Esculentoside A suppresses Aβ1-42-induced neuroinflammation by down-regulating MAPKs pathways in vivo
Esculentoside A suppresses Aβ1-42-induced neuroinflammation by down-regulating MAPKs pathways in vivo
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Esculentoside A 通过下调体内 MAPK 通路抑制 A beta(1-42) 诱导的神经炎症
DOI：
10.1179/1743132815y.0000000066
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发表时间：
2015-10-01
影响因子：
1.9
通讯作者：
Xu, Yun
中科院分区：
文献类型：
--
作者：
Yang, Hui;Wang, Sulei;Xu, Yun
简介：Esculentoside A (EsA) 是从商陆根中分离出来的皂苷。先前的研究表明，EsA 在外周免疫炎症中发挥强大的抗炎作用。本研究旨在确定EsA是否对炎症相关的神经退行性疾病，如阿尔茨海默病（AD）有效。方法：将雄性C57BL/6（B6）小鼠分为三组，每组6只小鼠，如下：（1）对照组；（2）对照组；（3）对照组。 (2)AD模型组(Aβ(1-42)生理盐水诱导AD小鼠)； (3)EsA组(Aβ(1-42)诱导的AD小鼠，EsA，5mg/kg/天，腹膜内注射15天)。 EsA 治疗 15 天后进行行为测试。使用实时 PCR 和蛋白质印迹来评估炎症因子和丝裂原激活蛋白激酶 (MAPK) 的水平。免疫染色用于测定活化的小胶质细胞和星形胶质细胞的水平。结果：结果表明，EsA 可以减轻 A beta(1-42) 诱导的 AD 小鼠的记忆缺陷。 Esculentoside A 降低 A beta(1-42) 诱导的 AD 小鼠海马中的促炎因子以及小胶质细胞和星形胶质细胞的活化。此外，A beta(1-42)激活AD模型组小鼠海马中ERK、JNK和p38 MAPK的磷酸化，而EsA显着降低磷酸化水平。结论：这些研究结果表明EsA对β-淀粉样蛋白引发的神经炎症具有保护作用。
Introduction: Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous studies have demonstrated that EsA exerts strong anti-inflammatory effects in peripheral immune inflammation. This study is to determine whether EsA is effective in inflammation-related neurodegenerative diseases, such as Alzheimer's disease (AD).Methods: Male C57BL/6(B6) mice were divided into three groups of six mice as follows: (1) control group; (2) AD model group (A beta(1-42)-induced AD mice with saline); (3) EsA group (A beta(1-42)-induced AD mice with EsA, 5 mg/kg/day, i.p. for 15 days). Behavioural testing was performed after 15 days of EsA treatment. Real time PCR and Western blot were used to assess the level of inflammation factors and mitogen-activated protein kinases (MAPKs). Immunostaining was used to determine the level of activated microglia and astrocyte.Results: The results showed that EsA attenuated memory deficits in A beta(1-42)-induced AD mice. Esculentoside A decreased the pro-inflammatory factors and microglia and astrocyte activation in the hippocampi of A beta(1-42)-induced AD mice. Moreover, A beta(1-42) activated phosphorylation of ERK, JNK and p38 MAPKs in the hippocampi of mice in the AD model group, while EsA significantly decreased the phosphorylation levels.Conclusion: These findings indicate that EsA provides protective effects against neuroinflammation triggered by beta-amyloid.