Vinoth Kumar R, Oh Tae Woo, Park Yong-Ki
Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju, 780-714, Republic of Korea.
Korean Medicine R&D Center, Dongguk University, Gyeongju, 780-714, Republic of Korea.
Neurochem Res. 2016 May;41(5):951-7. doi: 10.1007/s11064-015-1804-x. Epub 2016 Jan 6.
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.
小胶质细胞激活在神经炎症中起重要作用，并与多种神经系统疾病有关。因此，抑制小胶质细胞激活和促炎细胞因子可能会有效治疗神经退行性疾病。在本研究中，我们发现人参皂苷Rh2抑制对脂多糖（LPS）的炎症反应，并预防LPS诱导的小胶质细胞神经毒性。人参皂苷Rh2显著降低LPS诱导的活化小胶质细胞中一氧化氮生成、肿瘤坏死因子-α、白细胞介素（IL）-6、IL-1β、环氧合酶-2和诱导型一氧化氮合酶的产生。此外，人参皂苷Rh2（20和50μM）显著增加转化生长因子-β1表达并降低Smad表达。这些结果表明，人参皂苷Rh2通过调节转化生长因子-β1/Smad通路有效抑制小胶质细胞激活和促炎细胞因子的产生。
