Dihydroquercetin attenuates lipopolysaccharide-induced acute lung injury through modulating FOXO3-mediated NF-κB signaling via miR-132–3p

Abstract

BackgroundDihydroquercetin (DHQ) is a potent flavonoid which has been demonstrated to have multiple biological activities including anti-inflammation activity, antioxidant activity as well as anti-cancer activity etc. Recently, many studies have focused on the antioxidant activity of DHQ. However, the use of the anti-inflammation activity of DHQ in acute lung injury (ALI) has not been reported. MethodsCell viability was examined by CCK-8 assay. The relative expression of miR-132–3p, FOXO3 were detected by qPCR. The levels of TNF-α, IL-6 and IL-1β were detected using enzyme-linked immunosorbent assay. The amount of apoptosis cells was detected by flow cytometry. The protein levels of Bcl-2, Bax, p-p65 and p-IκBα were measured by western blot. ResultsWe found that DHQ-induced the expression of miR-132–3p in LPS-induced ALI. Overexpression of miR-132–3p resulted in the inhibition of FOXO3 expression and then suppressed FOXO3-activated NF-κB pathway, attenuating LPS-induced inflammatory response and apoptosis. ConclusionWe demonstrated FOXO3 to be a target of miR-132–3p, and DHQ could induce the expression of miR-132–3p, relieving LPS-induced ALI via miR-132–3p/FOXO3/NF-κB axis, providing a promising therapeutic target for ALI.