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Sedanolide is a natural compound produced in edible umbelliferous plants, such as Celery seed oil [1].

In HepG2 and CaCo-2 cells, treatment with sedanolide (7-500 μM) for 24h showed no effect on cell viability. In HepG2 cells cultured in sedanolide-free medium, sedanolide (500 μM) treatment for 72h decreased cell viability. Pretreatment with sedanolide (100 μM) for 24 h and exposement to either H2O2 or tBOOH did not exhibit statistically significant difference in viability from controls. In HepG2 following 24-h incubation with 500 μM sedanolide, a significant increase in DNA strand breaks was observed. Sedanolide did not modulate H2O2- and tBOOH-induced DNA damage. Sedanolide was relatively nontoxic to cells in culture [1]. Sedanolide (SN) possesses antioxidant effects. In human liver cancer (J5) cells, treatment with sedanolide suppressed J5 cell viability by inducing autophagy. Sedanolide decreased protein expression levels of phosphoinositide 3-kinase (PI3K)-I, mammalian target of rapamycin (mTOR) and Akt and increased PI3K-III, LC3-II and Beclin-1 protein levels. Sedanolide increased the cytosolic phosphorylation of inhibitor of kappa B (IκB) and nuclear p65 and the DNA-binding activity of NF-κB. Sedanolide induced J5 cell autophagy by regulating PI3K, p53 and NF-κB autophagy-associated signaling pathways in J5 cells [2]. Sedanolide (100 μg/ml) inhibited cyclooxygenases-1 and -2 at 250 pg/ml and blocked topoisomerase-I and-II activity [3].

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