Sulfated derivative of 20(S)-ginsenoside Rh2 inhibits inflammatory cytokines through MAPKs and NF-kappa B pathways in LPS-induced RAW264.7 macrophages.

Wen-Yan Bi, Ben-Dong Fu, Hai-Qing Shen, Qian Wei, Cui Zhang, Zhou Song, Qian-Qian Qin, Hui-Ping Li, Shuang Lv, Shuai-Cheng Wu, Peng-Fei Yi, Xu-Bin Wei

Index: Inflammation 35(5) , 1659-68, (2012)

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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.