Mechanisms of Qizhujianwei Granules in Blocking Malignant Progression of Gastric Intraepithelial Neoplasia
10.13422/j.cnki.syfjx.20251841
- VernacularTitle:芪术健胃颗粒阻断胃上皮内瘤变恶性进展机制
- Author:
Yuling YU
1
;
Yanmin WANG
1
;
Siqi WANG
1
;
Yateng SUN
1
;
Yunhe WANG
2
;
Yonghuang YAN
1
;
Xinyu YANG
1
;
Siqi HAN
1
;
Yuhong SONG
1
;
Yuhan WANG
1
;
Cai ZHANG
3
;
Zeqi SU
3
Author Information
1. School of Chinese Meteria Medica，Beijing University of Chinese Medicine，Beijing 100029，China
2. School of Acupuncture-Moxibustion and Tuina，Beijing University of Chinese Medicine，Beijing 100029，China
3. Beijing Research Institute of Chinese Medicine， Beijing University of Chinese Medicine， Beijing 100029，China
- Publication Type:Journal Article
- Keywords:
Qizhujianwei granules;
gastric intraepithelial neoplasia;
cell proliferation;
epithelial-mesenchymal transition;
traditional Chinese medicine compound formula
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(10):143-151
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effects of Qizhujianwei granules （QZJW） on abnormal proliferation and malignant transformation of gastric mucosal cells in rats with gastric intraepithelial neoplasia （GIN） and to explore the related mechanisms. MethodsA total of 80 SPF male Wistar rats were used. A GIN rat model was established using a four-factor comprehensive method consisting of methylnitronitrosoguanidine （MNNG）， ranitidine， irregular feeding patterns， and sodium salicylate. Except for the normal group， after successful modeling， the rats were randomly divided according to body weight into a model group， a Moluodan group （0.55 g·kg-1）， and a QZJW group （7.34 g·kg-1）， with 12 rats in each group. All groups were treated for 8 weeks. The general characteristics of the rats and morphological changes of the gastric mucosa were observed. Histopathological changes of the gastric mucosa were examined by hematoxylin-eosin （HE） staining. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of pepsinogenⅠ （PGⅠ）， pepsinogenⅡ （PGⅡ）， and gastrin （G-17）， as well as the expression level of transforming growth factor-β1 （TGF-β1） in gastric mucosal tissue， and the PGⅠ/PGⅡ ratio was calculated. Immunohistochemistry （IHC） was used to detect the localization and expression levels of proliferating cell nuclear antigen （Ki-67） and Vimentin in gastric mucosal tissue. Western blot analysis was used to determine the protein expression levels of Wnt family member 3A （Wnt3a）， β-catenin， CyclinD1， proto-oncogene Cmyc， transforming growth factor-β receptor Ⅰ （TGFβRⅠ）， intracellular signaling transducers Smad2/3， phosphorylated （p）-Smad2/3， twist family transcription factor （Twist1）， and Vimentin in gastric mucosal tissue. ResultsCompared with the normal group， the model group showed characteristic changes including dim eyes， pale ears and claws， dark-red tongue， and reduced luster of the tail. The gastric mucosa appeared pale， with surface congestion and erosion. The gastric mucosal glands were disordered， the nuclear-to-cytoplasmic ratio increased， and local tumor cells were observed. Serum PGⅠ and PGⅡ levels and the PGⅠ/PGⅡ ratio were significantly decreased （P<0.01）， while the level of G-17 was significantly increased （P<0.01）. The protein expression levels of Ki-67， Wnt3a， β-catenin， CyclinD1， Cmyc， TGF-β1， TGFβRⅠ， Smad2/3， Twist1， and Vimentin in gastric mucosal tissue were significantly increased （P<0.05， P<0.01）， whereas the ratio of p-Smad2/3 to Smad2/3 was significantly decreased （P<0.05）. Compared with the model group， the general characteristics and gastric mucosal conditions of rats in the Moluodan group and the QZJW group were improved. HE staining showed that QZJW could effectively block the malignant progression of GIN. Serum PGⅠ and PGⅡ levels and the PGⅠ/PGⅡ ratio were significantly increased （P<0.05， P<0.01）， while the level of G-17 was significantly decreased （P<0.01）. The protein expression levels of Ki-67， Wnt3a， β-catenin， CyclinD1， Cmyc， TGF-β1， TGFβRⅠ， Smad2/3， Twist1， and Vimentin in gastric mucosal tissue were significantly decreased （P<0.05， P<0.01）. ConclusionQZJW have a therapeutic effect on rats with GIN. The mechanism may involve inhibition of the Wnt/β-catenin signaling pathway to regulate the cell cycle and suppress abnormal cell proliferation. Meanwhile， it may inhibit epithelial-mesenchymal transition by suppressing the TGF-β1/Smad/Twist1 signaling pathway， thereby blocking the malignant progression of GIN.
