[CAS NO. 20283-92-5]  Rosmarinic acid

RA exerts a significant cytoprotective effect by scavenging intracellular ROS induced by UVB. RA also attenuates UVB-induced oxidative macromolecular damage, including protein carbonyl content, DNA strand breaks, and the level of 8-isoprostane. Furthermore, RA increases the expression and activity of superoxide dismutase, catalase, heme oxygenase-1, and their transcription factor Nrf2, which are decreased by UVB radiation. RA treatment recovers the protein expression levels of Nrf2 decreased by UVB exposure, and results in the translocation of Nrf2 protein from the cytosol into the nucleus. RA may protect cellular environments from free-radical damage and thereby, enhance the cellular antioxidant defense system. Rosmarinic acid inhibits TNF-α-induced phosphorylation and degradation of IκB-α, as well as nuclear translocation of NF-κB heterodimer induced by TNF-α. It downregulates the expression of CCL11 and CCR3 via the inhibition of NF-κB activation signaling. Rosmarinic acid inhibits the Ca2+-dependent pathways of TCR-mediated signaling by inhibiting PLC-γ1 and Itk activities.