益生菌治疗大鼠实验性结肠炎效果观察及对T细胞亚群的影响

目的评价益生菌对大鼠实验性结肠炎的疗效，以及研究治疗后体内T细胞亚群变化情况。方法选择北京大学人民医院消化内科与北京医院特需医疗科于2004年9月至2005年2月建立实验性结肠炎模型，设立不同剂量益生菌治疗组、阴性对照组和阳性对照治疗组（泼尼松治疗组及柳氮磺胺吡啶治疗组）。组织学积分评定疗效；流式细胞仪检测外周血、脾脏和结肠CD4^＋、CD8^＋T细胞亚群变化情况。结果大剂量益生菌对治疗大鼠实验性结肠炎有效；结肠炎大鼠结肠内CD4^＋、CD8^＋T细胞均增加，益生菌治疗后回落，而CD4^＋／CD8^＋比值及外周循环T细胞亚群无变化。结论大剂量益生菌治疗大鼠实验性结肠炎有效，可能与免疫调节机制有关。     

实验性大鼠结肠炎中血小板激活状态研究

国内外研究表明,炎症性肠病(IBD)患者病变活动期存在血液高凝状态且肠壁可能有微血栓形成。近十年来,已证实血小板除具有凝血功能外还在炎症的发生发展中发挥重要的作用,本研究通过三硝基苯磺酸(TNBS)诱导建立IBD动物模型,观察模型建立4周内动物血小板的激活状态改变,探讨血小板激活在IBD中的变化规律及其与肠道炎症严重度的相关性。     

益生菌治疗的实验性结肠炎中调节性T细胞的作用

目的评价不同剂量益生菌对大鼠实验性结肠炎的疗效,研究治疗后全身及肠道局部调节性T细胞(Tr)的变化情况,探讨益生菌作用机制。方法建立三硝基苯磺酸(TNBS)实验性结肠炎大鼠模型。所用益生菌为双歧三联活菌(商品名:培菲康)。设阴性对照组、泼尼松组、柳氮磺胺吡啶 (SASP)组、益生菌小、大剂量组(剂量分别为150和300 mg·kg-1·d-1)、益生菌+泼尼松或SASP(益生菌剂量为150 mg·kg-1·d-1)组。治疗2周后组织学积分评定疗效;流式细胞仪检测各组外周血、脾脏和结肠上皮内CD4+CD25+及CD8+CD28-两种Tr比例变化。采用t检验行统计学分析。结果组织学评分显示大剂量益生菌对实验性结肠炎有效(2．2±0．8比3．5±0．7,P<0．05),而小剂量益生菌单独作用无明显疗效,联合泼尼松或SASP治疗比单独应用疗效更强;大剂量益生菌治疗后CD4+ CD25+Tr比例在外周血(3．4±0．6比11．7±4．7,P<0．05)及脾脏(2．1±1.9比10．3±3．1,P<0．05) 中下降,在结肠内上升(36．6±15．0比7．9±4．7,P<0．05);CD8+CD28-Tr则相反,在外周血及脾脏中上升(91．7±4．5比59．0±4．2,97．3±0．1比88．2±6．9,P<0．05),在结肠内下降(42．2±6．0比68．5 ±8．6,P<0．05)。Tr的这种变化与泼尼松或SASP治疗存在一定差异。结论益生菌单独大剂量或小剂量联合泼尼松或SASP治疗TNBS诱导的结肠炎有效,CD4+CD25+和CD8+CD28-Tr在发挥疗效过程中可能起一定作用。     

益生菌治疗大鼠实验性结肠炎效果观察及对T细胞亚群的影响

目的评价益生菌对大鼠实验性结肠炎的疗效,以及研究治疗后体内T细胞亚群变化情况。方法选择北京大学人民医院消化内科与北京医院特需医疗科于2004年9月至2005年2月建立实验性结肠炎模型,设立不同剂量益生菌治疗组、阴性对照组和阳性对照治疗组(泼尼松治疗组及柳氮磺胺吡啶治疗组),组织学积分评定疗效;流式细胞仪检测外周血、脾脏和结肠CD4 、CD8 T细胞亚群变化情况。结果大剂量益生菌对治疗大鼠实验性结肠炎有效;结肠炎大鼠结肠内CD4 、CD8 T细胞均增加,益生菌治疗后回落,而CD4 /CD8 比值及外周循环T细胞亚群无变化。结论大剂量益生菌治疗大鼠实验性结肠炎有效,可能与免疫调节机制有关。     

大鼠溃疡性结肠炎模型的实验研究

[目的]探讨不同剂量的5％2，4，6，三硝基苯磺酸（TNBs），所建立的急性期溃疡性结肠炎（UC）动物模型。[方法]用聚丙烯管插入大鼠肛门上段8cm后，注入不同剂量混合试剂（TNBs 50～100mg／kg加50％乙醇0．25m1），1周后处死动物，进行组织形态学评分和光镜评估。[结果]TNBs 100mg/kg剂量下引起的UC模型，肉眼见结肠黏膜多处溃疡，黏膜显著充血水肿。组织学检查发现黏膜及黏膜下层有大量中性粒细胞及淋巴细胞、巨噬细胞、纤维细胞浸润，肉芽组织及隐窝脓肿形成，50mg／kg剂量时有一较轻度的损伤。[结论]用TNBs所致的UC模型简单易行，重复性好；其溃疡炎症类似人UC的改变。实验的最佳造模剂量为100mg／kg。     

TNBS诱导结肠炎大鼠Foxp3表达及其机制初探

目的 观察2、4、6-三硝基苯磺酸(TNBS)诱导的SD大鼠结肠炎模型结肠Foxp3、TGF-β1的表达及外周血IL-2、IL-10的变化,初步确定Foxp3在IBD中的作用及机制.方法 20只SD大鼠随机分组,三硝基苯磺酸/乙醇灌肠造模,观察炎症活动指数(DAI)、大体形态损伤、组织学改变及免疫组化检测结肠Foxp3及TGF-β1、ELISA法检测血清IL-2、IL-1.结果 模型大鼠结肠黏膜组织Foxp3阳性的细胞数4.040±1.088低于对照组6.920±1.834,P＜0.05;模型组结肠黏膜组织TGF-β1光密度值0.186±0.013低于对照组0.231±0.034,P＜0.05;模型组大鼠血清IL-10浓度(27.61±4.28 pg/m1)低于对照组(40.46±4.77 pg/na),P＜0.05;模型组大鼠血清IL-2浓度(66.70±3.51 pg/m1)高于对照组(50.39±3.92 pg/m1),P＜0.05.结论 Foxp3可能通过TGF-β1、IL-2、IL-10在IBD的发展过程中发挥作用.     

DSS、TNBS、OXZ诱导结肠炎动物模型的对比

目的 对比研究DSS、TNBS、OXZ诱导的结肠炎动物模型.方法 本研究选取了一般状态、DAI评分和组织学损伤评分几个方面来评价.结果 DSS组大鼠造模安全性较高,在整个实验过程中无大鼠出现死亡,而TNBS组及OXZ组均有2只大鼠出现死亡,DSS组大鼠DAI评分升高较快,于实验第7天时各模型组DAI评分差异无统计学意义,TNBS组组织学损伤最重,但各造模组之间差异无统计学意义.结论 三种造模方法均可以成功诱导大鼠实验性结肠炎模型,各造模组DAI评分和组织学损伤没有显著的差异.DSS造模方法具有较高的安全性.     

徐长卿对三硝基苯磺酸诱导的大鼠结肠炎的作用

目的:探讨徐长卿对2,4,6-三硝基苯磺酸(trinitrobenzenesulfonic acid,TNBS)诱导的大鼠结肠炎的作用.方法:将40只♂SD大鼠随机分为4组:正常组、模型组、徐长卿组和巴柳氮组.除正常组外,其余3组大鼠均以TNBS灌肠造模.灌肠24h后,徐长卿组开始每天给予徐长卿4g/kg;巴柳氮组给予巴柳氮钠1g/kg灌胃治疗10d.每天观察大鼠一般情况,给药结束后,观察大鼠结肠大体损伤及病理,酵素免疫分析法(enzyme-linked immunosorbant assay,ELISA)检测肠组织肿瘤坏死因子(tumor necrosis factor,TNF)-α、白介素(interleukin,IL)-1β及IL-10水平.结果:两治疗组体质量较模型组增加,但差异无统计学意义;两治疗组疾病活动指数(disease activity index,DAI)评分较模型组明显下降(0.70±1.06,0.67±0.71vs2.38±1.51,P<0.05).徐长卿组、巴柳氮组结肠大体损伤及病理评分较模型组显著下降(1.05±0.83,1.06±0.85vs2.94±0.94;1.65±1.67,2.00±1.80vs6.00±1.67,均P<0.01).徐长卿组较模型组TNF-α、IL-1β水平明显降低(P<0.01),IL-10水平无统计学差异.巴柳氮组较模型组TNF-α、IL-1β、IL-10水平均明显降低(P<0.01).结论:徐长卿能有效改善TNBS诱导的大鼠结肠炎,其机制可能与调节细胞因子水平有关.     

雷公藤红素对三硝基苯磺酸诱导的大鼠结肠炎的保护作用

背景：传统药物对炎症性肠病疗效不甚理想，寻找新型而有效的药物一直是该领域的研究热点。目的：观察雷公藤红素对三硝基苯磺酸（TNBS）诱导的大鼠结肠炎的保护作用，并初步探讨其可能机制。方法：以TNBS诱导大鼠结肠炎模型。将动物随机分为正常对照组、模型组、助溶剂对照组以及雷公藤红素低剂量组（每天0．5mg／kg）和高剂量组（每天1mg／kg）。以大体和组织学评分评价结肠炎症程度。以免疫组化方法检测结肠组织核因子（NF）-kBp65的表达，以半定量逆转录聚合酶链反应（RT-PCR）检测白细胞介素（IL）-1β和肿瘤坏死因子（TNF）-α mRNA的表达。结果：高、低剂量雷公藤红素均能显著改善结肠组织大体和组织学评分，降低NF-kB p65以及IL-1β、TNF-α mRNA的表达。结论：雷公藤红素对TNBS诱导的大鼠结肠炎具有显著保护作用，抑制促炎细胞因子的产生可能是其主要作用机制之一。     

银杏天宝对大鼠实验性结肠炎炎症损伤的保护作用

炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),病因和发病机制尚不清楚。肠黏膜局部免疫反应异常是UC发病的重要环节。炎症介质[包括活性氧簇(ROS)和细胞因子]在介导这一异常免疫反应中起重要作用。本研究观察银杏天宝(Ginkgo biloba extract,EGB)对2,4,6-三硝基苯磺酸(TNBS)诱导实验性结肠炎大鼠炎症介质的影响,探讨银杏天宝对大鼠实验性结肠炎的影响机制。一、材料和方法1．材料和试剂:TNBS购自Sigma公司。EGB为贵州     

垂盆草对小鼠和大鼠肝脏脂质过氧化损伤的防护作用

本实验观察了垂盆草水提物对急性酒清中毒所致小鼠肝脏脂质过氧化损伤的影响,同时又观察了垂盆草水提物对氧自由基损伤的作用。结果表明,口服垂盆草(10g/kg),无论是给药3次还是1次均能明显防止酒精所致小鼠肝脏谷胱苷肽(GSH)的耗竭及脂质过氧化产物丙二醛(MDA)的生成。垂盆草与大鼠肝微粒体体外温孵,对 NADPH—Vit C 所致微粒体脂质过氧化和 Fe_(2+)-半胱氨酸(cys)所致大鼠肝细胞的脂质过氧化损伤亦具有显著的防护作用。表明该药可保护肝细胞免受脂质过氧化损伤。     

Infliximab modifies mesenteric adipose tissue alterations and intestinal inflammation in rats with TNBS-induced colitis

Abstract

Objective. Infliximab is a monoclonal anti-TNF-α antibody that is used therapeutically to treat Crohn's disease (CD). High levels of pro-inflammatory cytokines, especially TNF-α, have been observed in the gastrointestinal tract of CD patients and were associated with alterations in the mesenteric adipose tissue, which also contributed to the high levels of adipokine release. The authors used a rat model of colitis that produces mesenteric adipose tissue alterations that are associated with intestinal inflammation to study the effects that infliximab treatment has on adipokine production, morphological alterations in adipose tissue and intestinal inflammation. Material and methods. The ability of infliximab to neutralize rat TNF-α was evaluated in vitro using U937 cells. Colitis was induced by repeated intracolonic trinitrobenzene sulfonic acid instillations and was evaluated by macroscopic score, histopathological analysis, myeloperoxidase activity, TNF-α and IL-10 expression as well as iNOS (inducible NO synthase) expression and JNK phosphorylation in colon samples. The alterations in adipose tissue were assessed by TNF-α, IL-10, leptin, adiponectin and resistin levels as well as adipocyte size and peroxisome proliferator-activated receptor (PPAR)-γ expression. Results. Infliximab treatment controlled intestinal inflammation, which reduced lesions and neutrophil infiltration. Inflammatory markers, such as iNOS expression and JNK phosphorylation, were also reduced. In mesenteric adipose tissue, infliximab increased the production of IL-10 and resistin, which was associated with the restoration of adipocyte morphology and PPAR-γ expression. Conclusions. Our results suggest that infliximab could contribute to the control of intestinal inflammation by modifying adipokine production by mesenteric adipose tissue.     

Expression and significance of nuclear factor κB p65 in colon tissues of rats with TNBS-induced colitis

AIM: To investigate the role of NF-κB in the pathogenesis of TNBS-induced colitis in rats.METHODS: Thirty-two healthy adult Sprague-Dawley (SD)rats were randomly divided into four groups of eight each:normal, NS, model I, model Ⅱ groups in our study. Rat colitis model was established through 2-,4-,6-trinitrobenzene sulfonic acid (TNBS) enema. At the end of four weeks,the macroscopical and histological changes of the colon were examined and mucosa myeloperoxidase (MPO)activities assayed. NF-κB p65 expression was determined by Western blot assessment in cytoplasmic and nuclear extracts of colon tissue, and the expressions of TNF-αand ICAM-1 protein in colon tissue were examined by immunohistochemistry. The relativities between expression of NF-κBp65 and other parameters were analyzed.RESULTS: TNBS enema resulted in pronounced pathological changes of colonic mucosa in model Ⅱ group (macroscopic and histological injury indices 6.25±1.39 and 6.24±1.04,respectively), which were in accordance with the significantly elevated MPO activity (1.69±0.11). And the nuclear level of NF-κB and expression of TNF-α, ICAM-1 in rats of model Ⅱ group were higher than that of normal control (9.7±1.96 vs1.7±0.15, 84.09±14.52 vs16.03±6.21,77.69±8.09 vs13.41±4.91 P＜0.01), Linear correlation analysis revealed that there were strong correlations between the nuclear level of NF-κB and the tissue positive expression of TNF-α and ICAM-1, MPO activities,macroscopical and histological indices in TNBS-induced colitis, respectively (r = 0.8235, 0.8780, 0.8572, 0.9152,0.8247; P＜0.05).CONCLUSION: NF-κB plays a pivotal role in the pathogenesis of ulcerative colitis, which might account for the up-regulation the expression of TNF-α and ICAM-1.     

日本血吸虫卵抗TNBS诱导的小鼠结肠炎的观察

目的 探讨日本血吸虫卵对2,4,6 三硝基苯磺酸（TNBS）诱导的小鼠结肠炎的抑制作用。 方法 50只6～8周龄BALB/c 雌性小鼠随机分为正常对照组、乙醇对照组、虫卵对照组、结肠炎组和虫卵免疫结肠炎组，10只/组。虫卵免疫结肠炎组以日本血吸虫卵经腹腔注射免疫小鼠 4次，10 000个卵/鼠，每次间隔1周，末次免疫后6 d用TNBS诱导结肠炎模型。观察对照组和实验组小鼠的体重、结肠病理改变及细胞因子水平的变化。 结果 结肠炎组小鼠经TNBS诱导后，出现明显的粘液血便、体重下降、结肠充血水肿，肠黏膜呈现严重炎性浸润伴溃疡，IFN-γ水平为（3.47±0.87） ng/ml，IL-4水平为（146.06±45.76） pg/ml。虫卵免疫结肠炎组小鼠症状较轻，体重恢复较快，IFN-γ表达被明显抑制，其水平为（1.53±0.51） ng/ml，IL-4水平显著升高至（598.50±135.90） pg/ml。 结论 日本血吸虫卵对TNBS诱导的BALB/c小鼠结肠炎具有抑制作用。     

Expression and significance of nuclear factor κB p65 in colon tissues of rats with TNBS-induced colitis

AIM: To investigate the role of NF-κB in the pathogenesis of TNBS-induced colitis in rats. METHODS: Thirty-two healthy adult Sprague-Dawley (SD) rats were randomly divided into four groups of eight each: normal, NS, model Ⅰ, model Ⅱ groups in our study. Rat colitis model was established through 2-,4-,6-trinitrobenzene sulfonic acid (TNBS) enema. At the end of four weeks, the macroscopical and histological changes of the colon were examined and mucosa myeloperoxidase (MPO)activities assayed. NF-~B p65 expression was determined by Western blot assessment in cytoplasmic and nuclear extracts of colon tissue, and the expressions of TNF-α (and ICAM-1 protein in colon tissue were examined by immunohistochemistry. The relativities between expression of NF-κB p65 and other parameters were analyzed. RESULTS: TNBS enema resulted in pronounced pathological changes of colonic mucosa in model Ⅱ group (macroscopic and histological injury indices 6.25&#177;1.39 and 6.24&#177;1.04, respectively), which were in accordance with the significantly elevated MPO activity (1.69+0.11). And the nuclear level of NF-κB and expression of TNF-α, ICAM-1 in rats of model Ⅱ group were higher than that of normal control(9.7&#177;1.96 vs 1.7&#177;0.15, 84.09&#177;14.52 vs 16.03&#177;6.21,77.69&#177;8.09 vs 13.41&#177;4.91 P&lt;0.01), Linear correlation analysis revealed that there were strong correlations between the nuclear level of NF-κB and the tissue positive expression of TNF-α and ICAM-1, MPO activities, macroscopical and histological indices in TNBS-induced colitis, respectively (r = 0.8235, 0.8780, 0.8572, 0.9152,0.8247; P&lt;0.05). CONCLUSION: NF-κB plays a pivotal role in the pathogenesis of ulcerative colitis, which might account for the up-regulation the expression of TNF-α and ICAM-1.     

Curcumin reverses attenuated carbachol-induced contraction of the colon in a rat model of colitis

Background- Curcumin ameliorates colitis whether it reverses colitis-induced reduction in colonic contractility remains to be investigated. Objectives- To investigate the effect of curcumin on colitis-induced reduction of carbachol-induced contraction in colon segments from rats treated with trinitrobenzenesulphonic acid. Methods- Colitis was induced in rats by intra rectal administration of trinitrobenzenesulphonic acid and followed for 5 days. A group of animals which received trinitobenzene sulphonic acids was treated with curcumin (100 mg/Kg and 200 mg/kg body weight) 2 hrs prior to induction of colitis. The controls received phosphate buffered saline in a similar fashion. Markers of inflammation and contractility of colon were assayed using standard procedures. Results- Induction of colitis was associated with increased myeloperoxidase activity and malondialdehyde levels, gross histological changes characterized by infiltration of inflammatory cells. All these changes were prevented by treatment with curcumin (100mg/kg). Treatment with curcumin also reduced the histological scores from 3.34±0.40 to 1.75±0.30 confirming an anti-inflammatory effect of curcumin in this experimental model of colitis. Colonic reactivity to carbachol was decreased in colitis affecting the maximum response but not sensitivity. Treatment with curcumin had no effect on sensitivity of the colon to carbachol in any of the preparations. Curcumin however reversed the decrease in carbachol-induced contraction associated with trinitrobenzenesulphonic acid treatment. The same dose of curcumin had no effect on either the potency of or the maximum response to carbachol in control rats. Tissue expression of NF-kB was increased in colon segments from trinitrobenzenesulphonic acid -treated rats and this was inhibited in rats treated with curcumin. Conclusions- Based on these findings it is concluded that curcumin prevented the reduction in carbachol-induced contraction in trinitrobenzenesulphonic acid -treated rats by modulating NF-kB signaling pathway.     

T细胞亚群在TNBS诱发大鼠实验性结肠炎发病及治疗后的变化

目的探讨T细胞亚群在TNBS诱发大鼠实验性结肠炎模型的外周血、脾、结肠中变化特点及经柳氮磺胺吡啶（SASP）和氢化泼尼松（PSL）治疗后这些细胞的变化。方法分为对照组、建模后1周及3周组、SASP及PSL治疗组，用流式细胞仪检测各组外周血、脾和结肠黏膜上皮细胞内CD4^＋，CD8^＋T细胞比例的变化；肠道积分评定组织学变化。结果CD4^＋T细胞：建模第1周外周血、脾明显低于对照组；建模第3周脾CD4^＋T细胞升至对照组水平，SASP治疗组外周血高于模型3周组，PSL治疗组外周血、脾、结肠均明显低于对照组和模型3周组。CD8^＋T细胞：建模第1周外周血、结肠低于对照组，建模第3周外周血中仍低，结肠升至对照组水平；SASP治疗组外周血高于模型3周组。PSL治疗组外周血、脾、结肠均明显低于对照组，脾、结肠低于模型3周组。结论大鼠实验性结肠炎发病过程中，机体免疫功能下调，以局部免疫异常为主，与整体的免疫异常可能关系较小。PSL导致机体免疫功能下调。SASP对全身免疫状态影响较小，其作用更集中于肠道。     

Activation of nuclear factor-kappa B and effects of pyrrolidine dithiocarbamate on TNBS-induced rat colitis

AIM: To explore the changes of nuclear factor-kappa B (NF-κB) DNA-binding activity, the expression of intercellular adhesion molecule-1(ICAM-1) regulated by IMF-κB at various times and to evaluate the effects of pyrrolidine dithiocarbamate (PDTC) on trinitrobenzene sulfonic acid (TNBS)-induced rat colitis. METHODS: TNBS of 0.6 mL was mixed with ethanol of 0.3 mL solution and instilled into the lumen of the rat colon. The rat models were divided into 6 groups, which were killed at 24 h, 3, 7,14, and 21 d after enema. Colonic inflammation and damage were assessed by macroscopical and histological criteria. Activity of NF-κB DNA-binding was analyzed by electrophoresis mobility shift assays (EMSA). Expression of ICAM-1 was detected by in situ hybridization (ISH) and immunohistochemistry (IH). Then various doses of PDTC were injected into rat abdomen 30 min before enema with TNBS/ethanol as pretreatment. The rats were killed 4 h after enema and the colonic inflammation, myeloperoxidase (MPO) activity, malondialdehyde (MDA) level, and DNA-binding activity of NF-κB were assessed. Finally, PDTC was injected intraperitoneally after colitis was induced. Changes of morphology were assayed. RESULTS: During the first week, hyperemia, hemorrhage, edema and ulceration of the colonic mucosa appeared with predominant infiltration of leukocytes. Neutrophils, macrophages, lymphocytes infiltrated in mucosa and submucosa 14 d later. Fibroblasts and granuloma-like structures were also obviously seen. The binding activity of NF-κB began to increase at 24 h time point and reached a peak at 14 d, then decreased but still was higher than control group at 21 d (P<0.01). Levels of ICAM-1 mRNA and protein significantly elevated at 24 h and the peak was at 21 d. Pretreatment with PDTC could attenuate the development of inflammation but not by reducing NF-KB activity. This attenuation of inflammation had a positive relationship with the dose of PDTC. PDTC at the dose of 100 mg/kg had no therapeutic effect after colitis was induced. CONCLUSION: NF-κB activation is an important event that may be involved in acute and chronic inflammation development and may contribute to self-protection against early inflammation damage. NF-κB also regulates ICAM-1 expression during colonic inflammation. Pretreatment of PDTC may attenuate the inflammation development. But PDTC has no therapeutic effect after the colitis is induced.     

Anti-inflammatory mechanism of oxymatrine in dextran sulfate sodium-induced colitis of rats

AIM: To investigate the anti-inflammatory mechanism of oxymatrine in dextran sulfate sodium (DSS)-induced colitis of rats. METHODS: Acute colitis was induced by giving 2% DSS orally in drinking water for 8 d. Twenty-six male rats were randomized into oxymatrine-treated group (group A, 10 rats), DSS control (group B, 10 rats) and normal control (group C, 6 rats). The rats in group A were injected muscularly with oxymatrine at the dosage of 63 mg/(kg·d) from d 1 to 11 and drank 2% DSS solution from d 4 to 11. The rats in group B were treated with 0.9% saline in an equal volume as group A and drank 2% DSS solution from d 4 to 11. The rats in group C were treated with 0.9% saline as group B from d 1 to 11 and drank water normally. Diarrhea and bloody stool as well as colonic histology were observed. The levels of serum tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) were determined by ELISA, and nuclear factor-κB (NF-κB) activity and the expression of inter-cellular adhesion molecule-1(ICAM-1) in colonic mucosa were detected by immunohistochemistry method. RESULTS: Compared with DSS contror group, the inflammatory symptoms and histological damages of colonic mucosa in oxymatrine-treated group were significantly improved, the serum levels of TNF-α, IL-6, and the expression of NF-κB, ICAM-1 in colonic mucosa were significantly reduced. CONCLUSION: The fact that oxymatrine can reduce the serum levels of TNF-α, IL-6, and the expression of NF-κB and ICAM-1 in colonic mucosa in DSS-induced colitis of rats indicates that oxymatrine may ameliorate the colonic inflammation and thus alleviate diarrhea and bloody stool.