Molecular nutrition & food research · 2025
Protective Effect of Piperine on Indomethacin-Induced Intestinal Damage.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Gervasoni Karine Nader, Iacia Maria Vitória Minzoni De Souza, Silva Kimberlly De Oliveira, Franco Letícia Gervasoni, Mendes Maria Eduarda Ferraz, Neves Thiago José Da Cruz, Sanches William Silva, Oliveira Lívia Batista, Saito Ellen Almeida, Vieira Karolinny Cristiny De Oliveira, Pereira Valéria Cataneli, Nai Gisele Alborghetti, Winkelstroter Lizziane Kretli
Аннотация
Nonsteroidal antiinflammatory drugs (NSAIDs) are widely prescribed for the treatment of inflammation and chronic pain. Chronic use of NSAIDs is associated with adverse events and organ damage, especially to the gastric mucosa and small intestine. This study evaluates the protective effect of piperine on indomethacin-induced intestinal damage. Eighteen male Mus musculus mice, aged 6-8 weeks, were used. Intestinal damage was induced with indomethacin (10 mg/mL) and cotreatment with piperine (20 mg/mL), both administered orally. After 14 days, the animals were euthanized. Biochemical serological analysis was performed. Intestinal inflammation was assessed based on macroscopic, histopathological, and metagenomic analyses. Histopathological analysis showed a reduction in small intestine inflammation (p < 0.05) and the disappearance of necrosis in the intestinal wall of the large intestine. Crypt and villus measurements showed increased values in the piperine-treated group (p < 0.05). An approximately six-fold increase in aspartate aminotransferase (AST) was observed in the Indomethacin group (p < 0.05). Regarding the intestinal microbiota, an increase in genus diversity was observed in the piperine-treated group (p < 0.05). There was a 50% reduction in micronucleus formation with the administration of piperine 20 mg/kg (p < 0.05). It was concluded that cotreatment with piperine has great potential in mitigating the side effects caused by NSAIDs.