Acute lung injury (ALI) is a serious respiratory syndrome featured with uncontrolled inflammatory response.
Biochanin A has been showed to possess and anti-inflammatory effect. This study intended to explore the suppression of
biochanin A on
lipopolysaccharide (LPS)-induced ALI in mice. Seven hours later LPS-induced ALI model established, the indexes including, pathological changes, MPO activity, wet/dry ratio, proinflammatory
cytokines TNF-α, IL-1β, and
IL-6, production, as well as and TLR4/NF-κB and
PPAR-γ signaling pathway expression were compared bwtween different groups. In addition, bronchoalveolar lavage fluid (BALF) was collected and the levels of total
protein, inflammatory cells and TNF-α, IL-1β, and
IL-6 were detected. The results revealed that LPS lead to significantly lung pathological injury, and damage of lung vascular permeability showing by higher
lung wet/dry ratio and total
protein levels in the BALF when compared to the control group mice. However, these changes significantly reversed by
biochanin A. Moreover, the levels of inflammatory cells in BALF, proinflammatory
cytokines TNF-α, IL-1β, and
IL-6, in both lung and BALF were also dose-dependently reduced by
biochanin A during ALI process. To investigate the anti-inflammatory mechanisms of
biochanin A, we found that
biochanin A significantly inhibited the activation of TLR4/NF-κB signaling pathway induced by LPS. Furthermore, the expression of
PPAR-γ also markedly increased in the mice after treated with
biochanin A. In conclusion,
biochanin A alleviated LPS-induced ALI by inhibiting the inflammatory response, which was mediated via down-regulating the activation of TLR4/NF-κB signaling pathway and enhancing the expression of
PPAR-γ.