氧化苦参碱对大鼠溃疡性结肠黏膜细胞NF-κB mRNA表达的影响

目的探讨氧化苦参碱对溃疡性结肠黏膜细胞中核因子-κB(NF-κB)mRNA表达的影响及机理。方法SPF级SD大鼠随机分成正常对照组、溃疡性结肠炎(UC)模型组、UC+氧化苦参碱组、UC+柳氮磺胺吡啶组,实验结束时,剖取病灶结肠,实时荧光定量PCR(RT-PCR)方法检测各实验组动物结肠黏膜细胞中NF-κB mRNA表达水平。结果氧化苦参碱可显著抑制NF-κB mRNA在溃疡性结肠炎症细胞中的表达(P<0.01)。结论氧化苦参碱可干预NF-κB mRNA在炎症性结肠黏膜细胞中的表达,进而抑制溃疡性结肠炎症反应。     

基于细胞信号通路探讨小檗碱治疗溃疡性结肠炎研究进展

小檗碱是黄连属植物的主要提取物,经现代研究已确证其有抗炎、抗氧化、抗菌及免疫调节等药理作用。溃疡性结肠炎(UC)是一种病因不明的慢性,特发性炎性肠病,其发病原因涉及遗传,肠道微生态和黏膜免疫系统失调等因素。该文通过查阅,梳理近年来小檗碱对溃疡性结肠炎的相关通路及其作用机制,为开展小檗碱治疗UC的药物开发及机制探讨提供方法与思路。结果显示,小檗碱通过调节JAK-STAT,NF-κB,PI3K-AKT,MAPK,Nrf2,ERS和MLCK-MLC等多条信号通路,发挥保护肠黏膜屏障、恢复机体正常免疫应答、抗氧化应激等作用,进而达到治疗UC的目的。     

风药对肝郁脾虚型UC大鼠结肠黏膜病理损伤的影响

目的:本研究主要观察中药风药对肝郁脾虚型UC大鼠肠黏膜病理损伤的影响。方法:50只Wistar大鼠随机分为空白对照组、模型组、痛泻要方加风药组、痛泻要方组、痛泻要方祛防风组,每组10只,用结肠黏膜组织致敏法加乙酸局部刺激法建立大鼠复合溃疡性结肠炎模型后,用药组分别给予痛泻要方加风药、痛泻要方、痛泻要方祛防风药灌胃,模型对照组和正常对照组给予生理盐水,均灌胃4周后处死大鼠,分离其结肠组织,计算肠重指数,评价黏膜充血、组织损伤。结果:痛泻要方加风药、痛泻要方组在改善大鼠肠重指数、结肠黏膜充血、组织损伤方面明显优于痛泻要方祛防风组。结论:风药通过减轻UC模型大鼠结肠组织炎性反应,减缓黏膜充血水肿来促进实验性UC大鼠溃疡愈合的作用。     

清肠化湿方对TNBS诱导大鼠UC模型紧密连接蛋白的影响

目的:观察三硝基苯磺酸(TNBS)法诱导大鼠溃疡性结肠炎模型结肠黏膜occludin、claudin-1蛋白的变化特点及清肠化湿方对occludin、claudin-1蛋白表达的影响。方法:采用TNBS诱导大鼠溃疡性结肠炎模型,并随机分为正常对照组、模型对照组、清肠化湿方组、SASP组,治疗10天后处死大鼠取新鲜结肠标本,观察黏膜大体形态及组织学改变,并采用Western blot法检测occludin、claudin-1蛋白表达水平。结果:模型对照组occludin、claudin-1蛋白表达均明显低于正常对照组,清肠化湿方组occludin、claudin-1的表达高于模型对照组,同时,清肠化湿方组大鼠结肠形态及组织学损伤评分均有降低。结论:清肠化湿方对UC模型大鼠具有治疗作用,增强occludin、claudin-1的表达,恢复正常的肠粘膜屏障功能可能是其作用机制之一。     

Pharmacological effects of ba-wei-xi-lei powder on ulcerative colitis in rats with enema application

Ba-wei-xi-lei powder is a classical herbal mixture, and is widely used for the treatment of oral ulcer and ulcerative colitis. This study aimed to explore the effect of Ba-wei-xi-lei powder with enema application on ulcerative colitis in rats. Ulcerative colitis was induced by immunization with rabbit's colonic mucosal protein emulsified with Completely Freund's Adjuvant. The mucosal inflammatory reaction and ulcer have been observed in the model rats. Characteristic changes of ulceractive colitis include that CD4 lymphocyte increased in peripheral blood while CD8 lymphocyte decreased; CD8 lymphocyte and TNF-alpha expression area increased in colonic mucosa, while CD4 lymphocyte decreased. Ba-wei-xi-lei powder and sulfasalazine with enema application could alleviate the pathological changes in the model rats. The results suggest that the pharmacological effects of Ba-wei-xi-lei powder on ulcerative colitis in rats are similar to the effect of sulfasalazine.     

复方蜚蠊提取物缓解噁唑酮诱导大鼠活动期溃疡性结肠炎的作用机制

目的 研究复方蜚蠊提取物Ento-PB对噁唑酮诱导的活动期溃疡性结肠炎(UC)大鼠的治疗作用,并初步探讨其可能作用机制.方法 采用噁唑酮诱导的溃疡性结肠炎大鼠模型,灌胃给予柳氮磺胺吡啶(SASP,0.3g/kg)和复方Ento-PB (0.05、0.1、0.2 g/kg),通过测定大鼠DAI (疾病活动指数)、CMDI...     

电针上巨虚、天枢穴对溃疡性结肠炎大鼠延髓Fos和GFAP表达的影响

目的:观察电针上巨虚穴和天枢穴对溃疡性结肠炎(UC)大鼠结肠黏膜损伤与延髓内Fos和GFAP免疫反应表达的影响。方法:40只雄性SD大鼠随机分为空白对照组、溃疡性结肠炎组(UC组)、UC+电针上巨虚穴组(上巨虚穴组)、UC+电针天枢穴组(天枢穴组)、UC+电针三阴交穴组(三阴交穴组),每组8只。采用三硝基苯磺酸乙醇液灌肠法诱导建立UC大鼠模型。实验结束后观察记录结肠黏膜大体形态损伤程度,取延髓组织切片进行抗Fos/抗GFAP双标记(标记神经元和星型胶质细胞)免疫组织化学染色。结果:针刺干预后,UC大鼠结肠黏膜损伤明显减轻,以上巨虚穴和天枢穴组减轻更明显,而三阴交穴组变化不明显;免疫组化观察发现各组Fos阳性神经元和GFAP阳性星型胶质细胞主要表达在延髓孤束核(NTS)内,以UC组表达最高,而上巨虚穴和天枢穴组表达最低,组间比较,差异有统计学意义(P<0.05)。结论:电针上巨虚穴和天枢穴对溃疡性结肠炎大鼠有治疗作用,延髓NTS内免疫阳性神经元和星形胶质细胞参与了此作用。     

调肠消炎片调控溃疡性结肠炎大鼠模式识别受体TLR-4信号通路的研究

目的:观察调肠消炎片对溃疡性结肠炎(UC)大鼠结肠的炎症反应及血清toll样受体4(TLR-4)浓度的影响。方法:用复合法(2,4,6-三硝基苯磺酸加乙醇)造模制备UC大鼠模型,将60只SD大鼠随机分为正常组、模型组、调肠消炎片组及柳氮磺胺吡啶(SASP)组,除正常组外,其余各组从造模后第3天开始分别每天灌胃给药1次,灌胃14天后取材观察大鼠结肠炎症反应情况及血清TLR-4浓度。结果:模型组CMDI及血清TLR-4浓度均高于正常组(P<0.01)。调肠消炎片组的CMDI及血清TLR-4浓度均低于模型组(P<0.05,P<0.01)。结论:调肠消炎片明显降低UC大鼠血清TLR-4浓度,提示其可能通过调控TLR-4信号通路,有效治疗溃疡性结肠炎模型大鼠。     

清胃理肠胶囊对实验性大鼠溃疡性结肠炎作用机制的研究

目的观察清胃理肠胶囊对溃疡性结肠炎大鼠结肠病理变化和T淋巴细胞亚群的影响。方法用二硝基氯苯-乙酸复合法制作溃疡性结肠炎大鼠模型,灌胃给药20d后,肉眼及光镜下观察结肠病理变化,流式细胞仪检测外周血CD4＋、CD8＋百分率,并计算CD4＋/CD8＋。结果造模后大鼠结肠肉眼可见溃疡、糜烂,大面积覆盖脓苔;镜下肠黏膜大面积受损,形成融合性溃疡,肠壁炎细胞浸润,组织水肿;CD4＋、CD8＋百分率降低,CD4＋/CD8＋升高。清胃理肠胶囊治疗后,结肠病理变化基本消失,与模型组比较CD4＋、CD8＋升高,CD4＋/CD8＋降低。结论清胃理肠胶囊能够改善溃疡性结肠炎大鼠结肠的病理变化,并调节其免疫功能。     

蒲公英水提物对大鼠溃疡性结肠炎的实验研究

目的:研究蒲公英水提物对大鼠溃疡性结肠炎疗效及机制.方法:将60只大鼠随机分成正常对照组(等容蒸馏水),模型组(等容蒸馏水),柳氮磺胺嘧啶(SASP,400 mg·kg-1)组,蒲公英水提物高、中、低剂量组(150,100,50 mg· kg-1).2,4,6-三硝基苯磺酸(TNBS)/乙醇溶液100 mg·kg-1灌肠制备溃疡性结肠炎大鼠模型,造模10d后,ig给药,2 mL/次,1次/d,连续14 d,实验第14天断头取血和结肠标本,观察黏膜大体形态及组织学改变,酶标记免疫吸附测定法(ELISA)法测定血清白细胞介素-6(IL-6),白细胞介素-10 (IL-10),肿瘤坏死因子-α(TNF-α)水平,SP免疫组织化学染色法检测结肠组织转录因子核因子-κB (NF-κB) p65表达.结果:蒲公英水提物高、中、低剂量组与模型组比较,大鼠组织大体形态评分显著下降,分别为(5.11±0.43),(6.11±0.31),(7.01±0.38),(7.89±0.31)分(P＜0.05).病理组织学评分显著下降,分别为(8.11±1.23),(9.37±1.12),(10.12±1.32),(12.17±1.56)分(P＜0.05).血清IL-6显著降低,分别为(68.53±18.21),(71.41±13.38),(80.24±15.29),(89.91±19.13) ng·L-1(P＜0.05).IL-10水平显著升高,分别为(35.61±4.19),(29.39±4.91),(21.83±5.63),(19.51±4.98) ng· L-1 (P ＜0.05).TNF-α显著下降,分别为(36.27±8.35),(46.29 ±9.32),(64.18±8.98),(71.27±8.81) ng· L-1 (P＜ 0.05,P＜0.01).NF-κB p65表达降低,分别为(0.301±0.038),(0.351±0.053),(0.389±0.041),(0.411±0.086)％,(P＜0.05,P＜0.01).高剂量组在各项检测指标与SASP组之间差异无显著性.结论:蒲公英水提物治疗溃疡性结肠炎具有一定的疗效.     

马齿苋对大鼠溃疡性结肠炎的治疗作用

目的:考察马齿苋对溃疡性结肠炎的治疗作用.方法:雄性SD大鼠72只随机分为6组.用2,4,6-三硝基苯磺酸灌肠制备大鼠溃疡性结肠炎模型.马齿苋高(10 g·kg-1)、中(5 g·kg-1)、低(2.5 g· kg-1)剂量组和柳氮磺吡啶组(0.5g·kg-1)从造模后第3天开始灌肠给药,每天1次,连续10 d.观察大鼠结肠组织形态学改变并进行评分,测定结肠组织内髓过氧化物酶(MPO)含量.结果:马齿苋中、高剂量组能够改善溃疡性结肠炎模型大鼠的大便性状,显著改善大鼠结肠组织的病理损害,降低大体形态损伤评分,降低髓过氧化物酶(MPO)含量.结论:马齿苋对溃疡性结肠炎急性期有良好疗效,能够改善溃疡性结肠炎模型大鼠的肠粘膜损伤,减少MPO含量,减轻肠道炎症.     

Boswellia serrata has Beneficial Anti‐Inflammatory and Antioxidant Properties in a Model of Experimental Colitis

Ulcerative colitis is an inflammatory disease that involves only the colon and rectum, being characterized by leukocyte infiltrate and superficial ulcers in the intestinal mucosa. To evaluate the anti‐inflammatory and antioxidant effects of extract from the Boswellia serrata plant in an experimental rat model of acute ulcerative colitis induced by the administration of acetic acid (AA). An extract of B. serrata (34.2 mg/kg/day) was administered by oral gavage for 2 days before and after the induction of colitis with 4 mL of 4% AA. The anal sphincter pressure in the colitis group showed a significant decrease compared to that of the control groups (p < 0.001). The analysis of the values of lipid peroxidation (LPO) obtained by substances that react with thiobarbituric acid (TBARS) showed a significantly increased LPO in the colitis group compared to the control groups (p < 0.001). The nitric oxide levels and the expression of inducible nitric oxide synthase (iNOS) showed a significant increase in the colitis group compared to control groups (p < 0.01). Both pretreatment and treatment with B. serrata exhibited significantly reduced lipid peroxidation, nitric oxide and iNOS and showed improvements in tissue injury and anal sphincter pressure in animals with ulcerative colitis. The B. serrata extract has protective anti‐inflammatory and antioxidant effects that inhibit inflammatory mediators in acute experimental colitis. Copyright © 2014 John Wiley & Sons, Ltd.     

氧化苦参碱干预IκB-α蛋白对溃疡性结肠炎的治疗作用机制研究

目的:研究氧化苦参碱抗溃疡性结肠炎作用机制.方法:SPF级大鼠随机分成正常组、UC模型组、氧化苦参碱+ UC模型组(ig给予氧化苦参碱180 mg·kg-1)、柳氮磺胺吡啶+UC模型组(ig给予柳氮磺胺吡啶600 mg·kg-1).采用2,4,6-三硝基苯磺酸(TNBS)致大鼠溃疡性结肠炎症,莲续给药21 d.实验结束后,剖取结肠病灶组织,采用免疫组织化学方法检测各组动物结肠组织细胞中核转录因子κB(NF-κB)的抑制蛋白(IκB-α)蛋白阳性细胞表达率,同时测定每组动物结肠组织中肿瘤坏死因子-α(TNF-α),白介素(interleukin,IL) 1β( IL-1β),IL-6,IL-8细胞因子表达.并对每只动物结肠病理切片做显微镜检查.结果:氧化苦参碱组动物结肠黏膜细胞中IκB-o阳性细胞表达率21.8％±5.0％,显著低于模型组(25.6％±2.9％)(P＜0.01);结肠细胞中TNF-α( 66.23±2.64)pg· mg-1,IL-1β( 149.42±64.69) pg·mg-1,IL-6(668.83±98.11)pg·mg-1和IL-8(91.83±23.14) pg·mg-14种细胞因子的表达率较模型组相比也显著降低(P＜0.01);结肠组织显微镜检查,治疗组动物结肠细胞炎症、淋巴细胞浸润、黏膜损伤修复率明显高于模型组.结论:氧化苦参碱通过干预IκB-ακ蛋白表达,进而抑制溃疡性结肠炎症细胞中核转录因子κB(NF-κB)活性,产生抗炎效果.     

香连胶囊对大鼠急性肠炎的作用

目的:观察香连胶囊对大鼠溃疡性结肠炎的疗效及其抗炎、镇痛、止泻作用.方法:大鼠随机分为正常对照组、模型组、泻痢消片组,香连低、中、高剂量组(0.122,0.243,0.486 g·kg-1),用乙酸法建立大鼠乙酸性结肠炎模型.连续给药10d后麻醉处死动物,观察大鼠结肠形态的变化并进行结肠黏膜损伤指数(CMDI)评分,测定大鼠结肠质量,HE染色病理观察.采用二甲苯致小鼠耳廓肿胀模型、番泻叶致小鼠腹泻模型,小肠推进实验及小鼠醋酸扭体实验观察其药效.结果:与模型组比较,香连胶囊中剂量组能够明显减轻醋酸对大鼠肠黏膜的损伤,减轻炎症坏死,水肿及炎细胞浸润;香连胶囊中剂量组抑制二甲苯所致小鼠耳肿胀(P＜0.01)、减少番泻叶致小鼠腹泻次数(P＜0.05)、缩短小肠推进距离(P＜0.05),减少醋酸引起的小鼠扭体次数(P＜0.01).结论:香连胶囊有明显的抑制溃疡,抗炎,镇痛作用及抑制肠蠕动的作用,是治疗肠炎的有效药物.     

Protective Effect of Hydroalcoholic Olive Leaf Extract on Experimental Model of Colitis in Rat: Involvement of Nitrergic and Opioidergic Systems

The aim of the present study is to investigate the possible protective effect of dry olive leaf extract (OLE) against acetic acid‐induced ulcerative colitis in rats, as well as the probable modulatory effect of nitrergic and opioidergic systems on this protective impact. Olive leaf extract was administered (250, 500 and 750 mg/kg) orally for two successive days, starting from the colitis induction. To assess the involvement of nitrergic and opioidergic systems in the possible protective effect of OLE, L‐NG‐Nitroarginine Methyl Ester (10 mg/kg) and naltrexone (5 mg/kg) intraperitoneal (i.p.) were applied 30 min before administration of the extract for two successive days, respectively. Colonic status was investigated 48 h following induction through macroscopic, histological and biochemical analyses. Olive leaf extract dose‐dependently attenuated acetic acid‐provoked chronic intestinal inflammation. The extract significantly reduces the severity of the ulcerative lesions and ameliorated macroscopic and microscopic scores. These observations were accompanied by a significant reduction in the elevated amounts of TNF‐α and interlukin‐2 markers. Moreover, both systems blockage reversed protective effects of OLE in the rat inflammatory bowel disease model. These finding demonstrated, for the first time, a possible role for nitrergic and opioidergic systems in the aforementioned protective effect, and the extract probably exerted its impact increasing nitric oxide and opioid tones. Copyright © 2014 John Wiley & Sons, Ltd.     

参苓白术散对溃疡性结肠炎大鼠超氧化物歧化酶及丙二醛的影响

目的 探讨参苓白术散对脾虚湿困型溃疡性结肠炎(UC)大鼠作用机制. 方法 将60只Wistar大鼠随机分为参苓白术散组(12g/kg)、柳氮磺吡啶组(0.5g/kg)、正常对照组和模型对照组(生理盐水10ml/kg),每组15只.除正常对照组外,其余各组采用2、4、6一三硝基苯磺酸(TNBS)/乙醇法结合高脂饮食、潮湿环境建立脾虚湿困型UC大鼠模型,造模成功后各组大鼠每天灌胃1次,14天后各组大鼠进行结肠组织损伤程度评分,检测结肠组织超氧化物歧化酶(SOD)活性及丙二醛( MDA)水平.结果 模型对照组大鼠结肠组织损伤程度评分与正常对照组比较差异有统计学意义(P＜0.01),参苓白术散组、柳氮磺吡啶组大鼠结肠组织损伤程度评分与模型对照组比较差异均有统计学意义(P＜0.05或P＜0.01),参苓白术散组大鼠结肠组织损伤程度评分低于柳氮磺吡啶组(P＜0.05).与正常对照组比较,模型对照组结肠组织SOD活性显著下降,MDA水平显著升高(P＜0.01);与模型对照组比较,参苓白术散组及柳氮磺吡啶组SOD活性显著升高、MDA水平明显降低(P＜0.01),参苓白术散组在降低MDA水平方面显著优于柳氮磺吡啶组(P＜0.05). 结论 参苓白术散能减少脾虚湿困型UC模型大鼠结肠黏膜充血、水肿及溃疡形成,提高大鼠结肠组织SOD活性,降低MDA水平,可能是其发挥临床疗效的作用机制之一.     

健脾益肠散对溃疡性结肠炎大鼠结肠组织HSP70表达的影响

目的:探讨健脾益肠散对溃疡性结肠炎(UC)大鼠结肠组织热休克蛋白70(HSP70)蛋白和mRNA表达的影响。方法:将健康SPF级雄性SD大鼠60只,随机分为2组,正常组和造模组;造模组采用二硝基苯磺酸(TNBS)/乙醇法复制UC大鼠模型;待复制模型成功后将造模组随机分为5组,分别为模型组、柳氮磺吡啶组(0.3 g·kg~(-1))以及健脾益肠散高、中、低剂量组(204,136,68 g·kg~(-1)),每组10只;灌胃相应药物21 d后,观察各组大鼠的一般状态和结肠黏膜组织损伤情况,免疫组化、蛋白免疫印迹法(Western blot)和实时荧光定量PCR(Real-time PCR)分别检测大鼠结肠组织中HSP70的蛋白和mRNA表达。结果:与正常组比较,模型组大鼠结肠黏膜损伤评分显著升高(P0.01),HSP70蛋白和mRNA表达均显著降低(P0.01)。与模型组比较,各给药组结肠黏膜损伤评分均显著降低(P0.01),各给药组均可增加结肠组织HSP70的蛋白和mRNA表达(P0.05,P0.01),其中以健脾益肠散高剂量组最为明显(P0.05,P0.01)。结论:健脾益肠散可能通过促进HSP70的表达而达到对UC大鼠结肠黏膜的免疫保护,从而发挥治疗作用。     

Effect of Jiaweiwumei decoction on regulatory T cells and interleukin-10 in a rat model of ulcerative colitis

OBJECTIVE:To investigate the effect of a decoction made from the Traditional Chinese Medicine Wumei pill,on regulatory T cells and interleukin-10(IL-10) in a rat model of ulcerative colitis induced by2,4,6-trinitrobenzene sulfonic acid(TNBS).METHODS:Rat ulcerative colitis was induced with TNBS.All modeled rats were randomly divided into six groups:normal control group;model group;sulfasalazine suppositories treatment group;and high,moderate,and low dosage of Jiaweiwumei decoction groups(12 rats each).Colon injury index was evaluated after 14 days.After peripheral blood lymphocyte separation,CD4 + T cells and CD4+/CD25+ T cell percentage was detected by flow cytometry.The content of IL-10 in serum and intestinal mucosa tissue was detected by sandwich enzyme-linked immunosorbent assay.RESULTS:Colon injury indices in the decoction groups were effectively reduced,compared with the model group(P 0.05).Compared with that of the control group,the CD4+/CD25+ to CD4+ T lymphocyte ratio of the model group was significantly lower,while the decoction treatment improved the CD4 +/CD25 + to CD4 + T lymphocyte ratio(P 0.05).The serum and mucosal IL-10 content of the model group was significantly lower(P 0.05) than that in the control group,while the decoction group had significantly higher serum and intestinal mucosal IL-10 content than that in the model group(P 0.05).The regulatory T cell content was negatively correlated with the colonic injury index(r = 0.68,P 0.05),and positively correlated with the content of serum IL-10(r = 0.87,P 0.05) and intestinal mucosal IL-10(r= 0.79,P 0.05).CONCLUSION:Jiaweiwumei decoction had significant effects on regulatory T cells and IL-10 in rats with TNBS-induced ulcerative colitis.     

不同灸量对溃疡性结肠炎大鼠结肠上皮形态学及血清中炎性细胞因子、结肠组织中炎性细胞信号转导通路的影响

目的:从形态学、免疫学、分子生物学角度探讨不同灸量治疗溃疡性结肠炎(UC)效果的异同。方法:32只SD大鼠随机分为空白组6只、模型复制组26只。采用三硝基苯甲酸/葡聚糖硫酸钠制备UC大鼠模型。模型复制成功后的大鼠按随机数字表分为模型组、3壮组、6壮组、9壮组,每组各6只。各治疗组所取穴位为"天枢""大横",艾炷直接灸法,每次分别施灸3壮(3min)、6壮(6min)、9壮(9min),共治疗14次。观察大鼠治疗前后疾病活动指数(DAI),电镜、光镜观察结肠组织形态学改变,酶联免疫法检测大鼠血清中白介素-8(IL-8)、白介素-10(IL-10)含量,Western blot法检测大鼠结肠中Toll样受体9(TLR-9)和核转录因子-κB(NF-κB)p 65表达。结果:灸法可明显降低大鼠DAI的评分(与模型组比较均P0.05);光镜与电镜结果显示,灸量越大,结肠组织腺体排列越规则。模型组血清IL-8含量升高,IL-10含量降低;与模型组比较,各治疗组IL-8降低,IL-10增高,其中9壮组和6壮组的变化较3壮组更明显(均P0.05)。模型组结肠组织中TLR-9、NF-κB p 65大量表达;与模型组比较,各治疗组TLR-9、NF-κB p 65表达均降低,且以9壮组的变化最为明显(均P0.05)。结论:艾灸可修复UC大鼠受损黏膜上皮,抑制血清中IL-8含量,提高血清中IL-10含量,通过抑制结肠组织中NF-κB p 65转录而下调TLR-9表达。灸量越大治疗效果越明显。     

Changtai granule, a traditional Chinese drug, protects hapten-induced colitis by attenuating inflammatory and immune dysfunctions

The study was aimed to investigate the effects and mechanism of action of Changtai granule (CT), a traditional compound Chinese medicinal formula, in rodent 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis. Rats with TNBS/ethanol-induced colitis were used. The colonic wet weight, myeloperoxidase (MPO) activity, macroscopic and histological colon injury was observed. Inflammation cytokines were determined by ELISA methods and semi-quantitative RT-PCR. When dosed orally once daily, CT markedly attenuated TNBS-induced colitis. CT significantly attenuated colonic wet weight, macroscopic and histological colon injury. CT decreased mucosal mRNA levels for several inflammatory mediators: inducible nitric oxide synthase, cyclooxygenase 2, and macrophage inflammatory protein 2. CT also decreased mucosal mRNA and protein levels of T effectors cytokines: tumor necrosis factor-alpha (TNF-alpha), interleukin-2 (IL-2) and interferon-gamma (IFN-gamma). Systemic levels of these cytokines were also dramatically attenuated. CD3/CD28-mediated costimulation of T helper 1 effector cytokines release in lamina propria mononuclear cells (LPMC) was markedly inhibited by CT ex vivo and in vitro. Also CT prevented cytokines production by nuclear factor-kappaB (NF-kappaB). The potential anti-inflammatory and immunomodulatory effect of CT in TNBS colitis suggests that CT may be an effective treatment approach for inflammatory bowel disease.