摘要
目的:观察大黄素对结肠炎大鼠模型肠纤维化的影响,探讨其抗纤维化作用机制.方法:以三硝基苯磺酸(trinitrobenzene sulphonic acid,TNBS)诱导的结肠炎大鼠为纤维化模型,将34只SD大鼠分成正常对照组、模型组和大黄素组,模型组和大黄素组予以TNBS诱导肠纤维化,大黄素组每日给予大黄素40mg/kg灌胃,其余组则给予等体积盐溶液.实验过程中观察小鼠体质量、大便性状和活动变化,给予DAI评分,实验结束后收集结肠组织标本,给予大体和组织学评分,并采用HE染色及Masson胶原三色染色观察大鼠结肠组织损伤和纤维化程度,采用荧光定量PCR法检测结肠黏膜中TGF-1、胶原Ⅰ、胶原Ⅲ、Smad3、-SMA和E-cad mRNA表达.结果:与模型组相比,大黄素组一般情况、结肠组织大体和组织学评分及纤维化程度均出现明显改善.大黄素组TGF-β1、胶原Ⅰ、胶原Ⅲ、Smad3和-SMA mRNA表达较模型组明显降低(1.27±0.78vs4.56±3.14;0.60±0.59vs2.15±1.22;0.92±1.38vs3.34±1.47;3.11±2.81vs8.77±6.40;0.87±0.62vs2.40±1.15,均P<0.05),而E-cad mRNA表达明显升高(1.01±0.34vs0.30±0.23,P<0.05).结论:大黄素对TNBS诱导的大鼠肠纤维化模型具有一定的抗纤维化作用,该作用可能与其下调TGF-1/Smad信号通路抑制EMT发生有关.
AIM： To investigate the anti±fibrotic effects of emodin in rats with experimental colitis, and to explore the possible mechanisms. METHODS： Rats with colitis induced with trinitrobenzene sulphonic acid （TNBS） were used as the model of intestinal fibrosis. Thirty four rats were randomly divided into normal group, model group and emodin group. Colitis was induced with TNBS in rats of the model group and emodin group. Rats in the emodin group were gavaged with 40 mg/kg of emodin daily, and the other groups were gavaged with an equal volume of 0.9% NaC1 solution. Body weight loss and changes in stool and activities were observed, and DAI was calculated. At the end of the experiment, colon tissue samples were collected, and the general and histological scores were given. The injury and fibrosis of the colon were detected by HE staining and Massoncollagen staining, respectively. Expression of transforming growth factor （TGF）±β1, collagen Ⅰ, collagen Ⅲ, Smad3 and α±SMA was determined by FQ±PCR.RESULTS： Compared to the model group, the general condition, general and histological scores, and fibrosis were improved significantly in the emodin group. Expression of TGF±β1, col lagen Ⅰ, collagen Ⅲ, Smad3 and α±SMA in co lonic mucosa in the emodin group were signifi cantly lower than that in the model group （1.27 ± 0.78 vs 4.56 ± 3.14; 0.60 ± 0.59 vs 2.15 ± 1.22; 0.92 ± 1.38 vs 3.34 ± 1.47; 3.11 ± 2.81 vs 8.77 ± 6.40; 0.87 ± 0.62 vs 2.40 ± 1.15, all P 〈 0.05）, while expres sion of E-cad was higher in the emodin group （1.01± 0.34 vs 0.30 ＋ 0.23, P 〈 0.05）.CONCLUSION： Emodin reduces intestinal fibro± sis in rats with TNBS±induced colitis possibly by down-regulation of TGF-β1/Smad3 signal ing and inhibition of epithelial±mesenchymal transition.
出处
《世界华人消化杂志》
CAS
北大核心
2012年第28期2703-2708,共6页
World Chinese Journal of Digestology
关键词
大黄素
三硝基苯磺酸
肠纤维化
克罗恩
病
上皮间质化
转化生长因子β1
Emodin
Trinitrobenzene sulphonicacid
Intestinal fibrosis
Crohn＇s disease
Epithelial-mesenchymal transition
Transforming growthfactor-βl
