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Gallic acid prevents 1, 2-Dimethylhydrazine induced colon inflammation, toxicity, mucin depletion, and goblet cell disintegration.

Abstract
1,2-Dimethylhydrazine (DMH), an environmental toxicant specifically targets the colon. The present study was aimed to evaluate the efficacy of gallic acid (GA) against colon toxicity induced by DMH in Wistar rats. GA, a phenolic acid has numerous beneficial properties, which include antiviral, antifungal and antioxidant properties which help cells to overcome oxidative stress and balance the redox homeostasis. GA was administered orally at two doses (25 and 50 mg/kg body weight) once daily for 14 days and a single dose (40 mg/kg body weight) of DMH was administered subcutaneously on 14th day. Animals were sacrificed on the 15th day and we could find that GA at both the doses significantly ameliorates DMH-induced increased toxicity markers and also substantially increases the glutathione content level and activities of detoxifying enzymes. It also ameliorates the expression of proliferation, inflammation, apoptosis, goblet cell disintegration, and mucin depletion in the colon that was elevated upon administration of DMH. Histological alterations provide further confirmation of the protective role of GA against DMH-induced colon toxicity. The results of this study clearly indicate supplementation of GA is beneficial in ameliorating DMH-induced oxidative stress, inflammation, proliferation, apoptosis, mucin depletion, and goblet cell disintegration in colon of Wistar rats.
AuthorsAlpa Shree, Johirul Islam, Abul Vafa, Sheikh Mohammad Afzal, Sarwat Sultana
JournalEnvironmental toxicology (Environ Toxicol) Vol. 35 Issue 6 Pg. 652-664 (Jun 2020) ISSN: 1522-7278 [Electronic] United States
PMID31925992 (Publication Type: Journal Article)
Copyright© 2020 Wiley Periodicals, Inc.
Chemical References
  • Anti-Inflammatory Agents
  • Antioxidants
  • Mucins
  • Gallic Acid
  • Glutathione
  • 1,2-Dimethylhydrazine
Topics
  • 1,2-Dimethylhydrazine (toxicity)
  • Animals
  • Anti-Inflammatory Agents (toxicity)
  • Antioxidants (metabolism)
  • Apoptosis (drug effects)
  • Cell Proliferation (drug effects)
  • Dose-Response Relationship, Drug
  • Female
  • Gallic Acid (pharmacology)
  • Glutathione (metabolism)
  • Goblet Cells (drug effects, metabolism, pathology)
  • Inflammation
  • Mucins (metabolism)
  • Oxidative Stress (drug effects)
  • Rats
  • Rats, Wistar

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