Inhibition of the TLR/NF-κB Signaling Pathway and Improvement of Autophagy Mediates Neuroprotective Effects of Plumbagin in Parkinson's Disease.
Inhibition of the TLR/NF-κB Signaling Pathway and Improvement of Autophagy Mediates Neuroprotective Effects of Plumbagin in Parkinson's Disease.
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TLR/NF-κB 信号通路的抑制和自噬的改善介导白花丹素对帕金森病的神经保护作用
DOI：
10.1155/2022/1837278
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发表时间：
2022
影响因子：
--
通讯作者：
Yan, Jianguo
中科院分区：
文献类型：
--
作者：
Su, Yan;Li, Mao;Wang, Qi;Xu, Xingfeng;Qin, Peifang;Huang, Haitao;Zhang, Yuting;Zhou, Yali;Yan, Jianguo
从药用植物Plumbago zeylanica L.的根中提取的一种被称为白丹素（plbagin， PL）的萘醌分子具有广泛的药理特性，包括抗肿瘤、抗氧化、抗炎症和神经保护作用。白丹素因其治疗帕金森病（PD）的潜力而被研究。然而，其有效性和机制尚不清楚。本研究旨在体外和体内评价白桦素对帕金森病的治疗效果。白桦素部分修复了MPTP或MPTP/probenecid引起的小鼠黑质多巴胺能神经元的缺失和由此引起的行为障碍。此外，白桦素显著抑制了TLR/NF-κB通路。降低MPTP或MPTP/probenecid诱导的PD小鼠TNF-α、IL-6、IL-1β mRNA的表达，这与MPP+或LPS诱导的BV2细胞炎症模型的结果一致。在MPTP或MPTP/probenecid诱导的PD小鼠中，白蜡苷处理提高了微管相关蛋白1轻链3 β (LC3) LC3- ii /LC3- i水平，降低了p-mTOR和p62蛋白的积累，这与MPP+诱导的SH-SY5Y和PC12细胞的实验结果相似。因此，我们的研究结果支持了一种假设，即白杨苷通过促进自噬和抑制TLR/NF-κB信号通路的激活，是治疗帕金森病（PD）的有希望的药物。然而，为了更彻底地证实白桦素的抗帕金森病作用，在未来的研究中必须使用其他动物和细胞PD模型。
A naphthoquinone molecule known as plumbagin (PL), which has a wide range of pharmacological properties including antitumor, antioxidation, anti-inflammation, and neuroprotective effects, is extracted from the roots of the medicinal herb Plumbago zeylanica L. Plumbagin has been studied for its potential to treat Parkinson's disease (PD). However, its effectiveness and mechanism are still unknown. This study intends to evaluate plumbagin's effectiveness against PD in vitro and in vivo. Plumbagin partially repaired the loss of dopaminergic neurons in the nigral substantia nigra and the resulting behavioural impairment caused by MPTP or MPTP/probenecid in mice. Furthermore, plumbagin treatment significantly inhibited the TLR/NF-κB pathways. It reduced the TNF-α, IL-6, and IL-1β mRNA expression in PD mice induced by MPTP or MPTP/probenecid, which was consistent with the findings in the inflammatory model of BV2 cells induced by MPP+ or LPS. In addition, plumbagin treatment enhanced the microtubule-associated protein 1 light chain 3 beta (LC3) LC3-II/LC3-I levels while decreasing the p-mTOR and p62 protein accumulation in PD mice induced by MPTP or MPTP/probenecid, which was similar to the results obtained from the experiments in SH-SY5Y and PC12 cells induced by MPP+. Consequently, our results support the hypothesis that plumbagin, by promoting autophagy and inhibiting the activation of the TLR/NF-κB signaling pathway, is a promising treatment agent for treating Parkinson's disease (PD). However, to confirm plumbagin's anti-PD action more thoroughly, other animal and cell PD models must be used in future studies.
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影响因子：
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作者：
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4
作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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