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Protective Effect of Lonicera japonica on PM 2.5 -Induced Pulmonary Damage in BALB/c Mice via the TGF-β and NF-κB Pathway.

Authors :
Lee, Hyo Lim
Kim, Jong Min
Go, Min Ji
Kim, Tae Yoon
Joo, Seung Gyum
Kim, Ju Hui
Lee, Han Su
Kim, Hyun-Jin
Heo, Ho Jin
Source :
Antioxidants; Apr2023, Vol. 12 Issue 4, p968, 21p
Publication Year :
2023

Abstract

This study aimed to assess the protective effect of an extract of Lonicera japonica against particulate-matter (PM)<subscript>2.5</subscript>-induced pulmonary inflammation and fibrosis. The compounds with physiological activity were identified as shanzhiside, secologanoside, loganic acid, chlorogenic acid, secologanic acid, secoxyloganin, quercetin pentoside, and dicaffeoyl quinic acids (DCQA), including 3,4-DCQA, 3,5-DCQA, 4,5-DCQA, and 1,4-DCQA using ultra-performance liquid chromatography–quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS<superscript>E</superscript>). The extract of Lonicera japonica reduced cell death, reactive oxygen species (ROS) production, and inflammation in A549 cells. The extract of Lonicera japonica decreased serum T cells, including CD4<superscript>+</superscript> T cells, CD8<superscript>+</superscript> T cells, and total T helper 2 (Th2) cells, and immunoglobulins, including immunoglobulin G (IgG) and immunoglobulin E (IgE), in PM<subscript>2.5</subscript>-induced BALB/c mice. The extract of Lonicera japonica protected the pulmonary antioxidant system by regulating superoxide dismutase (SOD) activity, reduced glutathione (GSH) contents, and malondialdehyde (MDA) levels. In addition, it ameliorated mitochondrial function by regulating the production of ROS, mitochondrial membrane potential (MMP), and ATP contents. Moreover, the extract of Lonicera japonica exhibited a protective activity of apoptosis, fibrosis, and matrix metalloproteinases (MMPs) via TGF-β and NF-κB signaling pathways in lung tissues. This study suggests that the extract of Lonicera japonica might be a potential material to improve PM<subscript>2.5</subscript>-induced pulmonary inflammation, apoptosis, and fibrosis. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
20763921
Volume :
12
Issue :
4
Database :
Complementary Index
Journal :
Antioxidants
Publication Type :
Academic Journal
Accession number :
163380056
Full Text :
https://doi.org/10.3390/antiox12040968