摘要
目的探讨RIP3参与的程序性细胞坏死在小鼠结肠炎中的作用。方法 24只C57BL/6J小鼠随机分为模型组和正常组。模型组自由饮用5%葡聚糖硫酸钠盐(dextran sulfate sodium salt,DSS)4 d,再自由饮用无菌水3 d;正常组自由饮用无菌水7 d。每天检测小鼠疾病活动指数(disease activity index,DAI),于7 d后处死小鼠,取出结肠,测量结肠长度;结肠HE染色进行病理学评分;运用Western blotting检测IL-1β、IL-6、RIP3、TNF-α在结肠中的表达;运用免疫组化检测RIP3在结肠组织中的表达位置。结果模型组结肠长度显著短于正常组(P<0.001);病理学评分显著高于正常组(P<0.001);模型组炎症因子IL-1β、IL-6表达量较正常组增高(P<0.05);RIP3、TNF-α表达量较正常组增高(P<0.05);RIP3主要表达于小鼠结肠上皮细胞中。结论在小鼠结肠炎中存在TNF-α/RIP3信号通路上调,RIP3参与的程序性细胞坏死可能是导致结肠炎的一个重要机制。
Objective To evaluate the effect of RIP3-mediated necroptosis in experimental C57BL/6J mice colitis. Methods Twenty-four C57BL/6J mice were randomly divided into model group and normal group. Mice in model group drank 5% DSS solution freely for 4 days, then drank sterile water for 3 days; mice in normal group just drank sterile water for 7 days. Disease activity index （DAI） was checked every day; after 7 days, mice were euthanized, co- lons were removed and the length of colons were measured; the histological score of colons was evaluated; the expres- sions of IL-1 β, IL-6, RIP3 and TNF-α in colons were detected by Western blotting and RIP3 in colons was analyzed by immunohistoehemistry-paraffin （IHC-P）. Results The length of colons in model group was shorter than that in normal group （P 〈 0. 001 ） ; the histological score in model group was significantly higher than that in normal group （P 〈 0. 001 ） ; the expressions of IL-1 β, IL-6 in model group were higher than those in normal group （P 〈 0.05） ; the levels of RIP3 and TNF-α in model group were higher than those in normal group （ P 〈 0.05 ） ; RIP3 was mainly expressed in colonic epithelial cells. Conclusion The expression of TNF-α/RIP3 signal pathway is increased in mice colitis, RIP3- mediated necroptosis may be involved in the pathogenesis of colitis.
出处
《胃肠病学和肝病学杂志》
CAS
2015年第8期935-938,共4页
Chinese Journal of Gastroenterology and Hepatology
作者简介
贾振宇，硕士研究生，研究方向：消化内科。E—mail：jzyg—host@163．com
通讯作者简介：许春芳，主任医师，研究方向：消化内科。E-mail：xcf601@163．com
