Anti-inflammatory activity and antioxidant capacity of Clerodendrum japonicum (Thunb.) sweet extract in LPS-stimulated macrophages.

BACKGROUND

Clerodendrum japonicum (Thunb.) Sweet is a medicinal plant native to East Asia, including Korea, Japan, and China. Its leaves have traditionally been used to relieve respiratory symptoms and inflammatory conditions. However, no studies have systematically explored its anti-inflammatory activity and antioxidant capacity.

OBJECTIVE

This study aimed to investigate the anti-inflammatory effects of C. japonicum (Thunb.) Sweet extract (CJSE) in a lipopolysaccharide (LPS)-induced inflammatory model and determine its antioxidant capacity.

METHODS

Anti-inflammatory activity was investigated in LPS-stimulated RAW 264.7 macrophages by evaluating nitric oxide (NO) production, inflammatory gene expression, and related signaling pathways. Antioxidant capacity was determined using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging assays and by determining total phenolic and flavonoid contents.

RESULTS

CJSE reduced LPS-induced NO production in a dose-dependent manner without detectable cytotoxicity. CJSE also decreased the expression of key inflammatory mediators, including inducible nitric oxide synthase and cyclooxygenase-2, and proinflammatory cytokine genes, such as tumor necrosis factor-α, interleukin-6, and interferon-β. Mechanistically, CJSE was associated with reduced phosphorylation of extracellular signal-regulated kinase (ERK) and nuclear factor-kappa B (NF-κB) in LPS-stimulated cells. Moreover, CJSE demonstrated strong DPPH and ABTS radical scavenging activities and contained substantial levels of phenolic and flavonoid compounds, which supported its antioxidant potential.

CONCLUSION

CJSE suppresses LPS-induced inflammatory responses in macrophages and exhibits remarkable antioxidant capacity, suggesting that it could serve as a potential natural source of bioactive compounds for managing inflammation and oxidative stress.