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多糖对缺氧诱导的神经元凋亡的神经保护作用。

Neuroprotective effects of polysaccharides against neuronal apoptosis induced by hypoxia.

作者信息

Xiang Qin, Zhou Wen-Yun, Hu Wei-Xu, Wen Zhu, He Dan, Wu Xiao-Mu, Wei Hui-Ping, Wang Wen-Ding, Hu Guo-Zhu

机构信息

State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Biology, Hunan University, Changsha, Hunan 410082, P.R. China.

Institute of Clinical Medical Sciences, Jiangxi Province People's Hospital, Nanchang, Jiangxi 330006, P.R. China.

出版信息

Exp Ther Med. 2015 Dec;10(6):2063-2070. doi: 10.3892/etm.2015.2819. Epub 2015 Oct 20.

Abstract

polysaccharides (RDPS) are the primary active ingredient of , which is a traditional Chinese medicine. RDPS have previously been shown to scavenge reactive oxygen species, and protect against D-galactose-induced mimetic aging. The present study aimed to investigate the neuroprotective effects of RDPS against hypoxia-induced neuronal cell apoptosis. Neuronal cells harvested from pregnant Sprague-Dawley rats were divided into groups, as follows: i) Normal control group; ii) hypoxia-induced apoptosis neuronal cell model; iii) 0.025 g/l RDPS-treated group; iv) 0.05 g/l RDPS-treated group; v) 0.1 g/l RDPS-treated group; and vi) 0.25 g/l RDPS treated group. Neuronal cell viability was investigated using an MTT assay, and neuronal cell apoptosis was analyzed using Annexin V-fluorescein isothiocyanate/propidium iodide double-staining, Hoechst 33342 fluorescent staining, Rhodamine 123 staining, polymerase chain reaction and immunocytochemical staining. The RDPS-treated neuronal cells exhibited improved viability, and decreased hypoxia-induced mitochondrial injury and apoptosis. In addition, the mRNA and protein expression levels of caspase-3 and B-cell lymphoma (Bcl)-2-associated X protein (Bax) were significantly downregulated, whereas the mRNA and protein expression levels of Bcl-2 were significantly upregulated, in the RDPS-treated hypoxic neurons, as compared with the apoptosis model (P<0.05). Furthermore, the ratio of Bcl-2 expression:Bax expression significantly increased following RDPS treatment, as compared with the apoptosis model (P<0.05). The results of the present study suggested that RDPS may attenuate hypoxia-induced neuronal cell apoptosis by altering the expression levels of key apoptosis-regulating proteins in hypoxic neurons.

摘要

红芪多糖(RDPS)是一种传统中药的主要活性成分。此前已表明,RDPS 具有清除活性氧的作用,并能预防 D-半乳糖诱导的模拟衰老。本研究旨在探讨 RDPS 对缺氧诱导的神经元细胞凋亡的神经保护作用。从怀孕的 Sprague-Dawley 大鼠中获取的神经元细胞被分为以下几组:i)正常对照组;ii)缺氧诱导凋亡神经元细胞模型组;iii)0.025 g/l RDPS 处理组;iv)0.05 g/l RDPS 处理组;v)0.1 g/l RDPS 处理组;和 vi)0.25 g/l RDPS 处理组。使用 MTT 法检测神经元细胞活力,并使用 Annexin V-异硫氰酸荧光素/碘化丙啶双染、Hoechst 33342 荧光染色、罗丹明 123 染色、聚合酶链反应和免疫细胞化学染色分析神经元细胞凋亡情况。经 RDPS 处理的神经元细胞活力提高,缺氧诱导的线粒体损伤和凋亡减少。此外,与凋亡模型相比,经 RDPS 处理的缺氧神经元中半胱天冬酶-3(caspase-3)和 B 细胞淋巴瘤(Bcl)-2 相关 X 蛋白(Bax)的 mRNA 和蛋白表达水平显著下调,而 Bcl-2 的 mRNA 和蛋白表达水平显著上调(P<0.05)。此外,与凋亡模型相比,RDPS 处理后 Bcl-2 表达与 Bax 表达的比值显著增加(P<0.05)。本研究结果表明,RDPS 可能通过改变缺氧神经元中关键凋亡调节蛋白的表达水平来减轻缺氧诱导的神经元细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a5a/4665171/736fbbdb29e1/etm-10-06-2063-g00.jpg

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