The anti-inflammatory effect of CA was supported by its ability to inhibit the mRNA expression of f IL-1β, TNF-α, and IL-6 after myocardial infarction while repressing the expression of NF-κB p65 and p-Ikkβ, an inhibitor of nuclear factor-κB kinase β. Here, NFKB1 is linked to myocardial infarction.