 12 and 16 and diamine oxidase level in model group at wk 12, 16 increased significantly compared with those in control group. There were notable differences of D-lactate and diamine oxidase level in model group between wk 8 and 12 as well as between wk 12 and 16. Serum lipids, liver transaminases and liver injury also increased with disease development. CONCLUSION: Increased intestinal permeability caused by intestinal bacterial overgrowth and endotoxin-induced intestinal destruction exists in rats with nonalcoholic steatohepatitis, which may partially explain the pathogenesis and progress of this disease.     

肝硬化对肠黏膜屏障的损害

肝硬化是一种多病因的慢性疾病。肝硬化造成患者肠黏膜屏障的损害,使肠道内毒素和细菌进入血液或腹腔,造成内毒素血症及自发性腹膜炎,进一步加重了患者的病情,引起恶性循环。此文就肝硬化对肠黏膜的损害及其机制作一综述。     

Acute pancreatitis is characterized by generalized intestinal barrier dysfunction in early stage

Background and aimsThe role of intestinal-barrier in acute pancreatitis(AP) is poorly understood. We aimed to assess structural and functional changes in the intestinal-barrier in patients with early AP (time from onset<2 weeks) and the effect of enteral nutrition on them.MethodsIn this prospective observational study, patients with early AP not on enteral nutrition were compared with controls for baseline intestinal-permeability(lactulose: mannitol ratio(L:M)), endotoxinemia(serum IgM/IgG anti-endotoxin antibodies), bacterial-translocation(serum bacterial 16S rRNA) and duodenal epithelial tight-junction structure by immunohistochemistry(IHC) for tight-junction proteins(claudin-2,-3,-4, zonula occludens-1(ZO1), junctional adhesion molecule(JAM) and occludin) and electron microscopy. These parameters were reassessed after 2 weeks enteral feeding in a AP patients subset.Results96 patients with AP(age: 38.0 ± 14.5 years; etiology: biliary[46.8%]/alcohol[39.6%]; severe:53.2%, mortality:11.4%) and 40 matched controls were recruited. Patients with AP had higher baseline intestinal permeability(median L:M 0.176(IQR 0.073–0.376) vs 0.049(0.024–0.075) in controls; p < 0.001) and more frequent bacteraemia(positive bacterial 16S rRNA in 24/48 AP vs 0/21 controls; p < 0.001) with trend towards higher serum endotoxinemia(median IgG anti-endotoxin 78(51.2–171.6) GMU/ml vs 51.2(26.16–79.2) in controls; p = 0.061). Claudin-2, claudin-3, ZO1 were downregulated in both duodenal crypts and villi while claudin-4 and JAM were downregulated in duodenal villi and crypts respectively. 22 AP patients reassessed after initiation of enteral nutrition showed trend towards improving intestinal permeability, serum endotoxinemia and bacteraemia, with significant improvement in claudin-2,-3 in duodenal villi.ConclusionPatients with AP have significant disturbances in intestinal barrier structure and function in first 2 weeks from onset that persist despite institution of enteral nutrition.     

肠道屏障功能障碍的干预研究进展

目前已知,肠道屏障功能在多种严重疾病如烧伤、重症胰腺炎、肿瘤、严重肝病等的发生、发展过程中发挥重要的“枢纽”作用.随着人们对肠黏膜功能障碍在各种严重疾病发生、发展中所起的重要病理生理作用的不断认识,针对患者肠黏膜屏障功能变化进行干预的基础和临床研究日益受到广大学者的关注.本文就近年来国内外对这一领域的研究进展作一综述.     

Effects of cardiopulmonary bypass on tight junction protein expressions in intestinal mucosa of rats

AIM： To investigate the tight junction protein expressions of intestinal mucosa in an experimental model of cardiopulmonary bypass （CPB） in rats. METHODS： Thirty anesthetized rats were randomly divided into two groups： Group S （n = 10） served as sham operation and group C （n = 20） served as CPB which underwent CPB for 1 h. Expression of occludin and zonula occludens-1 （ZO-1） were determined by Western blotting and immunotochemistry, respectively. Plasma levels of diamine oxidase （DAO） and d-lactate were determined using an enzymatic spectrophotometry. RESULTS： Immunohistochemical localization of occludin and ZO-1 showed disruption of the tight junctions in enterocytes lining villi at the end of CPB and 2 h after CPB. The intensities of the occludin and ZO-i at the end of CPB were lower than those of control group （76.4% ± 22.5% vs 96.5% ± 28.5% and 62.4% ± 10.1% vs 85.5% ±25.6%, P 〈 0.05） and were further lower at 2 h after CPB （50.5% ± 10.5% and 45.3% ± 9.5%, P 〈 0.05）. Plasma d-lactate and DAO levels increased significantly （8.688 ± 0.704 vs 5.745 ± 0.364 and 0.898 ± 0.062 vs 0.562 ± 0.035, P 〈 0.05） at the end of CPB compared with control group and were significantly higher at 2 h after CPB than those at the end of CPB （9.377 ± 0.769 and 1.038 ± 0.252, P 〈 0.05）. There were significant negative correlations between occludin or ZO-1 expression and DAO （r^2 = 0.5629,r^2 = 0.5424, P 〈 0.05） or d-lactate levels （r^2 = 0.6512,r^2 = 0.7073, P 〈 0.05） both at the end of CPB and 2 h after CPB. CONCLUSION： CPB markedly down-regulates the expression of occludin and ZO-1 proteins in intestinal mucosa of rats. The close correlation between expression of tight junctions （TJs） and plasma levels of DAO or d-lactate supports the hypothesis that intestinal permeability increases during and after CPB because of decreases in the expressions of TJs.     

炎症性肠病的肠道屏障功能研究

目的:探讨炎症性肠病患者肠道屏障功能损伤及其评价方法。方法:以180例炎症性肠病患者、65名健康体检者为研究对象,检测并比较2组血液中D-乳酸(D-LA)的浓度、二胺氧化酶(DAO)及细菌脂多糖(BET)的活性水平;结合欧洲重症监护医学协会提出的胃肠道功能障碍分级建议对胃肠道损伤进行分级,比较各级别患者胃肠功能异常比例。结果:180例炎症性肠病患者中,96例(53.3%)DAO、52例(28.9%)D-LA、33例(18.3%)BET水平升高;Ⅰ、Ⅱ、Ⅲ、Ⅳ级胃肠道损伤比例分别为31.1%、17.2%、10.6%、8.3%,与健康对照组(分别为17.8%、10.6%、3.9%和1.7%)相比差异显著(均P<0.05)。结论:炎症性肠病患者胃肠道损伤率和肠道屏障功能损伤率较高,应引起临床关注。     

Experimental obstructive jaundice alters claudin-4 expression in intestinal mucosa： Effect of bombesin and neurotensin

AIM: To investigate the influence of experimental obstructive jaundice and exogenous bombesin (BBS) and neurotensin (NT) administration on the expression of the tight junction (TJ)-protein claudin-4 in intestinal epithelium of rats. METHODS: Forty male Wistar rats were randomly divided into five groups:Ⅰ= controls,Ⅱ= sham operated,Ⅲ= bile duct ligation (BDL),Ⅳ= BDL BBS (30μg/kg per d),Ⅴ= BDL NT (300μg/kg per d). At the end of the experiment on d 10, endotoxin was measured in portal and aortic blood. Tissue sections of the terminal ileum were examined histologically and immunohistochemically for evaluation of claudin-4 expression in intestinal epithelium. RESULTS: Obstructive jaundice led to intestinal barrier failure demonstrated by significant portal and aortic endotoxemia. Claudin-4 expression was significantly increased in the upper third of the villi in jaundiced rats and an upregulation of its lateral distribution was noted. Administration of BBS or NT restored claudin-4 expression to the control state and significantly reduced portal and aortic endotoxemia. CONCLUSION: Experimental obstructive jaundice increases claudin-4 expression in intestinal epithelium, which may be a key factor contributing to the disruption of the mucosal barrier. Gut regulatory peptides BBS and NT can prevent this alteration and reduce portal and systemic endotoxemia.