International immunopharmacology
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Int. Immunopharmacol. · Nov 2016
Therapeutic effect of methyl salicylate 2-O-β-d-lactoside on LPS-induced acute lung injury by inhibiting TAK1/NF-kappaB phosphorylation and NLRP3 expression.
Acute lung injury (ALI), characterized by pulmonary edema and inflammatory cell infiltration, is a common syndrome of acute hypoxemic respiratory failure. Methyl salicylate 2-O-β-d-lactoside (MSL), a natural derivative of salicylate extracted from Gaultheria yunnanensis (Franch.) Rehder, was reported to have potent anti-inflammatory effects on the progression of collagen or adjuvant-induced arthritis in vivo and in vitro. The aim of this study is to investigate the therapeutic effect of MSL on lipopolysaccharide (LPS)-induced acute lung injury and reveal underlying molecular mechanisms. ⋯ Furthermore, MSL significantly inhibited LPS-induced TAK1 and NF-κB p65 phosphorylation in Raw264.7 cells. In addition, MSL significantly inhibited nuclear translocation of NF-κB p65 in cells treated with LPS in vitro. Taken together, our results suggested that MSL exhibited a therapeutic effect on LPS-induced ALI by inhibiting TAK1/NF-κB phosphorylation and NLRP3 expression.
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Int. Immunopharmacol. · Nov 2016
Cnidilide, an alkylphthalide isolated from the roots of Cnidium officinale, suppresses LPS-induced NO, PGE2, IL-1β, IL-6 and TNF-α production by AP-1 and NF-κB inactivation in RAW 264.7 macrophages.
Cnidilide, an alkyl phthalide isolated from the rhizome of Cnidium officinale, has been reported to possess antispasmodic and sedative effects. However, the anti-inflammatory capacity and molecular mechanism of cnidilide have not been studied to date. In the present study, we investigated the inhibitory effects of cnidilide on LPS-induced pro-inflammatory mediators and the underlying molecular mechanisms in RAW 264.7 macrophages. ⋯ In addition, cnidilide inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and mitogen- and stress-activated protein kinase 1(MSK-1), a downstream kinase. Moreover, the phosphorylation of c-Jun N-terminal kinase (JNK) was suppressed by cnidilide in a concentration-dependent manner, whereas it did not inhibit the extracellular signal-regulated kinase (ERK) phosphorylation in LPS-stimulated RAW 264.7 macrophages. Taken together, our findings suggest that cnidilide has anti-inflammatory properties by inhibiting p38 MAPK, JNK, AP-1, and the NF-κB pathway in LPS-stimulated RAW 264.7 macrophages.