Tea catechins induce crosstalk between signaling pathways and stabilize mast cells in ulcerative colitis

Giuseppe Bonaventura, Marie Noel Zeenny, Maria Laura Uzzo, Manfredi Rizzo, Angelo Leone, Giovanni Francesco Spatola, Rosalyn Jurjus, Angelo Leone, Assad Eid, Hajj Hussein, Spatola, Zeenny, Giuseppe Bonaventura, Manfredi Rizzo, Zgheib, Alice Gerges Geagea, Eid, Eid, Uzzo, Massaad-MassadeJurjus, Manfredi Rizzo

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

It is well documented that nutraceuticals, in general, and Green tea catechins, in particular, possess a potential therapeutic value in inflammatory bowel diseases (IBD) due to their anti-oxidative and anti-inflammatory effects. This study aimed to investigate the possible mechanism of action of catechins in a rat model of colitis induced by 2.4.6 trinitrobenzene sulfonic acid (TNBS). Thirty-five young adult Sprague-Dawley rats were divided into four groups: normal control (n=5), catechins (n=9), TNBS (n=9) and TNBS plus catechins (n=12) treated. Catechin in the form of Epigallocatechin-3-gallate (EGCG) was administered daily by intraperitoneal injection, 1 week before the induction date of UC. Biopsies of the descending colon were collected on days 3, 10 and 17, and partly frozen for molecular studies or fixed for light microscopy. The status of intestinal tissue alterations and mast cells number were also assessed, as well as the mRNA expressions of IL-6, TNF-a and NF-kB, and determination of ROS expression. Histological data depicted a significant amelioration in the TNBS- and EGCG-treated rats compared to the non-treated animals. Catechin expressed strong anti-inflammatory and anti-oxidant effects, ameliorated ulcerative colitis and stabilized mast cells. The mechanism of action occurred basically through the NF-kB pathway and possibly through a crosstalk with other pathways.
Original languageEnglish
Pages (from-to)865-877
Number of pages13
JournalJOURNAL OF BIOLOGICAL REGULATORS & HOMEOSTATIC AGENTS
Volume31
Publication statusPublished - 2017

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Immunology and Allergy
  • Physiology
  • Immunology
  • Oncology
  • Endocrinology
  • Physiology (medical)
  • Cancer Research

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