Curcumin analog exhibited anti-inflammatory activity through inhibiting ERK/JNK and NF-κB signaling pathway / 中草药

ABSTRACT

Objective: To study the anti-inflammatory activity and mechanism of mono-carbonyl curcumin analog 22. Methods: The cell cytotoxicity of compound 22 was detected by MTT assay. LPS activated peritoneal macrophages was used as cell model. The effect of compound 22 on inflammatory cytokines protein and gene expression was detected by ELISA and RT-qPCR, respectively. UV-absorbing assay was used to determine the stability of compound 22. The anti-inflammatory mechanism of compound 22 was detected by Western blotting assay. Results: Compound 22 showed no cytotoxicity after incubated cells 24 h. Compared with curcumin, compound 22 dose-dependently inhibited LPS-induced production of inflammatory cytokines TNF-α and IL-6. Compound 22 showed more stability than curcumin in vitro. Meanwhile, compound 22 inhibited LPS-induced inflammatory gene IL-1β, IL-12, IL-6, and TNF-α expression through qRT-PCR assay. Compound 22 inhibited the phosphorylation of ERK/JNK, also reversed the LPS-induced degradation of IκB. Conclusion: Compound 22 exhibits its anti-inflammatory activity through inhibiting ERK/JNK signaling pathway, as well as NF-κB activation.