Involvement of protein kinase Cδ and extracellular signal-regulated kinase-2 in the suppression of microglial inducible nitric oxide synthase expression by N-[3,4-dimethoxycinnamoyl]-anthranilic acid (tranilast)

Mechanisms of endotoxin-induced NO, IL-6, and TNF-α production in activated rat hepatic stellate cells: Role of p38 MAPK

“…32 Moreover, LPS-induced TNF-␣ expression is suppressed in microglia by pretreatment with the p38 inhibitor SB203580, 33 and some studies have shown regulation of iNOS induction by MAPKs. 34,35 LPS has also been re- ported to elicit iNOS expression and to stimulate the release of NO via NF-B in RAW264.7 cells, 32 N9 microglial cells, 36 and human myometrial cells. 37 In HSCs, although LPS caused activation of ERK1/2, p38 and JNK, only activated p38 was found to increase the expressions of iNOS, IL-6, and TNF-␣, as indicated by their strong inhibition by SB203580.…”

Puerarin suppresses production of nitric oxide and inducible nitric oxide synthase in lipopolysaccharide-induced N9 microglial cells through regulating MAPK phosphorylation, O-GlcNAcylation and NF-κB translocation

“…Our study revealed that, LPS encouraged NF-κB translocation into the nucleus, and the enhancement was significantly inhibited by puerarin at higher concentrations. Regulation of NO include two critical signal transduction molecules, MAPK and NF-κB (4,6,8). It has been documented that MAPKs, such as p38, JNK, and ERK, are major modulators for iNOS expression induced by LPS in microglial cells (6,7).…”

“…Lipopolysaccharide (LPS), which consist in outer membrane of gram-negative bacteria as potent pro-inflammatory agents, induce microglial cell inflammatory injury through releasing proinflammatory mediators such as NO generated by inducible nitric oxide synthase (iNOS) (3,4). NO is considered as a main risk factor of progressive damage in neurodegenerative diseases (5,6). Microglia cell inflammatory response to LPS is involved in speedy regulation of many signal transduction molecules.…”

“…Microglia cell inflammatory response to LPS is involved in speedy regulation of many signal transduction molecules. The regulation of a signal pathway, such as mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB), is implicated in major molecular mechanisms of LPS-induced NO and ROS production in microglial cells (4,(6)(7)(8).…”

“…Microglia cell inflammatory response to LPS is involved in speedy regulation of many signal transduction molecules. The regulation of a signal pathway, such as mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB), is implicated in major molecular mechanisms of LPS-induced NO and ROS production in microglial cells (4,(6)(7)(8).O-Linked O-GlcNAcylation of protein, a single monosaccharide N-acetylglucosamine (GlcNAc) attached to the hydroxyl groups of specific serine or threonine residues, is an important post-translational modification on nuclear and cytoplasmic proteins (9,10). More than 500 proteins have been identified to be O-GlcNAcylated, and these proteins are involved in regulation of cell processes including cell cycle, transcription, trafficking and signaling (11).…”