清肠化湿方对溃疡性结肠炎大鼠结肠组织PPAR-,NF-B及MUC2,TFF3的影响

顾培青; 沈洪; 朱磊; 刘亚军; 张露; 刘军楼; 徐艺; 成家飞

doi:10.13422/j.cnki.syfjx.2017030079

您当前的位置：

首页 >

文章列表页 >

清肠化湿方对溃疡性结肠炎大鼠结肠组织PPAR-,NF-B及MUC2,TFF3的影响

药理 | 更新时间：2024-01-04

- 清肠化湿方对溃疡性结肠炎大鼠结肠组织PPAR-,NF-B及MUC2,TFF3的影响
- Effect of Qingchang Huashi Decoction on Expressions of PPAR-, NF-B p65, MUC2 and TFF3 in Colonic Mucosa of Rats with Ulcerative Colitis
- 中国实验方剂学杂志 2017年23卷第3期页码：79-85
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家自然科学基金青年项目（81302919）;江苏省中医药局科技项目立项计划项目（LZ13048）;江苏省中医院高峰学术人才培养工程项目（k2014yrc13）;江苏省中医院院级课题（Y14076）
- DOI：10.13422/j.cnki.syfjx.2017030079
  中图分类号： R285.5
- 纸质出版日期：2017
- 稿件说明：
移动端阅览
顾培青, 沈洪, 朱磊, 等. 清肠化湿方对溃疡性结肠炎大鼠结肠组织PPAR-,NF-B及MUC2,TFF3的影响[J]. 中国实验方剂学杂志, 2017,23(3):79-85.

GU Pei-qing, SHEN Hong, ZHU Lei, et al. Effect of Qingchang Huashi Decoction on Expressions of PPAR-, NF-B p65, MUC2 and TFF3 in Colonic Mucosa of Rats with Ulcerative Colitis[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(3): 79-85.
顾培青, 沈洪, 朱磊, 等. 清肠化湿方对溃疡性结肠炎大鼠结肠组织PPAR-,NF-B及MUC2,TFF3的影响[J]. 中国实验方剂学杂志, 2017,23(3):79-85. DOI： 10.13422/j.cnki.syfjx.2017030079.

GU Pei-qing, SHEN Hong, ZHU Lei, et al. Effect of Qingchang Huashi Decoction on Expressions of PPAR-, NF-B p65, MUC2 and TFF3 in Colonic Mucosa of Rats with Ulcerative Colitis[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(3): 79-85. DOI： 10.13422/j.cnki.syfjx.2017030079.

摘要

目的：观察清肠化湿方对三硝基苯磺酸（TNBS）诱导的大鼠溃疡性结肠炎（UC）的治疗效果，以过氧化物酶体增殖物激活受体-γ（PPAR-γ）和核因子（NF）-κB为中心探讨其作用机制。方法：将雄性Wistar大鼠80只，随机分为8组，分别为正常组灌胃（ig）生理盐水2 mL·d-1]，模型组（ig生理盐水 2 mL·d-1），清肠化湿方低、中、高剂量组（ig清肠化湿方8，16，32 g·kg-1），柳氮磺胺吡啶（SASP）组（ig SASP 0.67 g·kg-1），SASP+双酚A-二甘氨酸醚（BADGE）组（ig SASP 0.67 g·kg-1+腹腔注射BADGE 20 mg·kg-1）及清肠化湿方中剂量+BADGE组（ig清肠化湿方16 g·kg-1+腹腔注射BADGE 20 mg·kg-1），每组10只。除正常组以生理盐水灌肠外，其余组采用TNBS/乙醇灌肠造UC大鼠模型。以柳氮磺胺吡啶（SASP）为阳性药物，同时联合使用PPAR-γ抑制剂双酚A-二甘氨酸醚（BADGE），观察大鼠疾病活动指数及结肠病理评分，蛋白质免疫印迹（Western blot）和实时荧光定量PCR（Real-time PCR）法分别检测大鼠结肠组织中PPAR-γ，NF-κB的蛋白和基因表达酶联免疫吸附测定（ELISA）法检测肠组织分泌蛋白黏蛋白2（MUC2）和三叶因子3（TFF3）的表达情况。结果：模型组大鼠结肠出现明显炎症和溃疡，提示造模成功。模型组PPAR-γ蛋白和基因表达较正常组显著降低（P<0.01）；与模型组比较，清肠化湿方组和SASP组PPAR-γ表达均有所增加（P<0.05）；联用PPAR-γ抑制剂BADGE后两组PPAR-γ表达又显著降低（P<0.05）。同时，模型组NF-κB的蛋白和基因表达显著升高（P<0.01），清肠化湿方各剂量组均能降低NF-κB的表达（P<0.05），而清肠化湿方中剂量+BADGE组较清肠化湿方中剂量组NF-κB的表达又显著增高（P<0.05）。此外，清肠化湿方组和SASP组能有效升高大鼠肠组织中MUC2和TFF3的表达，而当清肠化湿方或SASP联合使用BADGE时这一作用被减弱。结论：清肠化湿方能有效改善溃疡性结肠炎大鼠的病变程度，其作用机制与抑制NF-κB的激活，减轻炎症反应，并通过促进肠道黏膜MUC2与TFF3的分泌修复肠粘膜屏障有关，而这些作用可能主要是通过激活PPAR-γ信号通路完成的。

Abstract

Objective: To investigate the effects of Qingchang Huashi decoction (QHD) on the expressions of peroxidase body growth activated receptor-γ(PPAR-γ) and nuclear factor-κB(NF-κB) p65 in colonic mucosa of rats with ulcerative colitis

and study the mechanism of Qingchang Huashi decoction in rats with ulcerative colitis. Method: Eighty male Wistar rats were divided randomly into eight groups:normal group (ig NS 2 mL·d-1)

model group (ig NS 2 mL·d-1)

QHD low-dose group

QHD medium-dose group

QHD high-dose group (ig QHD 8

32 g·kg-1)

SASP group (ig SASP 0.67 g·kg-1)

SASP+BADGE group (ig SASP 0.67 g·kg-1+ip BADGE 20 mg·kg-1)

and QHD medium-dose+BADGE group (ig QHD 16 g·kg-1+ip BADGE 20 mg·kg-1)

with 10 rats in each group. TNBS was used in all of the groups except for normal group to establish the ulcerative colitis model in rats. SASP and BADGE that is the inhibitor of PPAR-γ were used as positive control drug. The general conditions and the colonic pathology morphology were observed. Western blot and Real-time PCR were performed to detect the protein and mRNA expressions of PPAR-γ and NF-κB p65.The expressions of mucoprotein2(MUC2) and trefoil factor3(TFF3) in colonic mucosa extract were detected by the method of ELISA. Result: Obvious inflammation and ulceration were observed in model group

which suggested that the model was successful. The protein and mRNA expressions of PPAR-γ in the model group were significantly lower than the normal group (P<0.01). Compared with the normal group

expressions of PPAR-γ in QHD and SASP increased slightly (P<0.05)

however

these effects were reduced when QHD and SASP were combined with BADGE (P<0.05). At the same time

the protein and mRNA expressions of NF-κB p65 increased significantly in model group (P<0.01). QHD could decline the expression of NF-κB (P<0.05)

while QHD combined with BADGE could not inhibit its expression any more (P<0.05). Moreover

SASP and QHD were able to increase the expressions of MUC2 and TFF3 in colonic mucosa

but these effects were weakened when combined with BADGE. Conclusion: Qingchang Huashi decoction can improve general conditions and colonic inflammation of TNBS-induced model rats. Its mechanisms may be that Qingchang Huashi decoction can activate PPAR-γ signaling pathway by inhibiting inflammation and expression of NF-κB p65

improving secretion of MUC2 and TFF3 at mucous membrane

and restoring the intestine barrier.

关键词

Keywords

references

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

暂无数据