title: Sulfated derivative of 20(S)-ginsenoside Rh2 inhibits inflammatory cytokines through MAPKs and NF-kappa B pathways in LPS-induced RAW264.7 macrophages.
abstract: In the previous study, we found that sulfated derivative B2 of ginsenoside Rh2 (Rh2-B2) has greater anti-inflammatory effects than 20(S)-ginsenoside Rh2. However, the anti-inflammatory mechanism of Rh2-B2 remains unclear. We therefore assessed the effects of Rh2-B2 on inflammatory cytokines in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. We found that Rh2-B2 (1-5 mg/L) significantly inhibited tumor necrosis factor alpha, interleukin (IL)-6, IL-1β, and increased IL-10 production from protein and mRNA levels. Furthermore, Rh2-B2 significantly inhibited the phosphorylation of p38 and c-Jun N-terminal kinase as well as decreased p65 nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) translocation into the nucleus by nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha degradation. The present results indicate that Rh2-B2 inhibits the production of inflammatory cytokines induced by LPS through blocking mitogen-activated protein kinases and NF-κB signaling pathways.
authors.affiliation: Department of Clinical Veterinary Medicine, College of Animal Science and Veterinary Medicine, Jilin University, 5333 Xi'an Road, Changchun, Jilin 130062, China.
authors.forename: Wen-Yan
authors.initials: WY
authors.lastname: Bi
authors.forename: Ben-Dong
authors.initials: BD
authors.lastname: Fu
authors.forename: Hai-Qing
authors.initials: HQ
authors.lastname: Shen
authors.forename: Qian
authors.initials: Q
authors.lastname: Wei
authors.forename: Cui
authors.initials: C
authors.lastname: Zhang
authors.forename: Zhou
authors.initials: Z
authors.lastname: Song
authors.forename: Qian-Qian
authors.initials: QQ
authors.lastname: Qin
authors.forename: Hui-Ping
authors.initials: HP
authors.lastname: Li
authors.forename: Shuang
authors.initials: S
authors.lastname: Lv
authors.forename: Shuai-Cheng
authors.initials: SC
authors.lastname: Wu
authors.forename: Peng-Fei
authors.initials: PF
authors.lastname: Yi
authors.forename: Xu-Bin
authors.initials: XB
authors.lastname: Wei
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000494:pharmacology*; D002478:Cells, Cultured; D036145:Ginsenosides / Q000737:chemistry / Q000494:pharmacology*; D007249:Inflammation / Q000378:metabolism; D016753:Interleukin-10 / Q000096:biosynthesis; D053583:Interleukin-1beta / Q000096:biosynthesis / Q000235:genetics; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008070:Lipopolysaccharides; D008264:Macrophages; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D010766:Phosphorylation; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013431:Sulfates / Q000737:chemistry; D051996:Transcription Factor RelA / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D036145:Ginsenosides; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; C498144:Rela protein, mouse; D013431:Sulfates; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; C055305:ginsenoside Rh2; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases