Effects of Weiyan I Decoction on Chronic Atrophy Gastritis and the Related Molecular Mechanism

WEI Yu-na; TAN Xiao; GUO Ya-lei; LIU You-zhang

doi:10.11653/syfj2013110276

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Effects of Weiyan I Decoction on Chronic Atrophy Gastritis and the Related Molecular Mechanism

更新时间：2024-01-04

- Effects of Weiyan I Decoction on Chronic Atrophy Gastritis and the Related Molecular Mechanism
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 19, Issue 11, Pages: 276-279(2013)
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- DOI：10.11653/syfj2013110276
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- Published：2013
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WEI Yu-na, TAN Xiao, GUO Ya-lei, et al. Effects of Weiyan I Decoction on Chronic Atrophy Gastritis and the Related Molecular Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(11): 276-279.
DOI：

WEI Yu-na, TAN Xiao, GUO Ya-lei, et al. Effects of Weiyan I Decoction on Chronic Atrophy Gastritis and the Related Molecular Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(11): 276-279. DOI： 10.11653/syfj2013110276.

摘要

目的: 探讨胃炎I号方对慢性萎缩性胃炎(CAG)的疗效及其分子机制。方法: 90只SD大鼠随机分为正常对照组、模型组、胃炎I号(1.08

0.54 g·kg-1)治疗组;除正常对照组外

所有大鼠进行CAG造模

20周后开始ig给药

1次/d

连续12周后处死大鼠

胃黏膜组织切片观察病变程度

采用RT-PCR测定β-链蛋白(β-catenin)和周期素D1(cyclin D1)表达水平。结果: 模型组大鼠胃黏膜出现CAG病变

治疗组大鼠CAG病变减轻;CAG大鼠模型组β-catenin和cyclin D1表达较正常对照组升高(P<0.01)

治疗组β-catenin和cyclin D1表达明显低于模型组(P<0.01)。结论: 胃炎I号对CAG有治疗作用

β-catenin和cyclin D1在CAG模型中表达升高

胃炎I号方可能通过抑制β-catenin和cyclin D1治疗CAG。

Abstract

Objective: To study the effects of Weiyan I decoction (WID) on chronic atrophy gastritis (CAG) and the related molecular mechanism. Method: Ninety SD rats were divided into 4 groups: control group

model group and two treatment groups(1.08

0.54 g·kg-1). The CAG model was established in model group and treatment group

and the treatment of WID was continued for 12 weeks started from 20 weeks after model establishment. Afterwards

the pathological specimens of gastric mucosa were collected and investigated. The expression level of β-catenin and cyclin D1 mRNA were examined by RT-PCR. Result: Compared with the control group

the expression of β-catenin and cyclin D1 were increased in the model group

while treatment with WID could reduce the induction. The difference were significant (P<0.01). Conclusion: WID has good therapeutic effect on CAG. The mechanism of WID in treating CAG may be related with inhibition of the expression of β-catenin and cyclin D1.

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