Inhibition of Epithelial-mesenchymal Transition Mechanism in Chronic Atrophic Gastritis Rats by Banxia Xiexintang via Regulating IL-17/ERK/C/EBP<italic style="font-style: italic">β</italic> Signaling Pathway

WU Wenyu; ZENG Xinyu; LI Hao; SUN Weiqi; REN Jiahui; YU Yang; ZHOU Tingting; XU Aili; WEI Wei

doi:10.13422/j.cnki.syfjx.20252404

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Inhibition of Epithelial-mesenchymal Transition Mechanism in Chronic Atrophic Gastritis Rats by Banxia Xiexintang via Regulating IL-17/ERK/C/EBPβ Signaling Pathway

更新时间：2026-01-23

- Inhibition of Epithelial-mesenchymal Transition Mechanism in Chronic Atrophic Gastritis Rats by Banxia Xiexintang via Regulating IL-17/ERK/C/EBPβ Signaling Pathway
  增强出版
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 32, Issue 4, Pages: 1-10(2026)
- 作者机构：
  
  1.中国中医科学院望京医院，北京 100102
  2.广州中医药大学，广州 510006
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20252404
  CLC： R289;R259;R285
- Received：15 September 2025，
  
  Revised：2025-10-29，
  
  Accepted：10 November 2025，
  
  Published Online：17 November 2025，
  
  Published：20 February 2026
- 稿件说明：
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武文玉,曾新雨,李浩等.半夏泻心汤调控IL-17/ERK/C/EBPβ信号通路抑制慢性萎缩性胃炎大鼠上皮间充质转化的机制[J].中国实验方剂学杂志,2026,32(04):1-10.

WU Wenyu,ZENG Xinyu,LI Hao,et al.Inhibition of Epithelial-mesenchymal Transition Mechanism in Chronic Atrophic Gastritis Rats by Banxia Xiexintang via Regulating IL-17/ERK/C/EBPβ Signaling Pathway[J].Chinese Journal of Experimental Traditional Medical Formulae,2026,32(04):1-10.
武文玉,曾新雨,李浩等.半夏泻心汤调控IL-17/ERK/C/EBPβ信号通路抑制慢性萎缩性胃炎大鼠上皮间充质转化的机制[J].中国实验方剂学杂志,2026,32(04):1-10. DOI： 10.13422/j.cnki.syfjx.20252404.

WU Wenyu,ZENG Xinyu,LI Hao,et al.Inhibition of Epithelial-mesenchymal Transition Mechanism in Chronic Atrophic Gastritis Rats by Banxia Xiexintang via Regulating IL-17/ERK/C/EBPβ Signaling Pathway[J].Chinese Journal of Experimental Traditional Medical Formulae,2026,32(04):1-10. DOI： 10.13422/j.cnki.syfjx.20252404.

摘要

目的

探讨半夏泻心汤调控白细胞介素-17（IL-17）/细胞外信号调节激酶（ERK）/CCAAT增强子结合蛋白

（C/EBP

）信号通路抑制慢性萎缩性胃炎（CAG）大鼠上皮间充质转化（EMT）的作用机制，为经典名方治疗CAG提供新的理论依据。

方法

采用复合因素法建立CAG大鼠模型，成模后随机分为模型组，半夏泻心汤低、中、高剂量（0.549、1.098、2.196 g·kg

-1

）组和阳性药（维酶素，0.3 g·kg

-1

）组，并设正常组。干预8周后，评估胃组织病理变化。采用酶联免疫吸附测定法（ELISA）检测血清中IL-17、肿瘤坏死因子-

（TNF-

）、环氧合酶-2（COX-2）、C/EBP

含量，以及胃黏膜组织上皮间充质转化（EMT）标志物E-钙黏蛋白（E-cadherin）、N-钙黏蛋白（N-cadherin）和波形蛋白（Vimentin）含量；免疫组化法检测胃黏膜组织中IL-17、磷酸化（p）-ERK及C/EBP

蛋白定位与表达水平；蛋白免疫印迹法（Western blot）检测胃黏膜中C/EBP

、ERK及磷酸化（p）-ERK蛋白表达；实时荧光定量聚合酶链式反应（Real-time PCR）检测胃黏膜中ERK、COX-2及C/EBP

mRNA表达水平。

结果

与正常组比较，模型组大鼠胃黏膜腺体萎缩，炎症细胞浸润；胃黏膜C/EBP

、ERK、p-ERK蛋白及相关mRNA表达明显升高（

0.05，

0.01）；血清IL-17、TNF-

、COX-2、C/EBP

水平显著升高（

0.01）；胃黏膜组织中N-cadherin、Vimentin含量升高，E-cadherin含量降低（

0.01）。与模型组比较，不同剂量半夏泻心汤干预后，胃黏膜病理损伤得到不同程度的改善，胃黏膜C/EBP

、ERK、p-ERK蛋白及mRNA表达明显降

低（

0.05，

0.01），血清IL-17、TNF-

、COX-2、C/EBP

水平显著降低（

0.01），胃黏膜组织中N-cadherin及Vimentin含量降低，E-cadherin含量升高（

0.05，

0.01）。

结论

半夏泻心汤能够有效改善CAG大鼠胃黏膜组织病理损伤，其作用机制可能与降低血清IL-17和TNF-

水平，调控IL-17/ERK/C/EBP

信号通路，抑制EMT进程有关。

Abstract

Objective

This study aimed to investigate the action mechanism by which Banxia Xiexintang （BXT） inhibits epithelial-mesenchymal transition （EMT） in chronic atrophic gastritis （CAG） rats by regulating the interleukin-17（IL-17）/extracellular regulated protein kinases（ERK）/CCAAT enhancer binding protein

（C/EBP

）signaling pathway， thereby providing new theoretical evidence for the treatment of CAG with classic traditional Chinese medicine formulas.

Methods

A CAG rat model was established by using the combined factor method. After successful modeling， the rats were randomly divided into the model group， low-， medium-， and high-dose groups （0.549， 1.098， 2.196 g·kg

-1

， respectively） of BXT， and the positive drug group （vitacoenzyme， 0.3 g·kg

-1

）. A normal control group was also set up. After 8 weeks of intervention， the pathological changes of gastric tissue were evaluated. The enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of IL-17， tumor necrosis factor-

（TNF-

）， cyclooxygenase-2 （COX-2）， and C/EBP

in serum， as well as the contents of EMT markers in gastric mucosal tissue including E-cadherin， N-cadherin， and vimentin. The immunohistochemistry method was employed to determine the localization and protein expression levels of IL-17， p-ERK， and C/EBP

in gastric mucosal tissue. Western blot was used to detect the protein expressions of C/EBP

， ERK， and its phosphorylated form （p）-ERK in gastric mucosa. Real-time polymerase chain reaction （Real-time PCR） was applied to measure the mRNA expression levels of ERK， COX-2， and C/EBP

in gastric mucosa.

Results

Compared with those in the normal control group， the rats in the model group showed gastric mucosal glandular atrophy and inflammatory cell infiltration. The protein and their related mRNA expressions of C/EBP

， ERK， and p-ERK in gastric mucosa were significantly increased （

0.05，

0.01）. The levels of IL-17， TNF-

， COX-2， and C/EBP

in serum were significantly increased （

0.01）. The contents of N-cadherin and vimentin in gastric mucosal tissue were significantly increased， while the content of E-cadherin was significantly decreased （

0.01）. Compared with the model group， after intervention with different doses of BXT， the pathological damage of the gastric mucosa was improved to varying degrees. The protein and mRNA expressions of C/EBP

， ERK， and p-ERK in gastric mucosa were significantly reduced （

0.05，

0.01）. The levels of IL-17， TNF-

， COX-2， and C/EBP

in serum were significantly decreased （

0.01）. The contents of N-cadherin and vimentin in gastric mucosa tissue were decreased， while the content of E-cadherin was increased （

0.05，

0.01）.

Conclusion

BXT can effectively improve the pathological damage of gastric mucosal tissue in CAG rats. Its action mechanism may be related to reducing the levels of IL-17 and TNF-

in serum， regulating the IL-17/ERK/C/EBP

signaling pathway and inhibiting the EMT process.

关键词

Keywords

references

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Inhibition of Epithelial-mesenchymal Transition Mechanism in Chronic Atrophic Gastritis Rats by Banxia Xiexintang via Regulating IL-17/ERK/C/EBPβ Signaling Pathway

DOI：10.13422/j.cnki.syfjx.20252404

摘要

Abstract

关键词

Keywords

references