Gallic Acid Alleviates Injury of Intestine Induced by Escherichia Coli: Protective Role of Metalloproteinase and Antioxidants on Small Intestine In-vivo
Gallic Acid Effects on Escherichia Coli Induced Intestine Injury
DOI:
https://doi.org/10.31661/gmj.v13i.3375Keywords:
Escherichia coli; Gallic acid; anti-inflammatory; antioxidant; MetalloproteinaseAbstract
Background: Escherichia coli (E. coli) is a common pathogen that can cause significant morbidity and mortality in hospitalized patients. The aim of this study was to investigate the effects of gallic acid (GA) on a mice infected with of E. coli enteritis and evaluate the serum levels of interleukin-6 (IL-6) and matrix metalloproteinase (MMP)-9, as well as any histopathological changes before and after exposure. Materials and Methods: Forty Swiss male mice were divided into four groups: Group I (negative control), Group II (received oral GA, 80 mg/kg/b.wt), Group III (orally inoculated with E. coli, 1×107 CFU, for four days), and Group IV (received oral GA, 80 mg/kg/b.wt, for 10 days after E. coli inoculation). Serum was collected to assess IL-6 and MMP-9 levels. Intestinal samples were examined for antioxidant parameters, including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase. Histopathology and immunohistochemistry were performed. Results: Group III exhibited significantly higher IL-6 and MMP-9 levels compared to the other groups (P<0.001). Antioxidant activity in the intestine, measured by SOD and GSH-Px, was lower in Group III compared to Group I. Conversely, Group IV showed significant improvements in biochemical, histopathological, and immunohistochemical outcomes, alongside reduced intestinal damage caused by E. coli. Conclusion: This study demonstrates that E. coli infection in mice increases IL-6 and MMP-9 levels while decreasing intestinal antioxidants. Concurrent administration of GA significantly improves outcomes, suggesting its potential as a therapeutic remedy for E. coli-induced intestinal damage. Furthers research is imperative to determine the underlying pathways by which GA exerts its beneficial outcomes.
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