Rosmarinic Acid Attenuates the Lipopolysaccharide-Provoked Inflammatory Response of Vascular Smooth Muscle Cell via Inhibition of MAPK/NF-κB Cascade

Rosmarinic acid (RA) is a phenolic compound that has several bioactivities, such as anti-inflammatory and antioxidant activities. Here, we further investigate the anti-inflammatory effect of RA on rat A7r5 aortic smooth muscle cells with exposure to lipopolysaccharide (LPS). Our findings showed that low-dose RA (10-25 mu M) did not influence the cell viability and morphology of A7r5 cells and significantly inhibited LPS-induced mRNA expression of the pro-inflammatory mediators TNF alpha, IL-8, and inducible NO synthase (iNOS). Consistently, RA reduced the production of TNF alpha, IL-8, and NO by A7r5 cells with exposure to LPS. Signaling cascade analysis showed that LPS induced activation of Erk, JNK, p38 mitogen-activated protein kinase (MAPK), and NF-kappa B, and RA treatments attenuated the activation of the three MAPKs and NF-kappa B. Moreover, cotreatment with RA and Erk, JNK, p38 MAPK, or NF-kappa B inhibitors further downregulated the mRNA expression of TNF alpha, IL-8, and iNOS, and decreased the production of TNF alpha, IL-8, and NO by A7r5 cells. Taken together, these findings indicate that RA may ameliorate the LPS-provoked inflammatory response of vascular smooth muscle cells by inhibition of MAPK/NF-kappa B signaling.

Automated summary

Rosmarinic acid (RA) has anti-inflammatory and antioxidant activities and can ameliorate the inflammatory response of vascular smooth muscle cells caused by lipopolysaccharide (LPS) through inhibition of the MAPK/NF-kappa B signaling pathway.