Codium fragile Suppressed Chronic PM2.5-Exposed Pulmonary Dysfunction via TLR/TGF-β Pathway in BALB/c Mice

Author:

Kim Tae Yoon1,Kim Jong Min1ORCID,Lee Hyo Lim1ORCID,Go Min Ji1,Joo Seung Gyum1,Kim Ju Hui1,Lee Han Su1,Jeong Won Min2,Lee Dong Yeol2ORCID,Kim Hyun-Jin1,Heo Ho Jin1ORCID

Affiliation:

1. Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeonsang National University, Jinju 52828, Republic of Korea

2. Research & Development Team, Gyeongnam Anti-Aging Research Institute, Sancheong 52215, Republic of Korea

Abstract

This study investigated the ameliorating effect of the aqueous extract of Codium fragile on PM2.5-induced pulmonary dysfunction. The major compounds of Codium fragile were identified as palmitic acid, stearic acid, and oleamide using GC/MS2 and hexadecanamide, oleamide, and 13-docosenamide using UPLC-Q-TOF/MSE. Codium fragile improved pulmonary antioxidant system deficit by regulating SOD activities and reducing GSH levels and MDA contents. It suppressed pulmonary mitochondrial dysfunction by regulating ROS contents and mitochondrial membrane potential levels. It regulated the inflammatory protein levels of TLR4, MyD88, p-JNK, p-NF-κB, iNOS, Caspase-1, TNF-α, and IL-1β. In addition, it improved the apoptotic protein expression of BCl-2, BAX, and Caspase-3 and attenuated the fibrous protein expression of TGF-β1, p-Smad-2, p-Smad-3, MMP-1, and MMP-2. In conclusion, this study suggests that Codium fragile might be a potential material for functional food or pharmaceuticals to improve lung damage by regulating oxidative stress inflammation, cytotoxicity, and fibrosis via the TLR/TGF-β1 signaling pathway.

Funder

Ministry of Education

Ministry of Oceans and Fisheries

Publisher

MDPI AG

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Biochemistry,Physiology

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