Anti-Inflammatory Effects of Ginsenoside-Rh2 Inhibits LPS-Induced Activation of Microglia and Overproduction of Inflammatory Mediators Via Modulation of TGF-β1/Smad Pathway

• DOI: 10.1007/s11064-015-1804-x
• Publication Date: 2016-01-06T05:20:10Z
• Authors: R Vinoth Kumar; Tae Woo Oh; Yong-Ki Park
• Keywords: Lipopolysaccharides; 0301 basic medicine; Ginsenosides; Interleukin-6; Tumor Necrosis Factor-alpha; Interleukin-1beta; Smad Proteins; Nitric Oxide; Cell Line; 3. Good health; Transforming Growth Factor beta1; Mice; 03 medical and health sciences; Neuroprotective Agents; Cyclooxygenase 2; Animals; Microglia; Inflammation Mediators; Nitric Oxide Synthase; Signal Transduction

Microglia activation plays an important role in neuroinflammation and contributes to several neurological disorders. Hence, inhibition of both microglia activation and pro-inflammatory cytokines may lead to the effective treatment of neurodegenerative diseases. In this study, we found that GRh2 inhibited the inflammatory response to lipopolysaccharide (LPS) and prevented the LPS-induced neurotoxicity in microglia cells. GRh2 significantly decreased the generation of nitric oxide production, and tumor necrosis factor-α, interleukin (IL)-6, IL-1β, cyclooxygenase-2 and inducible nitric oxide synthase in LPS-induced activated microglia cells. Furthermore, GRh2 (20 and 50 μM) significantly increased TGF-β1 expression and reduced the expression of Smad. These results suggest that GRh2 effectively inhibits microglia activation and production of pro-inflammatory cytokines via modulating the TGF-β1/Smad pathway.