Dioscin alleviates lipopolysaccharide-induced acute lung injury through suppression of TLR4 signaling pathways. (7th February 2020)

• Record Type: Journal Article
• Authors: Wang, Chuntao; Li, Qingnian; Li, Tianyu
• Is Part Of: Experimental lung research. Volume 46:Number 1/2(2020)
• Page Start: 11
• Page End: 22
• Publication Date: 2020-02-07
• Subjects: acute lung injury (ALI) -- dioscin -- lipopolysaccharide (LPS) -- nuclear factor-kappaB (NF-κB) -- Toll-like receptor 4 (TLR4); Lungs -- Periodicals; Lungs -- Diseases -- Periodicals; Lung Diseases; Lung -- physiology; Respiratory System; 616.24
• DOI: 10.1080/01902148.2020.1711830
• Languages: English
• ISSNs: 0190-2148

Abstract

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.