山茱萸苷 A 通过激活 PPAR-γ 抑制 LPS 诱导的 BV2 小胶质细胞活化。
Esculentoside A inhibits LPS-induced BV2 microglia activation through activating PPAR-γ.
机构信息
Department of Intensive Care Unit, The First Hospital of Jilin University, Changchun 130021, China.
Ultrasound Diagnosis Department, The First Hospital of Jilin University, Changchun 130021, China.
出版信息
Eur J Pharmacol. 2017 Oct 15;813:61-65. doi: 10.1016/j.ejphar.2017.07.029. Epub 2017 Jul 19.
Neuroinflammation has been recognized as a factor in the pathogenesis of neurodegenerative diseases. Esculentoside A (EsA), a saponin isolated from Phytolacca esculenta, has been reported to have anti-inflammatory activity. However, little research has been reported on the anti-neuroinflammatory effects of EsA. EsA concentration-dependently suppressed LPS-induced TNF-α, IL-1β, and PGE2 production. LPS-induced NF-κB activation was inhibited by treatment of EsA. Furthermore, EsA concentration-dependently up-regulated the expression of PPAR-γ. In addition, GW9662, a specific PPAR-γ inhibitor, reversed the anti-inflammatory effects of EsA. In conclusion, these results indicate that EsA exerts anti-inflammatory effects by activating PPAR-γ.
神经炎症已被认为是神经退行性疾病发病机制中的一个因素。已报道从商陆中分离得到的甾体皂苷 A（EsA）具有抗炎活性。然而，关于 EsA 的抗神经炎症作用的研究甚少。EsA 呈浓度依赖性地抑制 LPS 诱导的 TNF-α、IL-1β 和 PGE2 的产生。EsA 处理抑制 LPS 诱导的 NF-κB 活化。此外，EsA 呈浓度依赖性地上调 PPAR-γ 的表达。另外，PPAR-γ 的特异性抑制剂 GW9662 逆转了 EsA 的抗炎作用。总之，这些结果表明 EsA 通过激活 PPAR-γ 发挥抗炎作用。
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