2011
DOI: 10.1016/j.intimp.2011.03.014
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Ligustilide prevents LPS-induced iNOS expression in RAW 264.7 macrophages by preventing ROS production and down-regulating the MAPK, NF-κB and AP-1 signaling pathways

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Cited by 131 publications
(77 citation statements)
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“…In addition, we demonstrated that NF-κB and JNK contribute to the cytotoxicity induced by bafilomycin A1 or concanamycin A (Hong et al, 2006). With regard to the relationship between NO production and ROS production, Su et al (2011) suggested that ROS induce NO production in LPS-stimulated RAW 264 cells, and we reported previously that NO produced by treatment with bafilomycin A1 or concanamycin A plays a role in the cytotoxicity induced by these V-ATPase inhibitors (Hong et al, 2006). Therefore, the present findings suggest that concomitantly produced ROS and NO might comediate the cytotoxic effects of bafilomycin A1 or concanamycin A.…”
Section: Resultsmentioning
confidence: 84%
“…In addition, we demonstrated that NF-κB and JNK contribute to the cytotoxicity induced by bafilomycin A1 or concanamycin A (Hong et al, 2006). With regard to the relationship between NO production and ROS production, Su et al (2011) suggested that ROS induce NO production in LPS-stimulated RAW 264 cells, and we reported previously that NO produced by treatment with bafilomycin A1 or concanamycin A plays a role in the cytotoxicity induced by these V-ATPase inhibitors (Hong et al, 2006). Therefore, the present findings suggest that concomitantly produced ROS and NO might comediate the cytotoxic effects of bafilomycin A1 or concanamycin A.…”
Section: Resultsmentioning
confidence: 84%
“…Increased ROS generation can damage biological molecules and lead to cells or tissue injury (Rezaie et al 2007, Ziegler et al 2011 as well as induces inflammation by increasing the level of cytokines such as IL-1β, IL-6, and TNF-α (Geronikaki and Gavalas 2006). Furthermore, antioxidant polyphenol compounds inhibit nuclear facor-κB (NF-κB) activation and block the expression of NF-κB-dependent cytokines, iNOS, and COX-2 genes (Ahn et al 2005, Su et al 2011. Based on these studies, ROS and NO generation as well as cell death were assessed in LPS-induced inflammation zebrafish model.…”
Section: A C Bmentioning
confidence: 99%
“…We used an LPS-stimulated, murine macrophage cell line, RAW264.7, as a model of inflammation to determine the effects of LOME. The binding of LPS to downstream signaling cascades, including mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) pathways (14), led to the production of inflammatory mediators from macrophages, such as TNF-α, IL-1β, IL-6, PGE 2 and NO. Our results indicated that LOME inhibited NO, PGE 2 and the pro-inflammatory cytokines in LPS-stimulated macrophages through NF-κB signaling, as well as the MAPK, extracellular signal-regulated kinase (ERK)1/2, p38 and c-Jun N-terminal kinase (JNK)1/2 pathways.…”
Section: Introductionmentioning
confidence: 99%