Gamma-Terpinene, inhibits P38 and NFκB signaling pathway by supressing of TLR4 in a murine model of acute lung injure

Introduction. Gamma-terpinene (GT) is a component of essential oil classified as monoterpene of several plants. This molecule presents anti-inflammatory property. Objectives. The aim of this study was to investigate the mechanism of action of GT in acute lung injury (ALI) experimental model. Methods. For this purpose, lipopolysaccharide (LPS)-challenged BALB/c mice were treated with GT50 (50 mg/kg) one, 24 and 48 hours after the LPS-challenge. The inflammatory cell migration and cytokine production were measured in the fluid of bronchoalveolar lavage (BALF), cellular infiltration and mucus content were analyzed in the lung tissue and the p38/NFκB(p65) signaling pathway was analyzed in the BALF cells. Results. GT50 treatment inhibited inflammatory cell migration to the lung cavity as well as to the alveolar-capillary region. The treatment reduced the lung edema by decreasing protein content on the lung cavity as well as the lung wet/dry weight ratio. In addition, the GT50 treatment reduced IL-1β, IL-6 and TNF-α production and, the mechanism of action of the GT was by decreasing the TLR4 expression and p38 kinase and NFκB(p65) activities. Conclusion. These results indicate that the essential oil, gamma-terpinene, is a potential molecule to be tested in a clinical trial to prevent lung injury in acute lung injure syndrome.

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Journal
Brazilian Journal of Health Review
Published
2025-05-26
DOI
https://doi.org/10.34119/bjhrv8n3-145
Primary Topic
Immune Response and Inflammation
Type
article
Field-Weighted Citation Impact
0.00

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article

Gamma-Terpinene, inhibits P38 and NFκB signaling pathway by supressing of TLR4 in a murine model of acute lung injure

Laércia Karla Diega Paiva Ferreira, Francisco Allysson Assis Ferreira Gadelha, Márcia Regina Piuvezam, Raquel Fragoso Pereira Cavalcanti et al.
Brazilian Journal of Health Review
Immune Response and Inflammation
article

Gamma-Terpinene, inhibits P38 and NFκB signaling pathway by supressing of TLR4 in a murine model of acute lung injure

Laércia Karla Diega Paiva Ferreira, Francisco Allysson Assis Ferreira Gadelha, Márcia Regina Piuvezam, Raquel Fragoso Pereira Cavalcanti, Larissa Adilis Maria Paiva Ferreira, Talissa Mozzini Monteiro
article en

Abstract

Introduction. Gamma-terpinene (GT) is a component of essential oil classified as monoterpene of several plants. This molecule presents anti-inflammatory property. Objectives. The aim of this study was to investigate the mechanism of action of GT in acute lung injury (ALI) experimental model. Methods. For this purpose, lipopolysaccharide (LPS)-challenged BALB/c mice were treated with GT50 (50 mg/kg) one, 24 and 48 hours after the LPS-challenge. The inflammatory cell migration and cytokine production were measured in the fluid of bronchoalveolar lavage (BALF), cellular infiltration and mucus content were analyzed in the lung tissue and the p38/NFκB(p65) signaling pathway was analyzed in the BALF cells. Results. GT50 treatment inhibited inflammatory cell migration to the lung cavity as well as to the alveolar-capillary region. The treatment reduced the lung edema by decreasing protein content on the lung cavity as well as the lung wet/dry weight ratio. In addition, the GT50 treatment reduced IL-1β, IL-6 and TNF-α production and, the mechanism of action of the GT was by decreasing the TLR4 expression and p38 kinase and NFκB(p65) activities. Conclusion. These results indicate that the essential oil, gamma-terpinene, is a potential molecule to be tested in a clinical trial to prevent lung injury in acute lung injure syndrome.

Brazilian Journal of Health ReviewVol. 8(3)
Universidade Federal da Paraíba (BR), Software (Spain) (ES)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, Conselho Nacional de Desenvolvimento Científico e Tecnológico, Universidade Federal de Alagoas, Universidade Federal da Paraíba, Pró-Reitoria de Pesquisa, Universidade Federal do Rio Grande do Sul
Openalex Percentile: Top 87%
Immune Response and Inflammation
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