Ethyl rosmarinate inhibits lipopolysaccharide-induced nitric oxide and prostaglandin E2 production in alveolar macrophages

Eur J Pharmacol. 2018 Apr 5:824:17-23. doi: 10.1016/j.ejphar.2018.01.042. Epub 2018 Jan 31.

Abstract

In this study, a series of rosmarinic acid and analogs were investigated for their anti-inflammatory potential against LPS-induced alveolar macrophages (MH-S). Our results showed that, among the test compounds, ethyl rosmarinate (3) exhibited the most potent inhibitory effect on NO production in LPS-induced MH-S cells, with low cytotoxicity. Compound 3 exhibited remarkable inhibition of the production of PGE2 in LPS-induced MH-S cells. The inhibitory potency of compound 3 against LPS-induced NO and PGE2 release was approximately two-fold higher than that of dexamethasone. Compound 3 significantly decreased the mRNA and protein expression of iNOS and COX-2 and suppressed p65 expression in the nucleus in LPS-induced MH-S cells. These results suggested that compound 3 inhibited NO and PGE2 production, at least in part, through the down-regulation of NF-κB activation. Analysis of structure-activity relationship revealed that the free carboxylic group did not contribute to inhibitory activity and that the alkyl group of the corresponding alkyl ester analogs produced a strong inhibitory effect. We concluded that compound 3, a structurally modified rosmarinic acid, possessed potent inhibitory activity against lung inflammation, which strongly supported the development of this compound as a novel therapeutic agent for the treatment of macrophage-mediated lung inflammatory diseases, such as COPD.

Keywords: Alveolar macrophages; Chronic obstructive pulmonary disease; Ethyl rosmarinate; Nitric oxide; Prostaglandin E(2).

MeSH terms

  • Animals
  • Cell Line
  • Cell Survival / drug effects
  • Cinnamates / pharmacology*
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Depsides / pharmacology*
  • Dinoprostone / biosynthesis*
  • Gene Expression Regulation, Enzymologic / drug effects
  • Lipopolysaccharides / pharmacology*
  • Macrophages, Alveolar / cytology
  • Macrophages, Alveolar / drug effects*
  • Macrophages, Alveolar / metabolism*
  • Mice
  • NF-kappa B / metabolism
  • Nitric Oxide / biosynthesis*
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rosmarinic Acid

Substances

  • Cinnamates
  • Depsides
  • Lipopolysaccharides
  • NF-kappa B
  • RNA, Messenger
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • Dinoprostone