Inhibition of Epithelial-mesenchymal Transition Mechanism in Chronic Atrophic Gastritis Rats by Banxia Xiexintang via Regulating IL-17/ERK/C/EBPβ Signaling Pathway
10.13422/j.cnki.syfjx.20252404
- VernacularTitle: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
- Author:
Wenyu WU
1
;
Xinyu ZENG
1
;
Hao LI
1
;
Weiqi SUN
1
;
Jiahui REN
1
;
Yang YU
1
;
Tingting ZHOU
1
;
Aili XU
1
;
Wei WEI
1
Author Information
1. Wangjing Hospital， China Academy of Chinese Medical Sciences，Beijing 100102，China
- Publication Type:Journal Article
- Keywords:
Banxia Xiexintang;
chronic atrophic gastritis;
interleukin-17（IL-17）/extracellular regulated protein kinases（ERK）/CCAAT/enhancer binding protein β（C/EBPβ）pathway;
epithelial-mesenchymal transition
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(4):1-10
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveThis 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 β（C/EBPβ）signaling pathway， thereby providing new theoretical evidence for the treatment of CAG with classic traditional Chinese medicine formulas. MethodsA 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-α （TNF-α）， cyclooxygenase-2 （COX-2）， and C/EBPβ 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/EBPβ in gastric mucosal tissue. Western blot was used to detect the protein expressions of C/EBPβ， 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/EBPβ in gastric mucosa. ResultsCompared 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/EBPβ， ERK， and p-ERK in gastric mucosa were significantly increased （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBPβ in serum were significantly increased （P<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 （P<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/EBPβ， ERK， and p-ERK in gastric mucosa were significantly reduced （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBP β in serum were significantly decreased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosa tissue were decreased， while the content of E-cadherin was increased （P<0.05，P<0.01）. ConclusionBXT 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-α in serum， regulating the IL-17/ERK/C/EBPβ signaling pathway and inhibiting the EMT process.
