中华消化杂志
中華消化雜誌
중화소화잡지
Chinese Journal of Digestion
2010年
1期
28-32
,共5页
成家飞%林琳%宁月季%张蔚%李学良
成傢飛%林琳%寧月季%張蔚%李學良
성가비%림림%저월계%장위%리학량
结肠炎%纤维化%牛磺酸%疾病模型%动物
結腸炎%纖維化%牛磺痠%疾病模型%動物
결장염%섬유화%우광산%질병모형%동물
Colitis%Fibrosis%Taurine%Disease models%animal
目的 探讨牛磺酸对三硝基苯磺酸(TNBS)诱导的结肠炎大鼠肠纤维化的影响.方法 32只SD大鼠均分为对照组、模型组、低剂量和高剂量牛磺酸组.对照组以0.9%氯化钠溶液灌肠,其余3组以TNBS灌肠诱导建立结肠炎模型.低剂量和高剂量牛磺酸组于造模前1周每日分别给予牛磺酸400和800 mg/kg干预,直至造模结束.观察大鼠临床表现及疾病活动指数(DAI),行结肠大体评分和组织学评分,检测大鼠结肠长度、结肠重量.测定结肠组织中羟脯氨酸(Hyp)、Ⅰ型胶原蛋白、转化生长因子-β1(TGF-β1)蛋白和mRNA、Smad3蛋白和mRNA水平.结果 与对照组相比,模型组大鼠体重减轻、DAI评分升高、结肠狭窄伴近端扩张、结肠长度缩短、结肠重量增加、大体评分也显著升高(P<0.01).牛磺酸干预后,大鼠体重、DAI评分、结肠长度等指标均有所改善.模型组纤维化评分为1.88±0.35.较对照组明显增加(0.25±0.46,P<0.01);低剂量和高剂量牛磺酸组纤维化评分分别为1.25±0.71和0.75±0.47,较模型组下降(P<0.05).模型组大鼠结肠Hyp、TGF-β1、Ⅰ型胶原蛋白、Smad3蛋白和mRNA含量均较低剂量和高剂量牛磺酸组明显上升(P值均<0.05).结论 牛磺酸能有效抑制TNBS诱导的结肠炎大鼠肠纤维化,其抗纤维化机制可能与下调TGF-β1、抑制TGF-β/Smad3通路有关,为解决克罗恩病肠纤维化和肠狭窄提供一定的实验依据.
目的 探討牛磺痠對三硝基苯磺痠(TNBS)誘導的結腸炎大鼠腸纖維化的影響.方法 32隻SD大鼠均分為對照組、模型組、低劑量和高劑量牛磺痠組.對照組以0.9%氯化鈉溶液灌腸,其餘3組以TNBS灌腸誘導建立結腸炎模型.低劑量和高劑量牛磺痠組于造模前1週每日分彆給予牛磺痠400和800 mg/kg榦預,直至造模結束.觀察大鼠臨床錶現及疾病活動指數(DAI),行結腸大體評分和組織學評分,檢測大鼠結腸長度、結腸重量.測定結腸組織中羥脯氨痠(Hyp)、Ⅰ型膠原蛋白、轉化生長因子-β1(TGF-β1)蛋白和mRNA、Smad3蛋白和mRNA水平.結果 與對照組相比,模型組大鼠體重減輕、DAI評分升高、結腸狹窄伴近耑擴張、結腸長度縮短、結腸重量增加、大體評分也顯著升高(P<0.01).牛磺痠榦預後,大鼠體重、DAI評分、結腸長度等指標均有所改善.模型組纖維化評分為1.88±0.35.較對照組明顯增加(0.25±0.46,P<0.01);低劑量和高劑量牛磺痠組纖維化評分分彆為1.25±0.71和0.75±0.47,較模型組下降(P<0.05).模型組大鼠結腸Hyp、TGF-β1、Ⅰ型膠原蛋白、Smad3蛋白和mRNA含量均較低劑量和高劑量牛磺痠組明顯上升(P值均<0.05).結論 牛磺痠能有效抑製TNBS誘導的結腸炎大鼠腸纖維化,其抗纖維化機製可能與下調TGF-β1、抑製TGF-β/Smad3通路有關,為解決剋囉恩病腸纖維化和腸狹窄提供一定的實驗依據.
목적 탐토우광산대삼초기분광산(TNBS)유도적결장염대서장섬유화적영향.방법 32지SD대서균분위대조조、모형조、저제량화고제량우광산조.대조조이0.9%록화납용액관장,기여3조이TNBS관장유도건립결장염모형.저제량화고제량우광산조우조모전1주매일분별급여우광산400화800 mg/kg간예,직지조모결속.관찰대서림상표현급질병활동지수(DAI),행결장대체평분화조직학평분,검측대서결장장도、결장중량.측정결장조직중간포안산(Hyp)、Ⅰ형효원단백、전화생장인자-β1(TGF-β1)단백화mRNA、Smad3단백화mRNA수평.결과 여대조조상비,모형조대서체중감경、DAI평분승고、결장협착반근단확장、결장장도축단、결장중량증가、대체평분야현저승고(P<0.01).우광산간예후,대서체중、DAI평분、결장장도등지표균유소개선.모형조섬유화평분위1.88±0.35.교대조조명현증가(0.25±0.46,P<0.01);저제량화고제량우광산조섬유화평분분별위1.25±0.71화0.75±0.47,교모형조하강(P<0.05).모형조대서결장Hyp、TGF-β1、Ⅰ형효원단백、Smad3단백화mRNA함량균교저제량화고제량우광산조명현상승(P치균<0.05).결론 우광산능유효억제TNBS유도적결장염대서장섬유화,기항섬유화궤제가능여하조TGF-β1、억제TGF-β/Smad3통로유관,위해결극라은병장섬유화화장협착제공일정적실험의거.
Objective To investigate the effect of taurine on colonic fibrosis in rats with colitis induced by 2,4,6-trinitrobenzene sulphonic acid(TNBS). Methods Thirty-two SD rats were divided into normal control group, model group, low-dose (400 mg/kg) taurine group and high-dose (800 mg/kg) taurine group. Rats in normal group were administrated with 0.9% NaCl solution enema, and the other three groups received TNBS enema. The rats in low-dose and high-dose taurine groups were administrated with 400 mg/kg and 800 mg/kg of taurine daily, respectively, one week before TNBS enema. Morphology and disease activity index (DAI) were evaluated, and the colonic tissues were histologically examined. Colon length and weight of the rats were also measured. The concentrations of hydroxyproline, collagen type Ⅰ, transforming growth factor-betal(TGF-β1), and Smad3 protein and mRNA in colon tissues were tested. Results In comparison with control group, the body weight and colon length were decreased while DAI score and colon weight were increased obviously in model group (P`0.01). All above parameters were improved after intervention of taurine. The fibrotie score in model group (1.88±0.35) was significantly higher than that in control group (0.25±0.46), low-dose (1.25±0.71) and high-dose (0.75±0.47) taurine groups (all P values <0.05). High levels of hydroxyproline, collagen type Ⅰ, TGF-β1 and Smad3 were detected in model group compared with low-dose and high-dose taurine groups (all P values < 0.05). Conclusions Taurine is effective in prevention of colonic fibrosis induced by TNBS in rats, which is mediated by the down regulation of TGF-β1 and the inhibition of TGF-β/ Smad3 pathway. It may be beneficial in treatment of Crohn's disease with colonic fibrosis and strictures.
