The anti-inflammatory effect of ent-kaur-15-en-17-al-18-oic acid on lipopolysaccharide-stimulated RAW264.7 cells associated with NF-κB and P38/MAPK pathways

Abstract

Ent-kaur-15-en-17-al-18-oic acid (LL-3) was demonstrated that it can inhibit LPS-induced nitric oxide (NO) production and macrophage migration, maintain homeostasis of oxidative stress, including increased mitochondrial membrane potential (MMP), decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and maintenance of superoxide dismutase (SOD) and glutathione (GSH) activities and inhibit oxidative stress-induced P38 and nuclear factor κB (NF-κB) pathways to decrease inducible nitric oxide synthase (iNOS), cyclooxygense-2 (COX-2), and tumour necrosis factor (TNF)-α mRNA expressions without marked cytotoxicity. These findings revealed that LL-3 could serve as a candidate lead compound for further studying anti-inflammatory therapies.

Graphical Abstract

Keywords:

• Ent-kaur-15-en-17-al-18-oic acid
• inflammation
• LPS
• migration
• P38
• NF-κB

Disclosure statement

The authors declare that there are no potential conflicts of interest.

Additional information

Funding

This work was financially supported by the Natural Science Foundation of Shandong Province [grant number ZR2019MH001]; the Fundamental Research Funds for the Central Universities [grant number No.2019ZRJC004].