4.7 Article

Zuojin Pill ameliorates chronic atrophic gastritis induced by MNNG through TGF-β1/PI3K/Akt axis

Journal

JOURNAL OF ETHNOPHARMACOLOGY
Volume 271, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2021.113893

Keywords

Chronic atrophic gastritis; Zuojin pill; Coptis chinensis; Tetradium ruticarpum; TGF-beta 1/PI3K/Akt; MNNG

Funding

  1. National Key Research and Development Program [2018YFC1704500]

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The study demonstrated that ZJP significantly improved GES-1 damage induced by MNNG and enhanced the gastric histomorphology of CAG rats. ZJP intervention reduced the content of G-17 and inflammatory factors IL-8, TNF-alpha, IL-6, and IL-1 beta, inhibited the expression of TGF-beta 1, PI3K, and downstream signals p-Akt, p-mTOR, P70S6K, while promoting the expression level of PTEN, LC3-II, and Beclin-1. These findings suggest that ZJP may have a therapeutic effect on CAG through the inhibition of the TGF-beta 1/PI3K/Akt signaling pathway.
Ethnopharmacological relevance: Zuojin Pill (ZJP) is a classic prescription composed of Coptis chinensis and Tetradium ruticarpum (A.Juss.) T.G.Hartley, which is often used in the treatment of digestive system diseases. Aim of this study: The purpose of this study was to explore the therapeutic effect and potential mechanism of ZJP on chronic atrophic gastritis (CAG) induced by MNNG. Materials and methods: The GES-1 and rat model of CAG was established by MNNG. Detection of cell viability, morphological changes and proliferation of GES-1 by CCK-8 and high content screening (HCS) assay. G-17, IL-8 and TNF-alpha in rat serum were detected by ELISA kit. The expression of related mRNA and protein on TGF-beta 1/PI3K/Akt signal axis were detected by RT-PCR and Western blot. Results: The results showed that ZJP could significantly improve the GES-1 damage induced by MNNG and improve the gastric histomorphology of CAG rats. The intervention of ZJP could significantly reduce the content of G-17 and inflammatory factors IL-8, TNF-alpha, IL-6 and IL-1 beta, inhibit the expression of TGF-beta 1, PI3K and their downstream signals p-Akt, p-mTOR, P70S6K, and promote the expression level of PTEN, LC3-II and Beclin-1. Conclusion: ZJP has a good therapeutic effect on CAG induced by MNNG, which may be closely related to the inhibition of TGF-beta 1/PI3K/Akt signal pathway.

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