Abstract:
Particulate matter (PM) air pollution has gradually become a widespread problem in East Asia. PM may cause
unfamiliar inflammatory responses, oxidative stress, and pulmonary tissue damage, and a comprehensive un-
derstanding of the underlying mechanisms is required in order to develop effective anti-inflammatory agents. In
this study, fine dust collected from Beijing, China (CPM) (size < PM13 with majority < PM2.5) was evaluated
for its oxidative stress- and inflammation-inducing effects, which cause cell damage, in A459 human lung epi-
thelial cells. Oxidative stress was marked by an increase in intracellular ROS levels and the production of an-
tioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and heme oxygenase-1 (HO-1). Upon
induction of oxidative stress, a marked increase was observed in the expression of key inflammatory mediators
such as COX-2 and PGE2 and the pro-inflammatory cytokines TNF-α and IL-6 via NF-kB and MAPK pathways.
Cellular damage was marked by a reduction in viability, increased lactate dehydrogenase (LDH) release, for-
mation of apoptotic and necrotic bodies, accumulation of sub-G1 phase cells, and DNA damage. Apoptosis was
found to be mediated via the activation of caspases through the mitochondria-mediated pathway. Fucosterol,
purified from the brown alga Sargassum binderi (Sonder ex J. Agardh) by bio-assay-guided fractionation and
purification, exhibited potential therapeutic effects against CPM-induced detrimental effects. Further studies
could focus on developing fucosterol, in forms such as steroidal inhalers, against PM-induced pulmonary tissue inflammation.
