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Metabolites
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Exploring Innovations in Secondary Metabolites and Their Effects on Pain,...
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Exploring Innovations in Secondary Metabolites and Their Effects on Pain, Inflammation and Metabolic Syndrome

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Plant Metabolism".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 150

Special Issue Editors

Prof. Dr. Raquel Cariño-Cortés

E-Mail Website
Guest Editor
Academic Area of Medicine, Institute of Health Sciences, Autonomous University of the State of Hidalgo, Eliseo Ramírez Ulloa 400, Doctores Pachuca, Pachuca 42090, Mexico
Interests: secondary metabolites; pain; inflammation; chronic-degenerative diseases
Prof. Dr. Mario Ortiz

E-Mail Website
Guest Editor
Área Académica de Medicina del Instituto de Ciencias de la Salud, Universidad Autónoma del Estado de Hidalgo, Pachuca, México
Interests: obstetrics and gynecology

Special Issue Information

Dear Colleagues,

Metabolic syndrome remains a global public health challenge, affecting millions and serving as a critical driver of cardiovascular diseases, hypertension, type 2 diabetes, obesity, and other metabolic complications. Within this context, secondary metabolites, both natural and those derived from chemical synthesis, have emerged as promising therapeutic agents due to their antioxidant, anti-inflammatory, and metabolic regulatory properties. While all secondary metabolites originate from nature, chemical synthesis allows for their large-scale production or the generation of structural analogues. This Special Issue aims to highlight groundbreaking research on the pathophysiological mechanisms underlying pain and inflammation, with a particular emphasis on key biomarkers involved in hypertension, diabetes, obesity, and related complications. We welcome contributions from researchers worldwide, including original research articles, critical reviews, and preclinical or clinical studies that explore the role of secondary metabolites in addressing these pressing health concerns. We encourage you to take this opportunity to contribute to a multidisciplinary and impactful understanding of metabolic syndrome and its potential solutions. We look forward to receiving your submissions.

Prof. Dr. Raquel Cariño-Cortés
Prof. Dr. Mario Ortiz
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • secondary metabolites
  • pain
  • inflammation
  • chronic-degenerative diseases
  • chemoprevention
  • metabolic syndrome
  • plants

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Published Papers (1 paper)

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Research

17 pages, 1679 KiB  
Article
Peripheral Antinociception Induced by Carvacrol in the Formalin Test Involves the Opioid Receptor-NO-cGMP-K+ Channel Pathway
by Mario I. Ortiz, Raquel Cariño-Cortés, Eduardo Fernández-Martínez, Victor Manuel Muñoz-Pérez, Gilberto Castañeda-Hernández and Martha Patricia González-García
Metabolites 2025, 15(5), 314; https://doi.org/10.3390/metabo15050314 - 7 May 2025
Viewed by 66
Abstract
Background/Objectives: Carvacrol is a naturally occurring phenolic monoterpene that is one of the main constituents of the essential oils of oregano (Origanum vulgare) and other herbs. Carvacrol has anti-inflammatory and antinociceptive effects. Carvacrol can activate and inhibit several second messengers and [...] Read more.
Background/Objectives: Carvacrol is a naturally occurring phenolic monoterpene that is one of the main constituents of the essential oils of oregano (Origanum vulgare) and other herbs. Carvacrol has anti-inflammatory and antinociceptive effects. Carvacrol can activate and inhibit several second messengers and ionic channels at the systemic level. However, there is no evidence of the peripheral antinociception of carvacrol and its mechanism of action. This study was designed to determine whether the opioid receptor-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP)-K+ channel pathway is involved in the local antinociception of carvacrol. Methods: Wistar rats were injected with 1% formalin subcutaneously on the dorsal surface of the right hind paw with the vehicle or carvacrol (100–300 µg/paw). To determine whether the opioid receptor-NO-cGMP-K+ channel pathway and a biguanide-dependent mechanism are responsible for the local antinociception induced by carvacrol, the effect of the injection (10 min before the 1% formalin injection) with the corresponding vehicles, metformin, naltrexone, NG-L-nitro-arginine methyl ester (L-NAME), 1 H-(1,2,4)-oxadiazolo (4,2-a) quinoxalin-1-one (ODQ), and K+ channel blockers on the antinociception induced by local carvacrol (300 µg/paw) was determined. Results: In both phases of the formalin test, carvacrol produced antinociception. Naltrexone, metformin, L-NAME, ODQ, glibenclamide and glipizide (both ATP-sensitive K+ channel blockers), tetraethylammonium and 4-aminopyridine (voltage-gated K+ channel blockers), and apamin and charybdotoxin (Ca2+-activated K+ channel blockers) reversed the carvacrol-induced peripheral antinociception. Conclusions: The local peripheral administration of carvacrol produced significant antinociception and activated the opioid receptor-NO-cGMP-K+ channel pathway. Full article
(This article belongs to the Special Issue Exploring Innovations in Secondary Metabolites and Their Effects on Pain, Inflammation and Metabolic Syndrome)
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