Effects of Eugenol and Dehydrodieugenol B from Nectandra leucantha against Lipopolysaccharide (LPS)-Induced Experimental Acute Lung Inflammation

Acute lung injury (ALI) is an important public health problem. The present work investigated whether dehydrodieugenol B treatment, a compound isolated from Brazilian plant (Lauraceae), modulates experimental ALI and compared the observed effects to eugenol. Effects of dehydrodieugenol B in lipopolys...

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Bibliographic Details
Published in:Journal of natural products (Washington, D.C.) D.C.), 2021-08, Vol.84 (8), p.2282-2294
Main Authors: Bittencourt-Mernak, Márcia I, Pinheiro, Nathalia M, da Silva, Rafael C, Ponci, Vitor, Banzato, Rosana, Pinheiro, Aruanã J M C R, Olivo, Clarice R, Tibério, Iolanda F L C, Lima Neto, Lídio G, Santana, Fernanda P R, Lago, João H G, Prado, Carla M
Format: Article
Language:English
Subjects:
Acute Lung Injury - chemically induced
Acute Lung Injury - drug therapy
Animals
Anisoles - pharmacology
Brazil
Eugenol - pharmacology
Lauraceae - chemistry
Lipopolysaccharides
Male
Mice
Mice, Inbred BALB C
Phytochemicals - pharmacology
Plant Leaves - chemistry
Pneumonia - chemically induced
Pneumonia - drug therapy
RAW 264.7 Cells
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Summary:Acute lung injury (ALI) is an important public health problem. The present work investigated whether dehydrodieugenol B treatment, a compound isolated from Brazilian plant (Lauraceae), modulates experimental ALI and compared the observed effects to eugenol. Effects of dehydrodieugenol B in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells were evaluated. The lung and systemic inflammatory profile, lung function, and possible mechanisms involved in BALB/C male mice (6-8 weeks) with ALI induced by LPS instillation (5 mg/kg) was assayed. Dehydrodieugenol B did not affect the cell viability and inhibited the increase in NO release and IL-1β and IL-6 gene expression induced by LPS. , both compounds reduced lung edema, inflammatory cells, and the IL-6 and IL-1 β levels in bronchoalveolar lavage fluid, as well as reduced inflammatory cell infiltration and those positive to iNOS, MMP-9, and TIMP-1, and reduced the collagen content and the 8-isoprostane expression in lung tissue. Eugenol and dehydrodieugenol B also inhibited the phosphorylation of Jc-Jun-NH2 terminal Kinase (JNK), a signaling protein involved in the MAPKinase pathway. There was no effect of these compounds in lung function. Therefore, eugenol and dehydrodieugenol B ameliorates several features of experimental ALI and could be considered as a pharmacological tool to ameliorate acute lung inflammation.
ISSN:0163-3864
1520-6025
DOI:10.1021/acs.jnatprod.1c00386