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

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

Risultato della ricerca: Article

2 Citazioni (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.
Lingua originaleEnglish
pagine (da-a)865-877
Numero di pagine13
RivistaDefault journal
Volume31
Stato di pubblicazionePublished - 2017

All Science Journal Classification (ASJC) codes

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

Cita questo

Tea catechins induce crosstalk between signaling pathways and stabilize mast cells in ulcerative colitis. / Zeenny, Marie Noel; Bonaventura, Giuseppe; Rizzo, Manfredi; Leone, Angelo; Uzzo, Maria Laura; Spatola, Giovanni Francesco; Jurjus, Rosalyn; Leone, Angelo; Hajj Hussein; Spatola; Zeenny; Bonaventura, Giuseppe; Rizzo, Manfredi; Zgheib; Gerges Geagea, Alice; Eid; Uzzo; Massaad-Massade; Jurjus.

In: Default journal, Vol. 31, 2017, pag. 865-877.

Risultato della ricerca: Article

Zeenny, MN, Bonaventura, G, Rizzo, M, Leone, A, Uzzo, ML, Spatola, GF, Jurjus, R, Leone, A, Hajj Hussein, Spatola, Zeenny, Bonaventura, G, Rizzo, M, Zgheib, Gerges Geagea, A, Eid, Uzzo, Massaad-Massade & Jurjus 2017, 'Tea catechins induce crosstalk between signaling pathways and stabilize mast cells in ulcerative colitis', Default journal, vol. 31, pagg. 865-877.
Zeenny, Marie Noel ; Bonaventura, Giuseppe ; Rizzo, Manfredi ; Leone, Angelo ; Uzzo, Maria Laura ; Spatola, Giovanni Francesco ; Jurjus, Rosalyn ; Leone, Angelo ; Hajj Hussein ; Spatola ; Zeenny ; Bonaventura, Giuseppe ; Rizzo, Manfredi ; Zgheib ; Gerges Geagea, Alice ; Eid ; Uzzo ; Massaad-Massade ; Jurjus. / Tea catechins induce crosstalk between signaling pathways and stabilize mast cells in ulcerative colitis. In: Default journal. 2017 ; Vol. 31. pagg. 865-877.
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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.",
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AU - Zeenny, Marie Noel

AU - Bonaventura, Giuseppe

AU - Rizzo, Manfredi

AU - Leone, Angelo

AU - Uzzo, Maria Laura

AU - Spatola, Giovanni Francesco

AU - Jurjus, Rosalyn

AU - Leone, Angelo

AU - Hajj Hussein, null

AU - Spatola, null

AU - Zeenny, null

AU - Bonaventura, Giuseppe

AU - Rizzo, Manfredi

AU - Zgheib, null

AU - Gerges Geagea, Alice

AU - Eid, null

AU - Uzzo, null

AU - Massaad-Massade, null

AU - Jurjus, null

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

KW - Diabetes and Metabolism; Immunology and Allergy; Physiology; Immunology; Oncology; Endocrinology; Physiology (medical); Cancer Research

KW - Endocrinology

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SP - 865

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JO - Default journal

JF - Default journal

ER -