Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha 410011, China.
Hunan Provincial Engineering Research Centre of Translational Medicine and Innovative Drug, Changsha 410011, China.
Oxid Med Cell Longev. 2021 Jan 13;2021:8843899. doi: 10.1155/2021/8843899. eCollection 2021.
, a well-known life-prolonging tonic in Chinese medicine, has been widely used for nourishing nerves in the orient, but the underlying molecular mechanisms remain unclear. In this study, we found that polysaccharides (PSP) ameliorated 1-methyl-4-phenyl-1,2.3,6-tetrahydropyridine- (MPTP-) induced locomotor activity deficiency and dopaminergic neuronal loss in an Parkinson's disease (PD) mouse model. Additionally, PSP pretreatment inhibited -methyl-4-phenylpyridine (MPP+) induced the production of reactive oxygen species, increasing the ratio of reduced glutathione/oxidized glutathione. experiments showed that PSP promoted the proliferation of N2a cells in a dose-dependent manner, while exhibiting effects against oxidative stress and neuronal apoptosis elicited by MPP+. These effects were found to be associated with the activation of Akt/mTOR-mediated p70S6K and 4E-BP1 signaling pathways, as well as nuclear factor erythroid 2-related factor 2- (Nrf2-) mediated NAD(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (Gclc), and glutamate-cysteine ligase modulatory subunit (Gclm), resulting in antiapoptotic and antioxidative effects. Meanwhile, PSP exhibited no chronic toxicity in C57BJ/6 mice. Together, our results suggest that PSP can serve as a promising therapeutic candidate with neuroprotective properties in preventing PD.
, 一种在中医中被广泛应用的延年益寿的滋补品，在东方被广泛用于滋养神经，但潜在的分子机制仍不清楚。在这项研究中，我们发现 多糖（PSP）改善了 1-甲基-4-苯基-1,2,3,6-四氢吡啶-（MPTP-）诱导的运动活性缺陷和帕金森病（PD）小鼠模型中的多巴胺能神经元丧失。此外，PSP 预处理抑制了 -甲基-4-苯基吡啶（MPP+）诱导的活性氧的产生，增加了还原型谷胱甘肽/氧化型谷胱甘肽的比例。 实验表明，PSP 以剂量依赖的方式促进 N2a 细胞的增殖，同时对 MPP+诱导的氧化应激和神经元凋亡具有作用。这些作用与 Akt/mTOR 介导的 p70S6K 和 4E-BP1 信号通路的激活以及核因子红细胞 2 相关因子 2-（Nrf2-）介导的烟酰胺腺嘌呤二核苷酸（NAD（P）H）醌氧化还原酶 1（NQO1）、血红素加氧酶-1（HO-1）、谷氨酸-半胱氨酸连接酶催化亚基（Gclc）和谷氨酸-半胱氨酸连接酶调节亚基（Gclm）有关，导致抗凋亡和抗氧化作用。同时，PSP 在 C57BJ/6 小鼠中没有表现出慢性毒性。总之，我们的结果表明 PSP 可以作为一种有前途的治疗候选物，具有预防 PD 的神经保护特性。
