Oridonin attenuates Aβ1-42-induced neuroinflammation and inhibits NF-κB pathway.

Oridonin attenuates Aβ1-42-induced neuroinflammation and inhibits NF-κB pathway.
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冬凌草甲素可减轻 A beta(1-42) 诱导的神经炎症并抑制 NF-kappa B 通路

DOI:
10.1371/journal.pone.0104745
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Zhu X
Zhu X
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Wang S;Yang H;Yu L;Jin J;Qian L;Zhao H;Xu Y;Zhu X

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β-淀粉样蛋白(Aβ)诱导的神经炎症在阿尔茨海默病(AD)的发病机制中起重要作用,抑制Aβ诱导的神经炎症是AD治疗的一个潜在策略。冬凌草甲素(Oridonin,Ori)是冬凌草(Rabdosia rubescens)的一种化合物,具有抗炎作用。在这项研究中,我们证明了Ori抑制Aβ1-42诱导的AD小鼠海马中胶质细胞活化并减少炎性细胞因子的释放。此外,Ori还能抑制NF-κB通路和Aβ1-42诱导的细胞凋亡。Ori还能改善Aβ1-42诱导的AD小鼠的记忆障碍。结论:Ori可抑制Aβ1-42诱导的神经炎症反应,减轻Aβ1-42诱导的记忆障碍,有望成为治疗AD的有效药物。
Neuroinflammation induced by beta-amyloid (Aβ) plays a critical role in the pathogenesis of Alzheimer’s disease (AD), and inhibiting Aβ-induced neuroinflammation serves as a potential strategy for the treatment of AD. Oridonin (Ori), a compound of Rabdosia rubescens, has been shown to exert anti-inflammatory effects. In this study, we demonstrated that Ori inhibited glial activation and decreased the release of inflammatory cytokines in the hippocampus of Aβ1–42-induced AD mice. In addition, Ori inhibited the NF-κB pathway and Aβ1–42-induced apoptosis. Furthermore, Ori could attenuate memory deficits in Aβ1–42-induced AD mice. In conclusion, our study demonstrated that Ori inhibited the neuroinflammation and attenuated memory deficits induced by Aβ1–42, suggesting that Ori might be a promising candidate for AD treatment.
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