Use of Saccharomyces boulardii CNCM I-745 as therapeutic strategy for prevention of nonsteroidal anti-inflammatory drug-induced intestinal injury.


Journal

British journal of pharmacology
ISSN: 1476-5381
Titre abrégé: Br J Pharmacol
Pays: England
ID NLM: 7502536

Informations de publication

Date de publication:
12 2023
Historique:
revised: 21 02 2023
received: 16 09 2022
accepted: 28 03 2023
medline: 24 11 2023
pubmed: 31 7 2023
entrez: 31 7 2023
Statut: ppublish

Résumé

Nonsteroidal anti-inflammatory drugs (NSAIDs) can be associated with severe adverse digestive effects. This study examined the protective effects of the probiotic Saccharomyces boulardii CNCM I-745 in a rat model of diclofenac-induced enteropathy. Enteropathy was induced in 40-week-old male rats by intragastric diclofenac (4 mg·kg Diclofenac elicited intestinal damage, along with increments of myeloperoxidase, malondialdehyde, tumour necrosis factor and interleukin-1β, overexpression of TLR2/4, myeloid differentiation primary response 88 (Myd88) and NF-κB p65, increased faecal calprotectin and butyrate levels, and decreased blood haemoglobin levels, occludin and butyrate transporter monocarboxylate transporter 1 (MCT1) expression. In addition, diclofenac provoked a shift of bacterial taxa in both faecal and ileal samples. Treatment with S. boulardii CNCM I-745, in both preventive and curative protocols, counteracted the majority of these deleterious changes. Only preventive administration of the probiotic counteracted NSAID-induced decreased expression of MCT1 and increase in faecal butyrate levels. Occludin expression, after probiotic treatment, did not significantly change. Treatment with S. boulardii CNCM I-745 prevents diclofenac-induced enteropathy through anti-inflammatory and antioxidant activities. Such effects are likely to be related to increased tissue butyrate bioavailability, through an improvement of butyrate uptake by the enteric mucosa.

Sections du résumé

BACKGROUND AND PURPOSE
Nonsteroidal anti-inflammatory drugs (NSAIDs) can be associated with severe adverse digestive effects. This study examined the protective effects of the probiotic Saccharomyces boulardii CNCM I-745 in a rat model of diclofenac-induced enteropathy.
EXPERIMENTAL APPROACH
Enteropathy was induced in 40-week-old male rats by intragastric diclofenac (4 mg·kg
KEY RESULTS
Diclofenac elicited intestinal damage, along with increments of myeloperoxidase, malondialdehyde, tumour necrosis factor and interleukin-1β, overexpression of TLR2/4, myeloid differentiation primary response 88 (Myd88) and NF-κB p65, increased faecal calprotectin and butyrate levels, and decreased blood haemoglobin levels, occludin and butyrate transporter monocarboxylate transporter 1 (MCT1) expression. In addition, diclofenac provoked a shift of bacterial taxa in both faecal and ileal samples. Treatment with S. boulardii CNCM I-745, in both preventive and curative protocols, counteracted the majority of these deleterious changes. Only preventive administration of the probiotic counteracted NSAID-induced decreased expression of MCT1 and increase in faecal butyrate levels. Occludin expression, after probiotic treatment, did not significantly change.
CONCLUSIONS AND IMPLICATIONS
Treatment with S. boulardii CNCM I-745 prevents diclofenac-induced enteropathy through anti-inflammatory and antioxidant activities. Such effects are likely to be related to increased tissue butyrate bioavailability, through an improvement of butyrate uptake by the enteric mucosa.

Identifiants

pubmed: 37519261
doi: 10.1111/bph.16200
doi:

Substances chimiques

Diclofenac 144O8QL0L1
NF-kappa B 0
Occludin 0
Anti-Inflammatory Agents, Non-Steroidal 0
Butyrates 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3215-3233

Informations de copyright

© 2023 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.

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Auteurs

Vanessa D'Antongiovanni (V)

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Luca Antonioli (L)

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Laura Benvenuti (L)

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Carolina Pellegrini (C)

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Clelia Di Salvo (C)

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Marco Calvigioni (M)

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

Adelaide Panattoni (A)

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

Larisa Ryskalin (L)

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

Gianfranco Natale (G)

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

Sebastiano Banni (S)

Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy.

Gianfranca Carta (G)

Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy.

Emilia Ghelardi (E)

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

Matteo Fornai (M)

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

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