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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]

Sparstolonin B (SsnB) exists in the tubers of Scirpus yagara and Sparganium stoloniferum, and it is known to modulate inflammatory mediators. Here, we investigated whether SsnB could reduce the renal functional damage in a cecal ligation and puncture (CLP)-induced septic mice. The effect of SsnB was measured via assessment of blood urea nitrogen (BUN), serum creatinine, total glutathione, lipid peroxidation, catalase activity, glutathione peroxidase activity, and superoxide dismutase activity. Our findings showed that SsnB treatment in mice with CLP-induced renal damage elevated the BUN and creatinine levels in plasma and protein levels in the urine. In contrast, the excessive production of nitric acid and induction of nitric oxide synthase were decreased. Moreover, SsnB inhibited the activation of nuclear factor-kappa B, reduced the plasma levels of tumor necrosis factor-α and interleukin-6, and thus reduced lethality. SsnB also increased lipid peroxidation and restored the levels of superoxide dismutase, glutathione peroxidase, and catalase in kidney tissues, thereby enhancing the antioxidant defense system. Conclusively, our results indicate that SsnB can protect mice from sepsis-induced renal injury. [ABSTRACT FROM AUTHOR]