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International journal of molecular medicine

Oligomeric proanthocyanidins protects A549 cells against H2O2-induced oxidative stress via the Nrf2-ARE pathway.


PMID 28487966

Abstract

Oxidative signaling and oxidative stress contribute to aging, cancer and diseases resulting from lung fibrosis. In this study, we explored the anti-oxidative potential of oligomeric proanthocyanidinsxa0(OPCs), natural flavonoid compounds. We examined the protective effects of OPCs against hydrogen peroxidexa0(H2O2)-induced oxidative stress in non-small cell lung cancer cellsxa0(A549). We demonstrated that OPC markedly attenuated H2O2-induced A549 cell viability, as shown by by 3-[4,5-dimethylthiazol-2-yl)]-2,5-diphenyl-tetrazolium bromidexa0(MTT) assay. At the same time, OPC inhibited H2O2-induced oxidative stress by significantly increasing the activities of superoxide dismutase, catalase and glutathione, and reducing the levels of reactive oxygen speciesxa0(ROS) and malondialdehydexa0(MDA). Treatment of the A549 cells with OPC significantly promoted the nuclear translocation of NF-E2-related factorxa02xa0(Nrf2) and significantly enhanced the expression of its target genesxa0[heme oxygenase-1xa0(HO-1), NAD(P)H quinone dehydrogenasexa01xa0(NQO1) and thioredoxin reductasexa01xa0(TXNRD1)] with different fold change values at both the mRNA and protein level. The knockout of Nrf2 using CRISPR/Cas9 technology attenuated OPC-mediated ARE gene transcription, and almost abolished the OPC-mediated protective effects against H2O2-induced oxidative stress. On the whole, our study suggests that OPC plays an important role in controlling the antioxidant response of A549 cells via the Nrf2-ARE pathway.