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Chronic heart failure (CHF) reduces protein expression of voltage-gated sodium (Nav) channels in rat nodose neurons.Here, we investigated involvements of mitochondrial superoxide and NFκB in CHFdecreased Nav channel expression in rat nodose neurons.CHF was induced by left coronary ligation.CHF reduced protein expression of manganese superoxide dismutase (MnSOD) and elevated mitochondrial superoxide level in nodose neurons.Adenoviral MnSOD (Ad.MnSOD) gene transfection into nodose neurons normalized the MnSOD expression, reduced the elevation of mitochondrial superoxide, and partially reversed the reduced protein expression of Nav channels in CHF nodose neurons.Additionally, protein expression of NFκB p65 and phosphorylated-NFκB p65 in nodose neurons was higher in CHF rats than that in sham rats.An NFκB inhibitor (caffeic acid phenethyl ester) increased Nav channel density in CHF nodose neurons.Furthermore, Ad.MnSOD inhibited the NFκB p65 binding to Nav channel promoter in CHF nodose neurons.These results indicate that mitochondrial superoxide lowered protein expression of Nav channels in CHF nodose neurons via activating NFκB.