Qi-Dong-Huo-Xue-Yin Inhibits Inflammation in Acute Lung Injury in Mice via Toll-Like Receptor 4Caveolin-1 Signaling

Abstract EN

Acute lung injury (ALI) is a critical illness with no current effective treatment.

Caveolin-1 indirectly activates inflammation-associated signaling pathways by inhibiting endothelial nitric oxide synthase (eNOS).

This induces an imbalance between pro- and anti-inflammatory cytokine levels, which are involved in the pathogenesis of ALI.

The compound Chinese prescription Qi-Dong-Huo-Xue-Yin (QDHXY) is efficacious for ALI treatment via an anti-inflammatory effect; however, the exact underlying mechanism is unknown.

Therefore, we explored the protective effect of QDHXY against lipopolysaccharide- (LPS-) induced ALI in mice.

Histopathological changes in mouse lung tissues were studied.

Furthermore, alterations in the serum levels of pro- and anti-inflammatory cytokines were investigated.

The levels of tumor necrosis factor- (TNF-)α, interleukin- (IL-) 6, IL-1β, and interferon-γ-induced protein 10 in bronchoalveolar lavage fluid were measured.

Additionally, the expression levels of myeloid differentiation factor 88 (MyD88), caveolin-1, and eNOS were assessed.

QDHXY significantly reduced lung infiltration with inflammatory cells and the production of serum pro- and anti-inflammatory cytokines and inhibited the expression of TNF-α, IL-1β, caveolin-1, and MyD88 but not eNOS.

These indicate that QDHXY significantly improved the balance between pro- and anti-inflammatory cytokine levels, possibly by inhibiting the caveolin-1 signaling pathway.

Therefore, QDHXY may be a potential treatment for ALI.