Mechanistic Perspectives of Maslinic Acid in Targeting Inflammation

Figure 4

Molecular mechanism of maslinic acid in targeting inflammatory pathways. PKC plays a central role in the activation of NF-κB (p50/p65). Once activated, the IκB protein is degraded which allows NF-κB to translocate from cytoplasm to the nucleus, where it transcribes the expression of downstream proinflammatory genes such as TNF-α, COX-2, iNOS, and IL-6. It was shown that maslinic acid inhibited PKC activation, IκBα degradation, and NF-κB nuclear translocation, which might correlate to its anti-inflammatory properties. In addition, evidence also demonstrated the role of PKC in mediating PLA₂ phosphorylation and AA release. Once released from membrane phospholipids, AA can be converted into prostanoids through the action of COX enzymes. Considering that prostanoids are important mediators of inflammation, the anti-inflammatory effect of maslinic acid may be explained through its effect in inhibiting PKC activation and/or PLA₂ enzyme activity which reduces the substrate availability for COX-2-mediated prostanoids biosynthesis in inflammatory cells.