[1]姜从桥,朱平胜,时依,等.原花青素B2 对三硝基苯磺酸结肠炎模型小鼠肠炎及肠屏障的保护作用[J].南方医科大学学报,2019,(07):778.[doi:10.12122/j.issn.1673-4254.2019.07.05]
点击复制

原花青素B2 对三硝基苯磺酸结肠炎模型小鼠肠炎及肠屏障的保护作用()
分享到:

《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2019年07期
页码:
778
栏目:
出版日期:
2019-07-15

文章信息/Info

Title:
Protective effect of procyanidin B2 on intestinal barrier and against enteritis in a mouse model of trinitrobenzene sulphonic acid-induced colitis
作者:
姜从桥朱平胜时依项武军葛思堂张宗兵左芦根
关键词:
原花青素B2克罗恩病炎症肠粘膜屏障信号通路
Keywords:
procyanidin B2 Crohn’s disease inflammation intestinal mucosal barrier signaling pathway
DOI:
10.12122/j.issn.1673-4254.2019.07.05
摘要:
目的探讨原花青素B2(PCB2)对三硝基苯磺酸(TNBS)诱导的结肠炎小鼠肠炎及肠屏障的保护性作用及可能机制。方 法选取6~8周龄雄性Balb/c小鼠,建立TNBS结肠炎小鼠模型,将造模成功的小鼠随机分为PCB2治疗组(n=10)和对照组(n= 10)。PCB2治疗组小鼠每日给予PCB2灌胃(100 mg/kg,0.2 mL),对照组每日给予0.2 mL生理盐水灌胃。4周后处死小鼠,采 用H&E、免疫荧光及免疫印迹法等评估疾病症状、肠道炎症、肠粘膜细胞屏障功能和结构及PI3K/AKT信号改变情况。结果 PCB2治疗组小鼠疾病活动指数在干预第3周和第4周均低于对照组小鼠(P<0.05),而平均体质量在干预第3周和第4周均高于 对照组小鼠(P<0.05)。PCB2 治疗组小鼠结肠炎症评分及肠粘膜炎症介质白介素-1β及肿瘤坏死因子-α水平低于对照组(P< 0.05),而白介素-10高于TNBS组(P<0.05)。PCB2治疗组小鼠肠粘膜对硫氰酸荧光素-葡聚糖通透性及肠系膜淋巴结细菌移位阳 性率均低于对照组(P<0.05)。Western blot检测及半定量分析显示PCB2治疗提高了TNBS模型小鼠claudin-1及ZO-1的表达水 平(P<0.05)。同时,PCB2治疗组小鼠肠粘膜p-PI3K及p-AKT表达水平低于对照组,差异具有统计学意义(P>0.05)。结论PCB2 可能通过抑制肠道PI3K/AKT信号途径发挥抗炎及肠粘膜功能和结构保护作用,可能会成为克罗恩病治疗新的药物选择。
Abstract:
Objective To investigate the protective effect of procyanidin B2 (PCB2) on the intestinal barrier and against enteritis in mice with trinitrobenzene sulphonic acid (TNBS)-induced colitis and explore the possible mechanism. Methods A mouse model of TNBS-induced colitis was established in male Balb/c mice aged 6-8 weeks. The successfully established mouse models were randomly divided into PCB2 treatment group (n=10) and model group (n=10) and were treated with daily intragastric administration of PCB2 (100 mg/kg, 0.2 mL) and 0.2 mL normal saline, respectively. After 4 weeks, the disease symptoms, intestinal inflammation, intestinal mucosal cell barrier function and the changes in PI3K/AKT signaling were evaluated using HE staining, immunofluorescence assay and Western blotting. Results The disease activity index of the mice was significantly lower and the mean body weight was significantly greater in PCB2 group than in the model group in the 3rd and 4th weeks of intervention (P<0.05). The levels of colonic inflammation and intestinal mucosal inflammatory mediators IL-1β and TNF-α were significantly lower while IL-10 was significantly higher in PCB2 group than in the model group (P< 0.05). Compared with those in the model group, the mice in PCB2 treatment group showed a significantly lower positive rate of bacterial translocation in the mesenteric lymph nodes and a lower thiocyanate-dextran permeability of the intestinal mucosa (P<0.05). Western blotting showed that PCB2 treatment significantly increased the expressions of claudin-1 and ZO-1 (P<0.05) and significantly lowered the expression levels of p-PI3K and p-AKT in the intestinal mucosa as compared with those in the model group (P<0.05). Conclusion PCB2 suppresses intestinal inflammation and protects intestinal mucosal functions and structural integrity by inhibiting intestinal PI3K/AKT signaling pathway, suggesting the potential of PCB2 as a new drug for Crohn’s disease.

相似文献/References:

[1]张朝霞,赵芯梅,吕超蓝,等.膜联蛋白A2在炎症性肠病肠粘膜中的表达及临床意义[J].南方医科大学学报,2012,(11):1548.
[2]张萃,欧阳钦.局限性非特异性回盲部炎症66例的回顾与随访[J].南方医科大学学报,2016,(06):842.

更新日期/Last Update: 1900-01-01