Baicalin inhibits LPS-induced apoptosis and inflammation in WI- 38 cells by promoting FOXA2/TRIM27 Interaction: Implications for pediatric pneumonia mechanisms.

BACKGROUND

Pediatric pneumonia is lung inflammation in newborns caused by many factors, which can impair the respiratory, circulatory and nervous systems and affect their growth and development. Baicalin, a flavonoid separated from Scutellaria baicalensis Georgi, possesses anti-inflammatory effects in lung diseases. The aim of this study was to explore the molecular mechanism of baicalin in exerting a protective effect in neonatal pneumonia.

METHODS

Effect of baicalin on viability of human fibroblast cells (WI-38 cell) was detected by CCK-8 assay. Then, the WI-38 cells were treated with lipopolysaccharide (LPS). Cell apoptosis and inflammatory cytokines were assessed by flow cytometry and ELISA. Additionally, the oxidative stress and endoplasmic reticulum stress (ERS) were evaluated using specific assays. The mRNA and protein levels were assessed by qRT-PCR and western blot. Finally, the binding between FOXA2 and TRIM27 was predicted and verified by employing the Jaspar database, ChIP and dual luciferase reporter assays.

RESULTS

1-40 µM baicalin had no impact on the viability in WI-38 cells, and 40 µM baicalin increased the viability of LPS-inhibited cells. Besides, baicalin mitigated the effects of LPS on apoptosis, inflammation, oxidative stress and ERS in WI-38 cells. Moreover, TRIM27 exhibited low expression levels in pediatric pneumonia and LPS-induced cells. Furthermore, baicalin promoted TRIM27 expression and inhibited the effects of LPS induction on cell production. Mechanically, FOXA2 was positively correlated with TRIM27 expression and baicalin inhibited the adverse effects of LPS induction on WI-38 cells via FOXA2/TRIM27.

CONCLUSION

These findings suggested that baicalin miaght exert protective effects against pediatric pneumonia by modulating FOXA2/TRIM27-dependent pathways.