Article Publish Status: FREE
Abstract Title:

Ginsenoside Rh2 Downregulates LPS-Induced NF-κ B Activation through Inhibition of TAK1 Phosphorylation in RAW 264.7 Murine Macrophage.

Abstract Source:

Evid Based Complement Alternat Med. 2013 ;2013:646728. Epub 2013 Feb 17. PMID: 23483870

Abstract Author(s):

Li-Hua Lian, Quan Jin, Shun-Zong Song, Yan-Ling Wu, Ting Bai, Shuang Jiang, Qian Li, Ning Yang, Ji-Xing Nan

Article Affiliation:

Li-Hua Lian


The present study was carried out to evaluate the inhibitory effects of ginsenoside Rh2 on nuclear-factor- (NF-)κ B in lipopolysaccharide- (LPS-) activated RAW 264.7 murine macrophages. RAW 264.7 cells were pretreated with indicated concentrations of ginsenoside Rh2 for 1 h prior to the incubation of LPS (1  μ g/mL) for indicated time period. Ginsenoside Rh2 reduced CD14 and Toll-like receptor 4 (TLR4)expressions 24 h after LPS stimulation. Furthermore, ginsenoside Rh2 significantly inhibited TGF-beta-activated kinase 1 (TAK1) phosphorylation 30 min after LPS stimulation. Ginsenoside Rh2 was further shown to inhibit NF- κ B p65 translocation into the nucleus by suppressing I κ B- α degradation. Also, LPS increased mRNA expression of TNF- α and IL-1 α time-dependently, while TQ reduced TNF- α within 3 h and IL-1 α within 1 h. And we firstly found that pretreatment of ginsenoside Rh2 successively inhibited hypoxia-inducible factor- (HIF-) 1 α expression increased by LPS. In conclusion, ginsenoside Rh2 may inhibit LPS-induced NF- κ B activation and reduce HIF-1 α accumulation, suggesting that ginsenoside Rh2 may be considered as a potential therapeutic candidate for chronic inflammatory diseases.

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