This study aimed to assess the protective effect of an extract of against particulate-matter (PM)-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). The extract of reduced cell death, reactive oxygen species (ROS) production, and inflammation in A549 cells. The extract of decreased serum T cells, including CD4 T cells, CD8 T cells, and total T helper 2 (Th2) cells, and immunoglobulins, including immunoglobulin G (IgG) and immunoglobulin E (IgE), in PM-induced BALB/c mice. The extract of 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 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 might be a potential material to improve PM-induced pulmonary inflammation, apoptosis, and fibrosis.
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http://dx.doi.org/10.3390/antiox12040968 | DOI Listing |
J Appl Toxicol
December 2024
Cooperative Innovation Center of Industrial Fermentation, Ministry of Education & Hubei Province, Hubei University of Technology, Wuhan, Hubei, China.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder caused by the interaction of genetic and complex environmental factors. The prevalence of autism has dramatically increased in countries and regions undergoing rapid industrialization and urbanization. Recent studies have shown that particulate matter (PM) in air pollution affects the development of neurons and disrupts the function of the nervous system, leading to behavioral and cognitive problems and increasing the risk of ASD.
View Article and Find Full Text PDFAdv Healthc Mater
October 2024
Beijing Advanced Innovation Center for Soft Matter Science and Engineering, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, 100029, China.
Efficient personal protection has emerged as a crucial approach for reducing pulmonary injury induced by particulate matter (PM). However, current personal protective equipments usually lack essential biosafety concerns and fail to own adsorbing/antioxidant/antibacterial function together, making it a challenge to develop an integrated platform with the above characteristics. Herein, a facile oxygen-free hydrothermal strategy is proposed to synthesize new copper-based metal-organic frameworks, Cu-HHTPs, (HHTP: 2,3,6,7,10,11-hexahydroxytriphenylene), with great adsorbing/antioxidant/antibacterial activity and high biosafety.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Food Science and Biotechnology, College of BioNano Technology, Gachon University, Seongnam-si 13120, Republic of Korea.
Sci Total Environ
November 2024
Department of Pulmonary and Critical Care Medicine, Key Laboratory of Interventional Pulmonology of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China; Department of Pulmonary and Critical Care Medicine, The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital, Quzhou 324000, China. Electronic address:
Exposure to fine particulate matter (PM) disrupts the function of airway epithelial barriers causing cellular stress and damage. However, the precise mechanisms underlying PM-induced cellular injury and the associated molecular pathways remain incompletely understood. In this study, we used intratracheal instillation of PM in C57BL6 mice and PM treatment of the BEAS-2B cell line as in vivo and in vitro models, respectively, to simulate PM-induced cellular damage and inflammation.
View Article and Find Full Text PDFRespir Res
August 2024
Division of Allergy, Asthma, and Rheumatology, Department of Pediatrics, Chang Gung Memorial Hospital, 5 Fu-Hsin Street, Kweishan, Taoyuan, 33305, Taiwan.
Background: Mitochondria is prone to oxidative damage by endogenous and exogenous sources of free radicals, including particulate matter (PM). Given the role of mitochondria in inflammatory disorders, such as asthma and chronic obstructive pulmonary disease, we hypothesized that supplementation of vitamin D may play a protective role in PM-induced mitochondrial oxidative damages of human bronchial epithelial BEAS-2B cells.
Methods: BEAS-2B cells were pretreated with 1,25(OH)D, an active form of vitamin D, for 1 h prior to 24-hour exposure to PM (SRM-1648a).
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