Acute lung injury (ALI) is one of the representative "lung heat syndromes" in
traditional Chinese medicine (TCM). Scutellaria baicalensis is an herbal medicine used in TCM for treating
lung diseases, due to its remarkable anti-inflammatory and
antiviral effects. When used in TCM, S. baicalensis root is divided into two categories: S. baicalensis pith-not-decayed root (SN) and S. baicalensis pith-decayed root (SD). Compared to SN, SD has a better effect on
lung diseases. We constructed a
lipopolysaccharide (LPS)-induced
acute lung injury (ALI) mouse model to study the pharmacodynamic mechanism of SD. The ethanolic extract of Scutellaria baicalensis pith-decayed root (EESD) significantly affected LPS-induced ALI by reducing alveolar interstitial thickening,
pulmonary edema, and other pathological symptoms, decreasing the infiltration of inflammatory cells, especially macrophages, and inhibiting IL-1β, TNF-α, and
IL-6 transcription and translation. Furthermore, in the THP-1 macrophage model induced by LPS, EESD inhibited the expression of phosphorylated nuclear factor inhibitory
protein alpha (p-IκBα), phosphorylated nuclear factor-κB P65 (p-p65), cleaved-caspase-1, cleaved-IL-1β
protein, and the release of inflammatory factors in the NF-κB/NLRP3 pathway, inhibiting macrophage function. In vivo experiments yielded similar results. Therefore, the present study clarified the potential of EESD in the treatment of ALI and revealed its potential pharmacodynamic mechanism by inhibiting the NF-κB/NLRP3
inflammasome pathway and suppressing the pro-inflammatory phenotype activation of lung tissue macrophages.