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Fine particulate matter (PM2.5) is an air pollutant that causes severe lung injury. We investigated the effects of Jujuboside B (JB), a component of Zizyphi Spinosi Semen, on lung toxicity caused by PM2.5, and we identified the mechanism of its protective effect. Lung injury in an animal model was induced by intratracheal administration of a PM2.5 suspension. After 2 days of PM2.5 pretreatment, mice were administered JB via the tail vein three times over a 2-day period. JB significantly reduced the histological lung damage as well as the lung wet/dry weight ratio. JB also considerably reduced PM2.5-induced autophagy dysfunction, apoptosis, inflammatory cytokine levels, and the number of PM2.5-induced lymphocytes in the bronchial alveolar fluid. We conclude that by regulating TLR2, 4-MyD88, and mTOR-autophagy pathways, JB exerts a protective effect on lung injury. Thus, JB can be used as a potential therapeutic agent for PM2.5-induced lung damage. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]