Abstract
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.
Key words
Scutellaria baicalensis
- acute lung injury - macrophages - NF-
κB - NLRP3