ArticleAnnals of translational medicine2022
Jian-Pi-Yi-Qi-Fang ameliorates chronic atrophic gastritis in rats through promoting the proliferation and differentiation of gastric stem cells.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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8 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pharmacological mechanisms of traditional Chinese medicine in treating gastric cancer: a focus on the ferroptosis regulation.Frontiers in pharmacology · 2025Pooled it
- Chinese medicine boosts regenerative medicine in stem cell - based therapy.Stem cell research & therapy · 2025Review
- A web-based pharmacological approach to the mechanism of action of Radix Bupleuri in the treatment of chronic atrophic gastritis.Cytotechnology · 2025Article
- Investigation of c-Fos/c-Jun Signaling Pathways in Periostracum Cicadae's Inhibition of EMT in Gastric Tissue.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Traditional Chinese medicine for chronic atrophic gastritis: Efficacy, mechanisms and targets.World journal of gastroenterology · 2025Review
- Vitamin C Mediates IGFBP7 to Alleviate Chronic Atrophic Gastritis via the HIF-1α/VEGF Pathway.Journal of cellular and molecular medicine · 2025Article
- Research progress on the therapeutic effects of effective components of traditional Chinese medicine in the treatment of gastric cancer precursors through modulation of multiple signaling pathways.Frontiers in oncology · 2025Review
- Explore the active ingredients and potential mechanisms of JianPi QingRe HuaYu Methods in the treatment of gastric inflammation-cancer transformation by network pharmacology and experimental validation.BMC complementary medicine and therapies · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Jian-Pi-Yi-Qi-Fang (JPYQF) is a traditional Chinese medicine (TCM) herbal formula for treating chronic atrophic gastritis (CAG) in the clinic; however, its related mechanism remains unclear. The purpose of this study was to explore the potential mechanisms of JPYQF in treating CAG by examining proteins and genes related to the proliferation and differentiation of gastric stem cells and Wnt signaling. Methods: A CAG model was established in Sprague-Dawley (SD) rats which were induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and ranitidine. We randomly divided 25 CAG rats into 5 groups: the model group, positive drug group, low-dose group of JPYQF (JPYQF-L), middle-dose group of JPYQF (JPYQF-M), and high-dose group of JPYQF (JPYQF-H), with 5 rats of the same age classified into the control group. The body weight of rats was measured and their gastric morphology was visually assessed. Furthermore, pathological analysis of rat gastric tissue was performed. The expression levels of proteins and genes associated with the proliferation and differentiation of gastric stem cells and Wnt signaling were measured via immunohistochemistry and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Results: Compared with the model group, treatment with JPYQF increased the body weight of the rats, and relieved the gastric atrophy and inflammation. Compared with the control group, the protein and messenger RNA (mRNA) expression levels of gastric stem cell proliferation and differentiation markers Lgr5, Sox2, Ki67, PCNA, Muc5AC, and Wnt signaling initiator Wnt3A and enhancer R-spondin-1 (Rspo1) were decreased in the model group. Treatment with JPYQF increased the protein and mRNA expression levels of these markers. Conclusions: The Wnt signaling of CAG rats may be in a low activation state, which inhibits the proliferation and differentiation of gastric stem cells, so that gland cells cannot be replenished in time to repair the damaged gastric mucosa. The TCM formula JPYQF could enhance Wnt signaling to promote the restricted proliferation and normal differentiation of gastric stem cells, thereby improving gastric mucosal atrophy in CAG rats, which provides a novel and robust theoretical basis for CAG treatment.
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