18β-Glycyrrhetinic Acid Alleviates -Induced Vascular Endothelial Inflammation by PARP1-Mediated NF-κB and HMGB1 Signalling Suppression in PIEC Cells.

BACKGROUND

At present, the treatment and prevention of infections in pigs mainly rely on antibiotics and vaccines, but inflammatory injury cannot be eliminated. The compound 18β-glycyrrhetinic acid (GA), a pentacyclic triterpenoid extracted from . root (liquorice) and with a chemical structure similar to that of steroidal hormones, has become a research focus because of its anti-inflammatory, antiulcer, antimicrobial, antioxidant, immunomodulatory, hepatoprotective and neuroprotective effects, but its potential for the treatment of vascular endothelial inflammatory injury by infections has not been evaluated. This study aimed to investigate the effects and mechanisms of GA intervention in the treatment of vascular endothelial inflammatory injury by infections.

MATERIALS AND METHODS

Putative targets of GA intervention in the treatment of vascular endothelial inflammatory injury by infections were identified using network pharmacological screening and molecular docking simulation. The cell viability of PIEC cells was investigated via the CCK-8 assay. The mechanism of GA intervention in the treatment of vascular endothelial inflammatory injury by infections were investigated using cell transfection and western blot.

RESULTS

Through network pharmacological screening and molecular docking simulation, this study found that PARP1 may be a core target for GA to exert anti-inflammatory effects. Mechanistically, GA alleviates -induced vascular endothelial inflammation by PARP1-mediated NF-κB and HMGB1 signalling suppression.

CONCLUSION

These findings, for the first time, demonstrate the potential therapeutic relationship among GA, PARP1 and inflammatory injury, providing a candidate drug, therapeutic targets and explanation for treating vascular endothelial inflammatory injury caused by infection.