Effectiveness of a hydroxynaphthoquinone fraction from Arnebia euchroma in rats with experimental colitis

AIM:To evaluate the potential effectiveness of hydroxynaphthoquinone mixture(HM)in rats with 2,4,6-trinitrobenzene sulfonic acid(TNBS)-induced colitis.METHODS:Colitis was induced by intracolonic administration of TNBS(80 mg/kg,dissolved in 50%ethanol).Rats were treated daily for 7 d with HM(2.5,5,10 mg/kg)and mesalazine 100 mg/kg 24 h after TNBS instillation.Disease progression was monitored daily by observation of clinical signs and body weight change.At the end of the experiment,macroscopic and histopathologic lesions of rats were scored,and myeloperoxidase(MPO)activity was determined.We also determined inflammatory cytokine tumor necrosis factor(TNF)-αlevel by ELISA,Western blotting and immunochemistry to explore the potential mechanisms of HM.RESULTS:After intracolonic instillation of TNBS,animals developed colitis associated with soft stool,diarrhea and marked colonic destruction.Administration of HM significantly attenuated clinical and histopathologic severity of TNBS-induced colitis in a dose-dependent manner.It abrogated body weight loss,diarrhea and inflammation,decreased macroscopic damage score,and improved histological signs,with a significant reduction of inflammatory infiltration,ulcer size and the severity of goblet cell depletion(all P<0.05 vs TNBS alone group).HM could reduce MPO activity.In addition,it also decreased serum TNF-αlevel and down-regulated TNF-αexpression in colonic tissue.This reduction was statistically significant when the dose of HM was 10 mg/kg(P<0.05 vs TNBS alone group),and the effect was comparable to that of mesalazine and showed no apparent adverse effect.The underlying mechanism may be associated with TNF-αinhibition.CONCLUSION:These findings suggest that HM possesses favourable therapeutic action in TNBS-induced colitis,which provides direct pharmacological evidence for its clinical application.     

Favorable response to subcutaneous administration of infliximab in rats with experimental colitis

AIM: To investigate the influence of infliximab (Remicade) on experimental colitis produced by 2,4,6,trinitrobenzene sulfonic acid (TNBS) in rats. METHODS: Thirty-six Wistar rats were allocated into four groups (three groups of six animals each and a fourth of 12 animals). Six more healthy animals served as normal controls (Group 5). Group 1: colitis was induced by intracolonic installation of 25 mg of TNBS dissolved in 0.25 mL of 50% ethanol and infliximab was subcutaneously administered at a dose of 5 mg/kg BW; Group 2: colitis was induced and infliximab was subcutaneously administered at a dose of 10 mg/kg BW; Group 3: colitis was induced and infliximab was subcutaneously administered at a dose of 15 mg/kg BW; Group 4: colitis was induced without treatment with infliximab. Infliximab was administered on d 2-6. On the 7~(th) d, all animals were killed. The colon was fixed in 10% buffered formalin and examined by light microscopy for the presence and activity of colitis and the extent of tissue damage. Tumor necrosis factor-alpha (TNF-α) and malondialdehyde (MDA) were also measured. RESULTS: Significant differences concerning the presence of reparable lesions and the extent of bowel mucosa without active inflammation in all groups of animals treated with infliximab compared with controls were found. Significant reduction of the tissue levels of TNF-α in all groups of treated animals as compared with the untreated ones was found (0.47±0.44, 1.09±0.86, 0.43±0.31 vs 18.73±10.53 respectively). Significant reduction in the tissue levels of MDA was noticed in group 1 as compared to group 4, as well as between groups 2 and 4. CONCLUSION: Subcutaneous administration of infliximab reduces the inflammatory activity as well as tissue TNF-α and MDA levels in chemical colitis in rats. Infliximab at a dose of 5 mg/kg BW achieves better histological results and produces higher reduction of the levels of TNF-α than at a dose of 10 mg/kg BW. Infliximab at a dose of 5 mg/kg BW produces higher reduction of tissue MDA levels than at a dose of 15 mg/ kg BW.     

Curcumin improves regulatory T cells in gut-associated lymphoid tissue of colitis mice

AIM: To explore the probable pathway by which curcumin(Cur) regulates the function of Treg cells by observing the expression of costimulatory molecules of dendritic cells(DCs).METHODS: Experimental colitis was induced by administering 2, 4, 6-trinitrobenzene sulfonic acid(TNBS)/ethanol solution. Forty male C57BL/6 mice were randomly divided into four groups: normal, TNBS + Cur, TNBS + mesalazine(Mes) and TNBS groups. The mice in the TNBS + Cur and TNBS +Mes groups were treated with Cur and Mes, respectively, while those in the TNBS group were treated with physiological saline for 7 d. After treatment, the curative effect of Cur was evaluated by colonic weight, colonic length, weight index of the colon, and histological observation and score. The levels of CD4+CD25+Foxp3+ T cells(Treg cells) and costimulatory molecules of DCs were measured by flow cytometry. Also, related cytokines were analyzed by enzyme-linked immunosorbent assay. RESULTS: Cur alleviated inflammatory injury of the colonic mucosa, decreased colonic weigh and histological score, and restored colonic length. The number of Treg cells was increased, while the secretion of TNF-α, IL-2, IL-6, IL-12 p40, IL-17 and IL-21 and the expression of costimulatory molecules(CD205, CD54 [ICAM-1], TLR4, CD252[OX40 L], CD256 [RANK] and CD254 [RANK L]) of DCs were notably inhibited in colitis mice treated with Cur.CONCLUSION: Cur potentially modulates activation of DCs to enhance the suppressive functions of Treg cells and promote the recovery of damaged colonic mucosa in inflammatory bowel disease.     

Ameliorative effects of bombesin and neurotensin on trinitrobenzene sulphonic acid-induced colitis, oxidative damage and apoptosis in rats

AIM： TO investigate the effects of bombesin （BBS） and neurotensin （NTS） on apoptosis and colitis in an ulcerative colitis model.
METHODS： In this study, a total of 50 rats were divided equally into 5 groups. In the control group, no colitis induction or drug administration was performed. Colitis was induced in all other groups. Following the induction of colitis, BBS, NTS or both were applied to three groups of rats. The remaining group （colitis group） received no treatment. On the 11th d after induction of colitis and drug treatment, blood samples were collected for TNF-α and IL-6 level studies. Malondialdehyde （MDA）, carbonyl, myeloperoxidase （MPO） and caspase-3 activities, as well as histopathological findings, evaluated in colonic tissues.
RESULTS： According to the macroscopic and microscopic findings, the study groups treated with BBS, NTS and BBS ＋ NTS showed significantly lower damage and inflammation compared with the colitis group （macroscopic score, 2.1 ± 0.87, 3.7 ± 0.94 and 2.1 ± 0.87 vs 7.3 ± 0.94; microscopic score, 2.0 ± 0.66, 3.3 ± 0.82 and 1.8 ± 0.63 vs 5.2 ± 0.78, P 〈 0.01）. TNF-α and IL-6 levels were increased significantly in all groups
compared with the control group. These increases were significantly smaller in the BBS, NTS and BBS ＋ NTS groups compared with the colitis group （TNF-α levels, 169.69 ± 53.56, 245.86 ± 64.85 and 175.54 ± 42.19 vs 556.44 ± 49.82; IL-6 levels, 443.30 ± 53.99, 612.80 ± 70.39 and 396.80 ± 78.43 vs 1505.90 ± 222.23, P 〈 0.05）. The colonic MPO and MDA levels were significantly lower in control, BBS, NTS and BBS ＋ NTS groups than in the colitis group （MPO levels, 24.36 ± 8.10, 40.51 ± 8.67 and 25.83 ± 6.43 vs 161.47 ± 38.24; MDA levels, 4.70 ± 1.41, 6.55 ± 1.12 and 4.51 ± 0.54 vs 15.60 ± 1.88, P 〈 0.05）. Carbonyl content and caspase-3 levels were higher in the colitis and NTS groups than in control, BBS and BBS ＋ NTS groups （carbonyl levels, 553.99 ± 59.58 and 336.26 ± 35.72 vs 209.7     

Anti-inflammatory and anti-apoptotic effects of rosuvastatin by regulation of oxidative stress in a dextran sulfate sodium-induced colitis model

AIM To evaluate the anti-inflammatory and anti-apoptotic effects of rosuvastatin by regulation of oxidative stress in a dextran sulfate sodium(DSS)-induced colitis model.METHODS An acute colitis mouse model was induced by oral administration of 5% DSS in the drinking water for 7 d. In the treated group, rosuvastatin(0.3 mg/kg per day) was administered orally before and after DSS administration for 21 d. On day 21, mice were sacrificed and the colons were removed for macroscopic examination, histology, and Western blot analysis. In the in vitro study, IEC-6 cells were stimulated with50 ng/m L tumor necrosis factor(TNF)-α and then treated with or without rosuvastatin(2 μmol/L). The levels of reactive oxygen species(ROS), inflammatory mediators, and apoptotic markers were measured. RESULTS In DSS-induced colitis mice, rosuvastatin treatment significantly reduced the disease activity index and histological damage score compared to untreated mice(P 0.05). Rosuvastatin also attenuated the DSSinduced increase of 8-hydroxy-2'-deoxyguanosine and NADPH oxidase-1 expression in colon tissue. Multiplex ELISA analysis revealed that rosuvastatin treatment reduced the DSS-induced increase of serum IL-2, IL-4, IL-5, IL-6, IL-12 and IL-17, and G-CSF levels. The increased levels of cleaved caspase-3, caspase-7, and poly(ADP-ribose) polymerase in the DSS group were attenuated by rosuvastatin treatment. In vitro, rosuvastatin significantly reduced the production of ROS, inflammatory mediators and apoptotic markers in TNF-α-treated IEC-6 cells(P 0.05).CONCLUSION Rosuvastatin had the antioxidant, anti-inflammatory and anti-apoptotic effects in DSS-induced colitis model. Therefore, it might be a candidate anti-inflammatory drug in patients with inflammatory bowel disease.     

Effects of low molecular weight heparin on platelet surface P-selectin expression and serum interleukin-8 production in rats with trinitrobenzene sulphonic acid-induced colitis

AIM:To observe the effects of low molecular weight heparin(LMWH) on platelet surface P-selectin expression and serum interleukin-8 production in rats with trinitrobenzene sulphonic acid (TNBS) induced colitis.METHODS:Colitis was induced in female Sprauge-Dawley rats by colonic administration of 2, 4, 6-TNBS. LMWH, a dalteparin (150U/kg, 300U/kg) was subcutaneously administrated one hour before induction of colitis and went on once a day for 6 days. Then a half dose was given for the next 7 days. Control animals received the same volume of normal saline once a day for 14 days after treated by TNBS.Animals were sacrificed at 24h, days 7 and 14 after induction of colitis. The colon was excised for the evaluation of macroscopic and histological findings and TNF-α immunohistochemical assay. Platelet surface P-selectin expression was determined by radioimmunoassay and serum IL-8 production was assayed by ELISA method.RESULTS:LMWH treatment in a dose of 300U/kg for 14 days significantly improved colonic inflammation by histological examination. Serum IL-8 production in the 300U/kg treatment group was more significantly decreased at day 14 than that at 24h (P&lt;0.05). However, platelet surface P-selectin expression and TNF-α staining in colonic tissue were not significantly different among the three groups.CONCLUSION:LMWH has an anti-infiammatory effect on TNBS induced colitis in rats. The effect is possibly related to inhibition of proinflammatory cytokine IL-8, but not involved platelet surface P-selectin expression.     

Therapeutic and prophylactic thalidomide in TNBS-induced colitis: Synergistic effects on TNF-α, IL-12 and VEGF production

AIM: To evaluated the therapeutic and prophylactic effect of thalidomide on 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Thalidomide has been reported to downregulate the expression of tumor necrosis factor α (TNF-α), IL-12, and vascular endothelial growth factor (VEGF), hallmarks of intestinal inflammation in Crohn's disease (CD).METHODS: Male Wistar rats were divided in five groups of ten animals each. Four groups received a rectal infusion of TNBS in ethanol. The first group was sacrificed 7 d after colitis induction. The second and third groups received either thalidomide or placebo by gavage and were sacrificed at 14 d. The fourth group received thalidomide 6 h before TNBS administration, and was sacrificed 7 d after induction. The fifth group acted as the control group and colitis was not induced. Histological inflammatory scores of the colon were performed and lamina propria CD4+ T cells, macrophages, and VEGF+ cells were detected by immunohistochemistry. TNF-α and IL-12 were quantified in the supernatant of organ cultures by ELISA.RESULTS: Significant reduction in the inflammatory score and in the percentage of VEGF+ cells was observed in the group treated with thalidomide compared with animals not treated with thalidomide. Both TNF-α and IL-12 levels were significantly reduced among TNBS induced colitis animals treated with thalidomide compared with animals that did not receive thalidomide.TNF-α levels were also significantly reduced among the animals receiving thalidomide prophylaxis compared with untreated animals with TNBS-induced colitis. Intestinal levels of TNF-α and IL-12 were significantly correlated with the inflammatory score and the number of VEGF+ cells.CONCLUSION: Thalidomide significantly attenuates TNBS-induced colitis by inhibiting the intestinal production of TNF-α, IL-12, and VEGF. This effect may support the use of thalidomide as an alternate approach in selected patients with CD.     

Thalidomide and tuberculosis.

The anti-inflammatory and immunomodulatory effects of thalidomide have led scientists to explore its clinical therapeutic values. Thalidomide is now being considered as an adjuvant treatment for tuberculosis. This literature review examines the drug's mechanism of action and clinical applications. Thalidomide affects cytokine production and T lymphocyte proliferation. It appears that thalidomide suppresses TNF-alpha production by macrophages and thereby reduces inflammatory response. Thalidomide elevates the IFN-gamma level and modulates several other cytokines as well, noteworthily IL-2 and IL-12. Thalidomide costimulates T lymphocytes, with greater effect on CD8+ than on CD4+ T cells. This finding is important, since CD8+ T cells have been shown to be contributory to the protective immune response to Mycobacterium tuberculosis infection. The clinical application of thalidomide as part of standard tuberculosis therapy is inconclusive amid variability among reports. However, thalidomide has been shown to be an effective adjuvant for tuberculosis patients complicated with severe inflammatory reaction or wasting conditions.     

英夫利昔、沙利度胺对大鼠实验性结肠炎的治疗作用及其机制研究

炎症性肠病（IBD）是一种病因尚未明确的非特异性肠道炎症性疾病,传统治疗方法疗程长．疗效欠佳,容易反复发作。目的：观察并比较英夫利昔、沙利度胺对TNBS灌肠诱发的大鼠结肠炎治疗效果．并初步探讨两者治疗IBD的作用机制。方法：46只Sprague-Dawley大鼠随机分成正常对照组（n=10）、结肠炎组（n=12）、英夫利昔组（n=12）、沙利度胺组（n=12）,后三组给予TNBS／乙醇灌肠诱导大鼠结肠炎模型。造模后第1d,英夫利昔组、沙利度胺组分别给予英夫利昔腹腔注射5mg·kg-1．d～、沙利度胺管喂200mg．kg-．d～,连续7d后处死。行疾病活动指数（DAI）、大体形态损伤指数（CMDI）和组织损伤指数（TDI）评分;以Real．timePCR、蛋白质印迹法和免疫组化分别检测结肠组织TNF-d、VEGF、caspase-3mRNA和蛋白表达;TUNEL法检测结肠上皮细胞凋亡情况。结果：结肠炎组大鼠DAI、CMDI、TDI评分均显著高于正常对照组（P〈O．05）,TNF-a、VEGF、caspase-3mRNA和蛋白表达显著升高（P〈O．05）．结肠上皮细胞凋亡显著增加;给予英夫利昔或沙利度胺治疗后,上述指标均显著改善（P〈0．05）。结论：本实验成功构建了TNBS大鼠结肠炎模型,英夫利昔、沙利度胺对大鼠结肠炎均有明显的治疗效果,两者通过抑制TNF-a VEGF、caspase-3的表达,对IBD免疫、血管生成、凋亡过程起调节作用。     

白细胞介素-23/-17轴在小鼠急性实验性结肠炎中的表达及作用

目的 研究白细胞介素(IL)-23/IL-17轴在小鼠实验性结肠炎结肠组织中的表达和作用.方法 将64只小鼠分为对照组24只、模型组24只、抗体组8只、正常血清组8只.除对照组外,其余各组建立小鼠急性实验性结肠炎模型.对照组和模型组小鼠分别于造模后24 h、48 h、7 d处死.抗体组和正常血清组小鼠分别于造模前2 h腹腔内注射多克隆大鼠抗小鼠IL-17中和抗体和正常大鼠血清,于造模48 h后处死.检测各组小鼠组织学损伤评分、肠组织髓过氧化物酶(MPO)活性;酶联免疫吸附试验检测结肠组织IL-23p19、IL-17含量;免疫组化染色检测核因子(NF)-κB p65在结肠组织中的表达;实时荧光定量(RT)PCR检测IL-23p19、IL-17、IL-12p35的mRNA表达水平.结果 模型组24 h、48 h、7 d时IL-23p19蛋白表达水平和mRNA表达水平[分别为(15.53±3.32)、(31.16±4.98)、(14.03±3.56)ng/mg蛋白和4.09±0.34、3.39±0.46、6.54±1.82]、IL-17的蛋白表达水平和mRNA表达水平[分别为(0.35±0.06)、(0.38±0.08)、(0.26±0.05)ng/mg蛋白和4.21±2.61、2.65±0.91、5.63±1.43]均显著高于正常对照组(P值均＜0.05),48 h时达高峰.IL-23与IL-17蛋白表达水平和mRNA表达水平呈正相关(r值分别为0.745和0.793,P＜0.05).抗体组IL-23p19和IL-12p35高水平表达,但NF-κB p65阳性细胞率、组织学评分及MPO活性[分别为1.86%±0.36%、0.63±0.52、(0.40±0.03)U/g]明显低于48 h模型组[分别为4.35%±0.37%、5.13±0.64、(2.29±0.40)U/g],说明中和IL-17后能明显减轻结肠炎症,抑制NF-κB活性.结论 IL-23/IL-17轴在急性实验性结肠炎早期阶段起关键作用.IL-17有望成为炎症性肠病治疗的新靶标.     

Thalidomide reduces tumour necrosis factor alpha and interleukin 12 production in patients with chronic active Crohn's disease.

BACKGROUND: Thalidomide improves clinical symptoms in patients with therapy refractory Crohn's disease, as shown in two recent studies. The mechanism of this effect however is still unknown. Suppression of tumour necrosis factor alpha (TNF-alpha) by thalidomide has been suggested as a possible mechanism. However, effects on other cytokines have not been adequately investigated. AIM: The aim of our study was to investigate the effects of thalidomide on cytokine production in patients with inflammatory bowel disease (IBD). METHODS: Ten patients with therapy refractory IBD (nine Crohn's disease, one ulcerative colitis) received thalidomide 300 mg daily in a 12 week open label study. Production of TNF-alpha, interleukin (IL)-1 beta, IL-6, and IL-12 was investigated in short term cultures of stimulated colonic lamina propria mononuclear cells (LPMC) and peripheral blood monocytes (PBMC) before and after 12 weeks of treatment. LPMC were also cultured with graded doses of thalidomide. RESULTS: Three patients discontinued treatment because of sedative side effects. In the other patients, disease activity decreased significantly, with four patients achieving remission. Production of TNF-alpha and IL-12 decreased during treatment with thalidomide: LPMC (TNF-alpha: 42.3 (8.3) pg/ml v 16.4 (6.3); IL-12: 9.7 (3.3) v 5.0 (2.5); p<0.04) and PBMC (TNF-alpha: 62.8 (14.6) v 22.5 (9.2); p<0.02). Production of IL-1 beta and IL-6 did not change significantly. Culturing of LPMC with thalidomide showed a dose dependent decrease in TNF-alpha and IL-12 production. CONCLUSION: The clinical effects of thalidomide in Crohn's disease may be mediated by reduction of both TNF-alpha and IL-12.     

Faecalibacteriumprausnitzii对实验性结肠炎大鼠Foxp3＋Treg细胞的影响

Fxop3＋Treg细胞是-种免疫调节细胞,在免疫调节和维持机体免疫平衡中起重要作用。目的：研究Faecalibacterium口删nitzii（FP）对实验性结肠炎大鼠外周血和脾脏中CD4＋CD25＋Foxp3＋Treg细胞的影响,从而初步探讨FP治疗溃疡性结肠炎（UC）的作用机制。方法：采用2,4,6-三硝基苯磺酸（TNBS）灌肠制备实验性结肠炎大鼠模型．将大鼠随机分为正常对照组、结肠炎组、FP组、FP上清液组、培养基组和双歧杆菌组。观察大鼠结肠大体形态损伤、组织学变化．以流式细胞术测定外周血和脾脏中CD4＋CD25＋Foxp3＋rreg细胞比例,以ELISA法检测血浆IL-10、IL-12和TGF．B含量。结果：与正常对照组相比,结肠炎组结肠大体形态损伤明显,病理学评分显著增高（P〈O．01）;外周血和脾脏中CD4＋CD25＋Foxp3＋Treg细胞比例显著降低（P〈O．05）;血浆IL．10和TGF．B含量显著降低（P〈0．05）,IL-12含量显著升高（P〈O．01）,IL-IO／IL-12比值显著降低（P〈0．01）。经FP、FP上清液和双歧杆菌治疗后,除血浆IL-10含量无明显差异外．其余指标均显著改善（P〈0．05）。结论：FP及其上清液对TNBS诱导的实验性结肠炎大鼠有显著的治疗作用．其机制可能为提高外周血和脾脏中CD4＋CD25＋Foxp3＋Treg细胞比例。     

Regulatory role of the pituitary-adrenal axis in experimental colitis: effect of adrenalectomy on the clinical course and the TH1/TH2 immune profile

BACKGROUND: The hypothalamic-pituitary-adrenal (HPA) axis plays an important role in modulating immune reactions in inflammatory bowel disease. Our aim was to assess the role of the HPA axis in the pathogenesis of immunomediated colitis in mice. METHODS: Trinitrobenzene sulfonic acid (TNBS) colitis was induced in Balb/c mice. Sham operation (sham+TNBS) or bilateral adrenalectomy (Adex+TNBS) was performed 3 days later. Control groups underwent adrenalectomy without colitis induction (Adex) or were untreated [na?ve mice (Na?ve)]. Mice were monitored for survival, weight loss, and macroscopic and microscopic scores of colitis. FACS analysis of CD4, CD8, natural killer T lymphocytes, and serum levels of adrenocorticotropic hormone (ACTH), corticosterone (CS), interferon-gamma (IFN-gamma), interleukin-10 (IL-10), and IL-1beta were measured. Production of prostaglandin E2 (PGE2) and binding capacity to glucocorticoid receptor (GR) in colonic mucosa were also assessed. RESULTS: By day 7 following induction of colitis there was a marked increase in ACTH and CS levels in the colitis as compared with the control group (86 +/- 6.5 pg/mL and 16 +/- 1.9 pg/mL, and 23.3 +/- 2 pg/mL and 2.8 +/- 0.8 pg/mL, respectively). There was a decrease in ACTH and CS levels by day 28 in the colitis group, but the levels were still significantly higher than the levels in controls. Adrenalectomy markedly exacerbated colitis. The macroscopic and microscopic scores increased from 2.79 +/- 0.03 and 2.0 +/- 0.1 in the sham+TNBS group to 3.3 +/- 0.3 and 3.2 +/- 0.3 in the Adex+TNBS group. Survival and weight loss correlated with these differences. A significant increase in IL-10, IFN-gamma, and PGE2 was noted in the Adex+TNBS group compared with the sham+TNBS group. Splenic CD4 lymphocytes decreased in the sham+TNBS and Adex+TNBS groups as compared with control groups (Adex and na?ve). The CD8/CD4 ratio was significantly higher in the Adex+TNBS compared with the sham+TNBS group. Colitis also caused a significant decrease in the specific binding capacity of labeled dexamethasone to colonic mucosa. CONCLUSIONS: TNBS induced colitis activated the HPA axis and reduced the sensitivity of the inflamed mucosa to circulating glucocorticoids. Adrenalectomy markedly exacerbated TNBS-induced colitis. The effect was associated with changes in the peripheral CD8/CD4 ratio and with a TH1 cytokine shift. Our results suggest that adrenocortical hormones play an important role in the regulation of the immune system in experimental colitis.     

大蒜素对三硝基苯磺酸诱导大鼠结肠炎的保护作用及其机制研究

背景：溃疡性结肠炎（UC）是一种病因未明的结直肠炎症,大蒜素对其防治的作用目前尚未有结论。目的：探讨大蒜素对TNBS诱导的大鼠结肠炎的保护作用及其机制。方法：80只大鼠随机分为对照组、TNBS组、大蒜素预防组、大蒜素灌胃组、大蒜素灌肠组、地塞米松组、柳氮磺吡啶组、巴柳氮钠组。以含150mg／kgTNBS的50％乙醇溶液灌肠制备大鼠结肠炎模型。造模2周后处死大鼠。行大体评分和病理学评分,以ELISA法测定血清TNF-α、IL-1β、IL-10、IL4含量,蛋白质印迹法检测NF—κB表达。结果：与对照组相比,TNBS组大体和病理学评分均明显升高（P〈0．05）,体质量明显降低（P〈0．05）,血清TNF-α、IL-1B含量显著升高（P〈0．05）,血清IL-4、IL-10含量显著降低（P〈0．05）,NF-κB表达明显升高（P〈0．05）;给予大蒜素预防或治疗后,上述指标均明显改善（P〈0．05）,但疗效低于地塞米松组、柳氮磺吡啶组、巴柳氮钠组。结论：大蒜素对TNBS诱导的大鼠结肠炎有保护作用,可能是通过调控细胞因子和NF—κB而发挥作用的。