Evidence map›Paper›PMID 39834822›Full record

ArticleFrontiers in pharmacology2024

Elucidation of the mechanism of berberine against gastric mucosa injury in a rat model with chronic atrophic gastritis based on a combined strategy of multi-omics and molecular biology.

Lisheng Chen, Xin Wang, Jianyu Li, Lijuan Zhang, Wenbin Wu, Shizhang Wei, Wenjun Zou, Yanling Zhao

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Lisheng ChenCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Xin WangCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Jianyu LiDepartment of Pharmacy, The Fifth Medical Center of Chinese PLA General Hospital, Beijing, China.
Lijuan ZhangDepartment of Pharmacy, The Fifth Medical Center of Chinese PLA General Hospital, Beijing, China.
Wenbin WuHealthcare Office of the Service Bureau of Agency for Offices Administration of the Central Military Commission, Beijing, China.
Shizhang WeiNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Wenjun ZouCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Yanling ZhaoCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Berberine (BBR) is widely used to treat gastrointestinal diseases. However, the pharmacological mechanism of action of BBR in anti-chronic atrophic gastritis (CAG) remains unclear. This study aimed to investigate the mechanism of action of BBR in CAG by integration of molecular biology and multi-omics studies strategy. Methods: The CAG model was established by alternating drinking water of 0.1% ammonia and 20 mmol/L sodium deoxycholate, accompanied by an irregular diet. Serum biochemical indices including PGI, PGII, GAS-17, IL-6, IL-1β, and TNF-α were analyzed. HE and AB-PAS staining were employed to assess pathological damage in gastric tissue. The underlying molecular mechanism of BBR in CAG treatment was explored via the integration of network pharmacology, transcriptomics, widely targeted metabolomics and intestinal flora analysis. Finally, relevant key targets and pathway were verified. Results: The results showed that BBR exerted therapeutic effects in improving CAG via alleviating inflammation response, maintaining the gastric mucosal barrier's integrity and repairing gastric mucosal tissues. Network pharmacology showed that the treatment of CAG by BBR mainly involved in inflammatory response, apoptosis, angiogenesis and metabolic processes. Furthermore, 234 different expression genes were identified in the gastric tissue transcriptome, which were mainly involved in biological processes such as cell adhesion, angiogenesis, apoptosis, cell migration and lipids metabolism by regulating the MAPK signaling pathway. Metabolomics results showed that 125 differential metabolites were also identified, while the pathways were mainly involved in D-glutamine and D-glutamate metabolism, and tyrosine metabolism, etc. Integrating transcriptomics and metabolomics analyses indicated that BBR directly regulated Carnitine C3:0, LPC (0:0/20:3), L-Glutamic Acid and FFA (15:0) by acting on SLC25A20, PNLIPRP1, PLA2G4C, GSR, GFPT2, GCLM, CTPS1, ACSL1, ACOT4 and ACOT2. 16S rRNA sequencing revealed that BBR could restore the balance of gut microbiota dysbiosis by significantly regulating the relative abundance of Conclusion: This study demonstrated that BBR alleviates CAG through the regulation of the MAPK signaling pathway, metabolic disorders and gut microbiota dysbiosis, thereby revealing the complex mechanism of BBR in relation to alleviating CAG from multiple levels and perspectives.

Indexed as

16S rRNA sequencingberberinechronic atrophic gastritistranscriptomicswidely targeted metabolomics

Identifiers

PMID39834822
PMCPMC11743660

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