Literature DB >> 31931639

Dioscin alleviates lipopolysaccharide-induced acute lung injury through suppression of TLR4 signaling pathways.

Chuntao Wang1, Qingnian Li2, Tianyu Li1.   

Abstract

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)-α, interleukin (IL)-6, and keratinocyte chemoattractant (KC). Moreover, dioscin inhibited LPS-induced nuclear factor-kappaB (NF-κB) 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.

Entities:  

Keywords:  Toll-like receptor 4 (TLR4); acute lung injury (ALI); dioscin; lipopolysaccharide (LPS); nuclear factor-kappaB (NF-κB)

Mesh:

Substances:

Year:  2020        PMID: 31931639     DOI: 10.1080/01902148.2020.1711830

Source DB:  PubMed          Journal:  Exp Lung Res        ISSN: 0190-2148            Impact factor:   2.459


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