Journal
EXPERIMENTAL LUNG RESEARCH
Volume 46, Issue 1-2, Pages 11-22Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/01902148.2020.1711830
Keywords
acute lung injury (ALI); dioscin; lipopolysaccharide (LPS); nuclear factor-kappaB (NF-kappa B); Toll-like receptor 4 (TLR4)
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Aim:Acute lung injury (ALI) is a life-threatening inflammatory syndrome that lacks an effective therapy. Dioscin, a natural steroid saponin isolated from a variety of herbs, could serve as an anti-inflammatory agent, as suggested in previous reports. The purpose of this study was to explore the effects of dioscin on lipopolysaccharide (LPS)-induced ALI and validate the potential mechanisms. Materials and Methods:An ALI model was induced by intratracheal administration of LPS. Dioscin (20, 40, and 80 mg/kg) was administered intragastrically once daily for seven consecutive days prior to LPS challenge. Results:Our data revealed that dioscin significantly suppressed LPS-induced lung pathological changes, pulmonary capillary permeability, pulmonary edema, inflammatory cell infiltration, myeloperoxidase (MPO) activity, and cytokine production, including tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and keratinocyte chemoattractant (KC). Moreover, dioscin inhibited LPS-induced nuclear factor-kappaB (NF-kappa B) activation as well as Toll-like receptor 4 (TLR4) expression. Conclusions:In brief, the results indicated that dioscin alleviates LPS-induced ALI through suppression of TLR4 signaling pathways.
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