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Royal Jelly and its dual role in TNBS colitis in mice.

Abstract
Royal Jelly (RJ) is widely consumed in diets throughout the world due to its beneficial effects: antioxidant, antitumor and anti-inflammatory. We have investigated the role of RJ in the development of TNBS colitis in mice. Colitis was induced by a rectal instillation of TNBS at 0.1 mL per mouse. Intestine samples of the animals orally treated with RJ (100, 150, and 200 mg/kg) were collected for antioxidant assays (GSH and GSH-Px), proinflammatory protein quantification (COX-2 and NF-κB), and histological analyses. RJ 100 mg/kg maintained GSH levels and increased the activity of GSH-Px, downregulated key inflammatory mediators (COX-2 and NF-κB), and decreased the lesions caused by TNBS as shown by the histological analyses. In conclusion, RJ showed anti-inflammatory and antioxidant properties in experimental colitis, resulting in the amelioration of the macroscopic and histological analyses. These results corroborate with the RJ supplementation in diets.
AuthorsLuis Paulo Manzo, Felipe Meira de-Faria, Ricardo José Dunder, Eduardo Augusto Rabelo-Socca, Silvio Roberto Consonni, Ana Cristina Alves de Almeida, Alba Regina Monteiro Souza-Brito, Anderson Luiz-Ferreira
JournalTheScientificWorldJournal (ScientificWorldJournal) Vol. 2015 Pg. 956235 ( 2015) ISSN: 1537-744X [Electronic] United States
PMID25821860 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Anti-Inflammatory Agents
  • Antioxidants
  • Fatty Acids
  • NF-kappa B
  • Trinitrobenzenesulfonic Acid
  • Glutathione Peroxidase
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • Glutathione
  • royal jelly
Topics
  • Animals
  • Anti-Inflammatory Agents (therapeutic use)
  • Antioxidants (metabolism, therapeutic use)
  • Colitis (diet therapy, metabolism, pathology)
  • Cyclooxygenase 2 (metabolism)
  • Disease Models, Animal
  • Fatty Acids (therapeutic use)
  • Female
  • Functional Food
  • Glutathione (metabolism)
  • Glutathione Peroxidase (metabolism)
  • Humans
  • Mice
  • NF-kappa B (metabolism)
  • Trinitrobenzenesulfonic Acid (toxicity)

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