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Psoralidin is a dual inhibitor of COX-2 and 5-LOX. Psoralidin, a coumestan derivative isolated from seed of Psoralea corylifolia, has been widely used in traditional medicine for bleeding, pollakiuria, enuresis, vitiligo, and psoriasis. Psoralidin shows a variety of biological activities such as anti-cancer, anti-bacterial, anti-oxidant, anti-depressant activities and regulation of insulin signaling [1].

Psoralidin (100 μM) inhibited COX-2 in IR-irradiated normal lung fibroblasts in HFL-1 and MRC-5 cells [1]. Psoralidin significantly inhibited IR-induced NF-κB-luciferase activity. Psoralidin inhibited the IR-induced COX-2 expression and PGE2 production through regulation of PI3K/Akt and NF-κB pathway. Also, psoralidin blocked IR-induced LTB4 production through direct interaction with 5-lipoxygenase activating protein (FLAP) in 5-LOX pathway. Psoralidin significantly attenuated IR-induced fibroblast migration [1]. Psoralidin inhibited LPS-induced iNOS expression via repressing Syk-mediated activation of PI3K-IKK-IκB signaling pathways [2]. Psoralidin enhanced TRAIL-induced apoptosis in HeLa cells through increased expression of TRAIL-R2 death receptor and depolarization of mitochondrial membrane potential [3].

In male BALB/c strain mice (eight weeks, average weight 22–25 g), psoralidin (5 mg/kg) suppressed IR-induced expression of pro-inflammatory cytokines (TNF-α, TGF-β, IL-6 and IL-1 α/β) and ICAM-1 [1].

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