These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Effects of florfenicol on LPS-induced nitric oxide and prostaglandin E₂ production in RAW 264.7 macrophages. Author: Zhang X, Xiong H, Li H, Yu L, Deng X. Journal: Fundam Clin Pharmacol; 2011 Oct; 25(5):591-8. PubMed ID: 21077941. Abstract: Florfenicol, an antibiotic commonly used to treat infections, has previously been shown to modulate lipopolysaccharide (LPS)-induced early cytokine responses by blocking the nuclear factor-κB (NF-κB) pathway. In this study, we investigated the effects of florfenicol on nitric oxide (NO) and prostaglandin E₂ (PGE₂) production as well as on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated murine RAW 264.7 macrophages. We also analysed the effects of florfenicol on mitogen-activated protein kinase (MAPK) pathways. Florfenicol significantly inhibited LPS-induced NO and PGE₂ production. Consistent with these observations, mRNA and protein expression of iNOS and COX-2 were also inhibited by florfenicol in a dose-dependent manner. Furthermore, phosphorylation of p38 and extracellular signal-regulated kinase 1/2 (ERK1/2) in LPS-stimulated RAW 264.7 cells was suppressed by florfenicol. However, c-Jun N-terminal kinase (JNK) phosphorylation remained unaffected. Using specific inhibitors of ERK and p38, we found that florfenicol may inhibit NO and PGE₂ mostly through ERK and p38 pathway. These results suggest that florfenicol inhibits NO and PGE₂ production in conjunction with an inhibition of iNOS and COX-2 expression, at least partially via suppression of ERK1/2 and p38 MAPK phosphorylation.[Abstract] [Full Text] [Related] [New Search]