Evaluation of the beneficial effects of a GABA-based product containing

GABA Melissa officinalis abdominal pain colitis irritable bowel syndrome

Journal

Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923

Informations de publication

Date de publication:
2024
Historique:
received: 18 07 2024
accepted: 02 09 2024
medline: 7 10 2024
pubmed: 7 10 2024
entrez: 7 10 2024
Statut: epublish

Résumé

Visceral pain represents the most common digestive issue, frequently resulting from long-term inflammation, such as inflammatory bowel diseases. The lack of effective drugs prompted search of new therapeutic approaches. In this regard, gamma-aminobutyric acid (GABA) and Colitis was induced in rats by intrarectal 2,4-dinitrobenzenesulfonic acid (DNBS) administration. DNBS-treated animals received GABA-Mo (80 mg/kg BID), starting 3 days before DNBS administration, until 14 days after colitis induction (preventive protocol), or starting 7 days after DNBS until day 21 (curative protocol). Visceral pain was assessed by measuring the viscero-motor response (VMR) and the abdominal withdrawal reflex (AWR) to colorectal distension on day 7, 14 (both protocols) and 21 (curative protocol) after DNBS administration. In the preventive protocol, GABA-Mo reduced AWR at day 14 but had no effect on VMR. In the spinal cord, treatment with GABA-Mo significantly prevented microglia reactivity (Iba-1 positive cells). In the colon, the supplement significantly decreased malondialdehyde (MDA, index of oxidative stress) and IL-1β levels and counteracted the decreased expression of claudin-1. Moreover, GABA-Mo normalized the increased levels of plasma lipopolysaccharide binding protein (LBP, index of altered intestinal permeability). In the curative protocol, GABA-Mo significantly counteracted visceral hypersensitivity persistence in DNBS-treated animals (day 14 and 21). In the spinal cord, GABA-Mo significantly reduced GFAP positive cell density (astrocytes). Histological evaluations highlighted a mild but significant effect of GABA-Mo in promoting healing from DNBS-induced colon damage. Colonic MDA and myeloperoxidase (index of leukocyte infiltration) levels were reduced, while the decreased colonic claudin-1 expression was normalized. In addition, the increased levels of plasma LBP were normalized by GABA-Mo administration. In conclusion GABA-Mo, particularly in the curative protocol, was able to reduce visceral pain and intestinal inflammation, likely through a reinforcement of intestinal barrier integrity, thus representing a suitable approach for the management of abdominal pain, especially in the remission stages of colitis.

Identifiants

pubmed: 39372212
doi: 10.3389/fphar.2024.1466824
pii: 1466824
pmc: PMC11449869
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1466824

Informations de copyright

Copyright © 2024 Lucarini, Benvenuti, Di Salvo, D’Antongiovanni, Pellegrini, Valdiserra, Ciampi, Antonioli, Lambiase, Cancelli, Grosso, Di Cesare Mannelli, Bellini, Ghelardini and Fornai.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Auteurs

Elena Lucarini (E)

Pharmacology and Toxicology Section, Department of Neuroscience, Psychology, Drug Research and Child Health, Neurofarba, University of Florence, Florence, Italy.

Laura Benvenuti (L)

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.

Vanessa D'Antongiovanni (V)

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.

Giulia Valdiserra (G)

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

Clara Ciampi (C)

Pharmacology and Toxicology Section, Department of Neuroscience, Psychology, Drug Research and Child Health, Neurofarba, University of Florence, Florence, Italy.

Luca Antonioli (L)

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

Christian Lambiase (C)

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

Lorenzo Cancelli (L)

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

Antonio Grosso (A)

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

Lorenzo Di Cesare Mannelli (L)

Pharmacology and Toxicology Section, Department of Neuroscience, Psychology, Drug Research and Child Health, Neurofarba, University of Florence, Florence, Italy.

Massimo Bellini (M)

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

Carla Ghelardini (C)

Pharmacology and Toxicology Section, Department of Neuroscience, Psychology, Drug Research and Child Health, Neurofarba, University of Florence, Florence, Italy.

Matteo Fornai (M)

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

Classifications MeSH