Abeliophyllum distichum Nakai is known as a monotypic genus endemic to Korea. It is various classified according to the color phenotype of petals and sepals within the species. A. distichum has been reported to have bioactivities including antioxidants, protecting against oxidative DNA damage, anti-inflammatory, and anti-cancer. However, a study on A. distichum cultivated variety "Okhwang 1" has not been elucidated.In this study, callus (CAO) was induced from A. distichum cv. Okhwang 1. It was designed to analyze the content of bioactive compounds and to investigate molecular mechanisms of CAO on the regulation of DNA damage, inflammation, and cancer cell proliferation. Two glycosides which are acteoside and isoacteoside were identified and quantified by analysis of HPLC.CAO protected against the oxidative DNA damage induced Fenton reaction of mouse fibroblast cell line NIH/3T3 cells. CAO reduced the conversion of DNA structures into open-circular forms by DNA breaks in plasmid DNA levels. CAO induced a decrease in p53 and phosphorylated H2AX in both protein and mRNA levels. It effectively suppresses oxidative stress has been reported to be closely related to anti-inflammatory activity.Since various regulatory factors are involved in the alleviation of inflammation, further study for the potential mechanisms of CAO associated with the induction of anti-inflammatory effects may be important. In this study, the mechanisms were elucidated for PI3K/Akt, MAPK, and NF-κB signaling pathways in RAW 264.7 cells. CAO treatments in LPS-induced RAW 264.7 cells decrease NO production, iNOS, and COX-2 in both protein and mRNA levels. Akt phosphorylation by CAO treatment attenuated, while LPS stimulation mediated phosphorylated Akt. ERK1/2, JNK, p38 phosphorylation attenuated by CAO treatment under LPS-mediated inflammation. IκB-alpha and p65 phosphorylation attenuated, while total p65 did not change. In addition, p65 of translocation into nucleus inhibited by CAO treatment.CAO suppressed the proliferation and induced apoptosis in human colorectal cancer cell lines HCT116. CAO decreased PARP cleavage, Bax, p53, phospho-p53. An increase of ERK1/2, JNK, p38 phosphorylation by CAO treatment can cause apoptosis in HCT116 cells. To demonstrate a correlation with autophagy and apoptosis, regulation of Akt phosphorylation, Beclin-1, Atg12-Atg5 conjugation, p62, and LC3 investigated. Related factors to the formation of autophagosomes were regulated by CAO treatment. Also, expression of phospho-GSK-3β and β-catenin which are related in cell cycle arrest decreased.