Tubeimoside-1 attenuates LPS-induced inflammation in RAW 264.7 macrophages and mouse models

Abstract

Context: Acute lung injury (ALI), characterized by severe hypoxemia, pulmonary edema and neutrophil accumulation in the lung, is a common clinical problem associated with significant morbidity and mortality in shock, sepsis, ischemia reperfusion, etc.

Objective: In this study, we aimed at investigating the protective effect of tubeimoside-1 (TBMS1) on inflammation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and a LPS-induced in vivo lung injury model.

Materials and methods: We evaluated the effect of TBMS1 on LPS-induced production of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β in the culture supernatants of RAW 264.7 cells by enzyme-linked immunosorbent assay. LPS (0.5 mg/kg) was instilled intranasally in phosphate-buffered saline to induce ALI, and the severity of pulmonary injury was evaluated 6 h after LPS challenge.

Results: TBMS1 significantly inhibited the production of the pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β in vitro and in vivo. Pretreatment with TBMS1 markedly attenuated the development of pulmonary edema, histological severities and inflammatory cells infiltration in mice with ALI. In addition, we further demonstrated that TBMS1 exerts an anti-inflammatory effect in vivo model of ALI through suppression of IκB activation and p38/extracellular signal-regulated kinase mitogen-activated protein kinases signaling in a dose-dependent manner.

Discussion and conclusion: Overall, our data suggest that TBMS1 inhibits inflammation both in vitro and in vivo, and may be a potential therapeutic candidate for the prevention of inflammatory diseases.

• Acute lung injury
• cytokines
• lipopolysaccharide
• macrophages
• tubeimoside-1