Essential oil from Chimonanthus nitens Oliv. Leaves ameliorate inflammation and oxidative stress in LPS-induced ALI through NF-κB and Nrf2 signaling pathways.

J Ethnopharmacol

Jiangxi University of Chinese Medicine, Jiangxi, 330004, China; State Key Laboratory for the Modernization of Classical and Famous Prescriptions of Chinese Medicine, Jiangxi, 330004, China. Electronic address:

Published: October 2024

AI Article Synopsis

  • The essential oil from Chimonanthus nitens Oliv. leaves (CLO) has shown promise in reducing inflammation and repairing lung injury in a mouse model of Acute Lung Injury (ALI), although its exact mechanisms are still unclear.
  • The study aims to validate CLO's effects on ALI and investigate the underlying mechanisms, using established cell and animal models induced by lipopolysaccharide (LPS).
  • Results demonstrated that CLO significantly lowered inflammatory cytokine levels, oxidative stress markers, and structural damage in lung tissues, suggesting that its therapeutic effects may involve the NF-κB and Nrf2 signaling pathways, revealing potential for pharmacological treatment of ALI.

Article Abstract

Ethnopharmacological Relevance: Initial investigative research indicated that the essential oil from Chimonanthus nitens Oliv. Leaves (CLO) significantly reduces lung tissues inflammation and effectively repairs Acute lung injury (ALI) mice model. However, the mechanism underlying is not clear, and the impacts of CLO on oxidative stress require further investigation.

Aim Of The Study: The purpose of the experiment was to validate the influence of CLO in ALI model mice, as well as its potential mechanisms.

Materials And Methods: Lipopolysaccharide-induced establishment of the A549 cell inflammation model, and ALI mice model was established by intrathecal administration of LPS.

Results: CLO significantly reduced the release of inflammatory cytokines in A549 cells, lowered MDA and ROS levels, and enhanced SOD activity. Animal experiment results showed that CLO dramatically decreased white blood cell count, the expression of inflammatory cytokines, and the destruction of alveolar structures. CLO enhances the activity of antioxidant enzymes. Western Blot and q-PCR analyses have revealed that the mechanism of CLO is correlation with the NF-κB and Nrf2 signaling pathways in cellular and animal models. Pathway inhibitor experiments indicated that there might be functional crosstalk between these two pathways.

Conclusions: CLO may regulate inflammation and oxidative stress in LPS-induced ALI through NF-κB and Nrf2 signaling pathways. This finding could be novel in the pharmacological treatment of ALI.

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Source
http://dx.doi.org/10.1016/j.jep.2024.118470DOI Listing

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