TY - JOUR
T1 - The Inhibitory Functions of Sparstolonin B against Ambient Fine Particulate Matter Induced Lung Injury
AU - Kim, Chaeyeong
AU - Ryu, Soo Ho
AU - Choi, Hyukjae
AU - Park, Dong Ho
AU - Bae, Jong Sup
N1 - Publisher Copyright:
© 2022, The Korean Society for Biotechnology and Bioengineering and Springer.
PY - 2022/12
Y1 - 2022/12
N2 - Particulate matter, with an aerodynamic diameter equal to or less than 2.5 µm (PM2.5), is an air pollutant that causes serious pulmonary injury when inhaled. Sparstolonin B (SsnB) from the Chinese herb, Sparganium stoloniferum inhibits the expression of inflammatory cytokines and is involved in survival pathways. We investigated the protective effects of SsnB against PM2.5-induced lung damage. PM2.5 was pretreated intranasally and 30 minutes later, SsnB was injected via a vein in the tail of mouse. The effects of SsnB on PM2.5-induced lung damages, barrier disruptive responses, and pulmonary inflammation and the underlying mechanism of SsnB were investigated. SsnB significantly reduced pathological lung injury, the lung wet/dry weight ratio, and the levels of permeability. It also considerably attenuated PM2.5-induced myeloperoxidase activity in lung tissue, reduced PM2.5-induced inflammatory cytokine levels, and suppressed PM2.5-induced lymphocytes in bronchial alveolar fluid. Moreover, SsnB increased the phosphorylation of the mammalian target of rapamycin (mTOR) and significantly inhibited the expression of PM2.5-stimulated toll-like receptor 2, 4 (TLR2, 4), MyD88, and autophagy-related proteins, LC3II and Beclin 1. We concluded that SsnB regulates both the TLR2, 4-MyD88 and mTOR-autophagy pathways, therefore SsnB can be used as a potential therapeutic agent for preventing PM2.5-induced pulmonary damage.
AB - Particulate matter, with an aerodynamic diameter equal to or less than 2.5 µm (PM2.5), is an air pollutant that causes serious pulmonary injury when inhaled. Sparstolonin B (SsnB) from the Chinese herb, Sparganium stoloniferum inhibits the expression of inflammatory cytokines and is involved in survival pathways. We investigated the protective effects of SsnB against PM2.5-induced lung damage. PM2.5 was pretreated intranasally and 30 minutes later, SsnB was injected via a vein in the tail of mouse. The effects of SsnB on PM2.5-induced lung damages, barrier disruptive responses, and pulmonary inflammation and the underlying mechanism of SsnB were investigated. SsnB significantly reduced pathological lung injury, the lung wet/dry weight ratio, and the levels of permeability. It also considerably attenuated PM2.5-induced myeloperoxidase activity in lung tissue, reduced PM2.5-induced inflammatory cytokine levels, and suppressed PM2.5-induced lymphocytes in bronchial alveolar fluid. Moreover, SsnB increased the phosphorylation of the mammalian target of rapamycin (mTOR) and significantly inhibited the expression of PM2.5-stimulated toll-like receptor 2, 4 (TLR2, 4), MyD88, and autophagy-related proteins, LC3II and Beclin 1. We concluded that SsnB regulates both the TLR2, 4-MyD88 and mTOR-autophagy pathways, therefore SsnB can be used as a potential therapeutic agent for preventing PM2.5-induced pulmonary damage.
KW - 4-mTOR-autophagy
KW - Sparstolonin B
KW - TLR2
KW - lung injury
KW - particulate matter
UR - http://www.scopus.com/inward/record.url?scp=85144583806&partnerID=8YFLogxK
U2 - 10.1007/s12257-022-0286-3
DO - 10.1007/s12257-022-0286-3
M3 - Article
AN - SCOPUS:85144583806
SN - 1226-8372
VL - 27
SP - 949
EP - 960
JO - Biotechnology and Bioprocess Engineering
JF - Biotechnology and Bioprocess Engineering
IS - 6
ER -