ArticleAging2023
Modified Chaishao Liujunzi Decoction inhibits bile acid-induced gastric intestinal metaplasia: from network prediction to experimental verification.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Autophagy: Mechanisms and therapeutic perspectives in intestinal metaplasia (Review).Molecular medicine reports · 2026Review
- Bridging Traditions: Integrating TCM Into ERAS for Enhanced Gastrointestinal Recovery -A Scoping Review.Drug design, development and therapy · 2026Article
- KRT23 promotes proliferation invasion and metastasis of gastric cancer through epithelial-mesenchymal transition mediated by the PI3K/AKT/mTOR signaling pathway.Translational cancer research · 2025Article
- Combined detection of P53, Ki67, P504S, and IMP3: Diagnostic implications for gastric cancer and precursor lesions.World journal of gastrointestinal oncology · 2025Article
- Solamargine inhibits gastric cancer progression via inactivation of STAT3/PD‑L1 signaling.Molecular medicine reports · 2025Article
- Crosstalk between bile acids and gut microbiota: a potential target for precancerous lesions of gastric cancer.Frontiers in pharmacology · 2025Review
- Optimized therapeutic potential of Sijunzi-similar formulae for chronic atrophic gastritis via Bayesian network meta-analysis.EXCLI journal · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modified Chaishao Liujunzi Decoction (MCLD) is a traditional Chinese medicine formula that is used mainly to improve clinical symptoms, alleviate gastric mucosal inflammation, and improve gastric mucosal lesions in patients with gastric intestinal metaplasia (GIM). GIM is considered a precancerous gastric cancer (GC) lesion (PLGC) and exploring effective intervention measures for GIM is of great importance for the prevention of GC. The purpose of this study was to reveal the potential molecular mechanism of MCLD in improving GIM induced by bile acid (BA) using network pharmacology and experimental validation. Through network pharmacology, we speculated that MCLD could act on GIM by driving the epidermal growth factor receptor (EGFR)/PI3K/AKT/mammalian target of rapamycin (mTOR) pathway. After that, we used deoxycholic acid (DCA) to treat GES-1 cells to simulate BA-induced GIM and observed the effects of MCLD treatment. The results indicate that MCLD can significantly inhibit DCA-induced cell proliferation and down-regulate the expression of pro-inflammatory cytokines and intestinal-specific markers. At the same time, MCLD also negatively regulated the expression of genes and proteins of the EGFR/PI3K/AKT/mTOR pathway. Combination with EGFR agonists and inhibitors suggested that MCLD may improve GIM by inhibiting the EGFR/PI3K/AKT/mTOR pathway, which may be related to its inhibition of DCA-induced cell proliferation through this pathway. In conclusion, MCLD may improve BA-induced GIM through the EGFR/PI3K/AKT/mTOR pathway, as predicted by network pharmacology, and is a potential Chinese medicine prescription for the treatment or reversal of GIM.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.