deoxycholic-acid and Gastritis--Atrophic

deoxycholic-acid has been researched along with Gastritis--Atrophic* in 3 studies

Other Studies

3 other study(ies) available for deoxycholic-acid and Gastritis--Atrophic

ArticleYear
Regulation of gut microbiota of Astragali Radix in treating for chronic atrophic gastritis rats based on metabolomics coupled with 16S rRNA gene sequencing.
    Chemico-biological interactions, 2022, Sep-25, Volume: 365

    Astragali Radix (HQ), a common traditional Chinese medicine (TCM), is widely used to treat chronic atrophic gastritis (CAG). However, its mechanism in treating CAG is still not clear. Accumulating evidence highlights the link between gut microbiota and CAG. We hypothesized that the gut microbiota might be involved in the effect of HQ. Ultra-performance liquid chromatography coupled with time-of-flight mass spectrometry (UPLC-Q-TOF/MS) based metabolomics and 16S rRNA gene sequencing techniques of the cecal contents were applied to study its mechanisms. As a result, nine metabolites and fifteen gut microbiotas changed significantly in cecal contents samples between control group and model group. Among them, two metabolites (7-keto-3A ·12-α-hydroxyalkanoic acid and deoxycholic acid) and two gut microbiota genera (Acetobacter and Escherichia), had the most obvious callback effect after the administration of HQ. Sixty-seven correlated pairs exhibited the significant link between the involved metabolites and gut microbiotas through the correlation analysis, where two strong correlation pairs: Tetrahydrohydroxone ∼ Bacteroides (r = 0.895) and Deoxycholic acid ∼ Acetobacter (r = -0.843) were regulated by HQ. The results showed that HQ had the potential protection from metabolic perturbation involved into gut microbiotas induced by CAG. Two gut microbiotas, Acetobacter and Escherichia, and two metabolites, 7-keto-3A ·12-α-hydroxyalkanoic acid and deoxycholic acid were the potential targets of HQ.

    Topics: Animals; Deoxycholic Acid; Drugs, Chinese Herbal; Gastritis, Atrophic; Gastrointestinal Microbiome; Genes, rRNA; Metabolomics; Rats; RNA, Ribosomal, 16S

2022
Establishment of an animal model of chronic atrophic gastritis and a study on the factors inducing atrophy.
    Chinese medical journal, 2001, Volume: 114, Issue:12

    To establish a rat model of chronic atrophic gastritis and explore the factors inducing atrophy.. In accordance with repeated orthogonal design of L8(2(7)), 60% alcohol and 20 mmol/L sodium deoxycholate (served as factor A), 0.05%-0.1% ammonia water (factor B), 0.05% indomethacin (factor C) were given, alone or in combination, to rats in three experiments for 3 months, 6 months or 9 months respectively. Then the rats were dissected, and their pathologic changes of the gastric mucosa were assessed.. Typical signs of chronic atrophic gastritis (CAG) were found in all rats which were treated with factor A, B, C alone or in combination for 6 or 9 months. No significant difference of pathologic changes of gastric mucosa was found between the rats treated for 6 months and those for 9 months. No obvious CAG signs were found in the rats treated with factor A, B, C for 3 months.. Sixty percent of alcohol, 20 mmol/L sodium deoxycholate, 0.05%-0.1% ammonia water and 0.05% indomethacin given to Sprague-Dawley rats for 6 months can successfully establish the animal model of CAG. Prolongation of the model-establishment time is not able to further facilitate the atrophy of gastric mucosa.

    Topics: Ammonia; Animals; Atrophy; Deoxycholic Acid; Disease Models, Animal; Ethanol; Gastric Mucosa; Gastritis, Atrophic; Indomethacin; Male; Rats; Rats, Sprague-Dawley; Time Factors

2001
Antral mucosal bile acids in two types of chronic atrophic gastritis.
    The Tokai journal of experimental and clinical medicine, 1988, Volume: 13, Issue:1

    Bile acids may damage the gastric mucosa, and they are cocarcinogenic in experimental colonic and gastric cancer. Chronic atrophic gastritis (CAG) and chronic atrophic gastritis with intestinal metaplasia (CAGIM) are associated with gastric carcinoma. We, therefore, analysed bile acids in the antral mucosa in controls (n = 10), in patients with CAG (n = 12) and CAGIM (n = 20). In both forms of chronic antral gastritis, total mucosal bile acid concentrations drop, caused mainly by lower primary bile acids. The proportions of secondary bile acids rise, in particular of toxic lithocholic acid. This is probably caused by bacterial activity in the stomach. Whether secondary bile acids, especially lithocholic acid, alone or in combination with other bacterial degradation products, influence gastric carcinogenesis remains to be elucidated in further studies.

    Topics: Adult; Aged; Bile Acids and Salts; Chenodeoxycholic Acid; Cholic Acid; Cholic Acids; Deoxycholic Acid; Female; Gastric Mucosa; Gastritis; Gastritis, Atrophic; Humans; Intestines; Lithocholic Acid; Male; Metaplasia; Middle Aged; Pyloric Antrum; Stomach Neoplasms; Ursodeoxycholic Acid

1988