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Ramalin inhibits LPS‐induced autophagic response in macrophages through the downregulation of iNOS expression
Author(s) -
Park HyeJin,
Yim Joung Han,
Lee Hong Kum,
Pyo Suhkneung
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.888.2
Subject(s) - autophagy , downregulation and upregulation , microbiology and biotechnology , macrophage , mapk/erk pathway , chemistry , inflammation , secretion , blot , nf κb , cancer research , biology , signal transduction , immunology , apoptosis , in vitro , biochemistry , gene
Activation of macrophages is essential for the host defense system and accumulating evidence suggests that autophagy is an important component in macrophage activity. Prolonged activation of macrophages, however, becomes detrimental and contributes to the progression of chronic inflammatory diseases with abnormal cell death. Therefore, controlling the overactivation of macrophages may be a new therapeutic strategy for various inflammatory diseases. Here we showed that ramalin, an antioxidant compound from the Antarctic lichen Ramalina terebrata , inhibited both LPS‐induced autophagy and iNOS in macrophages. To verify the role of NO in autophagy, we compared autophagy‐related gene expression in LPS‐stimulated and SNP‐stimulated macrophages by western blotting. Interestingly, ramalin did not suppress NO and autophagy in macrophages exposed to NO donor, SNP. In addition, inhibition of NO production by SMT significantly reduced LPS‐induced autophagy. These finding imply that ramalin might suppress LPS‐induced autophagy by inhibiting NO secretion. Ramalin also showed inhibitory effect on LPS‐induced NF‐κB and MAPK activation. Overall, these finding indicate that ramalin suppresses autophagy in LPS‐stimulated macrophages by preventing NO production and downregulating both NF‐κB and MAPK activation.