Ozone Exposure Controls Oxidative Stress and the Inflammatory Process of Hepatocytes in Murine Models

Author:

Pelinsari Silvania Mol1,Sarandy Mariáurea Matias12,Vilela Emerson Ferreira3,Novaes Rômulo Dias45,Schlamb Jade2,Gonçalves Reggiani Vilela15

Affiliation:

1. Departament of General Biology, Federal University of Viçosa, Viçosa 36570-900, MG, Brazil

2. Plants for Human Health Institute, North Carolina Research Campus, North Carolina State University, Kannapolis, NC 28081, USA

3. Agriculture and Livestock Research Enterprise of Minas Gerais (EPAMIG-Sudeste), Viçosa 36570-000, MG, Brazil

4. Departament of Structural Biology, Federal University of Alfenas, Alfenas 37130-001, MG, Brazil

5. Departament of Animal Biology, Federal University of Viçosa, Viçosa 36570-900, MG, Brazil

Abstract

(1) Background: Ozone exposure is a promising tool for treating liver damage since it is known to control the release of free radicals and increase the expression of antioxidant enzymes. The objective is to investigate the main intracellular pathways activated after exposure to ozone, considering the dosage of antioxidant enzymes and markers of oxidative stress. (2) Methods: This systematic review was performed based on the PRISMA guidelines and using a structured search in MEDLINE (PubMed), Scopus, and Web of Science. Bias analysis and methodological quality assessments were examined using the SYRCLE Risk of Bias tool. (3) Results: Nineteen studies were selected. The results showed that the exposure to ozone has a protective effect on liver tissue, promoting a decrease in inflammatory markers and a reduction in oxidative stress in liver tissue. In addition, ozone exposure also promoted an increase in antioxidant enzymes. The morphological consequences of controlling these intracellular pathways were reducing the tissue inflammatory process and reducing areas of degeneration and necrosis. (4) Conclusions: Ozone exposure has a beneficial effect on models of liver injury through the decrease in oxidative stress in tissue and inflammatory markers. In addition, it regulates the Nrf2/ARE antioxidant pathway and blocks the NF-κB inflammatory pathway.

Funder

Fundação do Amparo à Pesquisa do Estado de Minas Gerais

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior—Brasil

Publisher

MDPI AG

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