Carnosic acid protects against ROS/RNS-induced protein damage and upregulates HO-1 expression in RAW264.7 macrophages

Abstract

The overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is a deleterious process that can be an important mediator of damage to cell structures including protein, lipid and DNA, and consequently leads to various disease states and senescence. In the present study, the protective effects of carnosic acid (CA) on ROS/RNS-induced protein damages were examined. CA dose-dependently decreased the fragmentation, carbonylation, and nitration of bovine serum albumin (BSA) in AAPH and Hemin/nitrite/H2O2 incubation systems, respectively. Moreover, CA effectively attenuated protein carbonylations in the radical-treated RAW264.7 cells. Furthermore, after pretreatments of RAW264.7 macrophages with CA, the generation of ROS and NO induced by AAPH and H2O2 or LPS were significantly suppressed, and heme oxygenase-1 (HO-1) protein expression was time- and dose-dependently upregulated. Hence, our results indicated that CA might be beneficial for cellular proteins in oxidative stress or inflammation conditions by alleviating ROS/RNS generation and inducing the expression of antioxidant enzyme HO-1.