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多糖对氧化应激诱导的神经元凋亡的神经保护作用。

Neuroprotective effects of polysaccharides against oxidative stress-induced neuronal apoptosis.

作者信息

Sun Xin-Zhi, Liao Ying, Li Wei, Guo Li-Mei

机构信息

Department of Orthopedics, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.

Department of Public Security Technology, Railway Police College, Zhengzhou, Henan Province, China.

出版信息

Neural Regen Res. 2017 Jun;12(6):953-958. doi: 10.4103/1673-5374.208590.

Abstract

polysaccharides have protective effects against apoptosis in neurons exposed to ischemia/reperfusion injury, but the mechanisms are unclear. The goal of this study was to investigate the underlying mechanisms of the effects of ganoderma polysaccharides against oxidative stress-induced neuronal apoptosis. Hydrogen peroxide (HO) was used to induce apoptosis in cultured cerebellar granule cells. In these cells, polysaccharides remarkably suppressed HO-induced apoptosis, decreased expression of caspase-3, Bax and Bim and increased that of Bcl-2. These findings suggested that polysaccharides regulate expression of apoptosis-associated proteins, inhibit oxidative stress-induced neuronal apoptosis and, therefore, have significant neuroprotective effects.

摘要

多糖对暴露于缺血/再灌注损伤的神经元凋亡具有保护作用,但其机制尚不清楚。本研究的目的是探讨灵芝多糖抗氧化应激诱导的神经元凋亡作用的潜在机制。用过氧化氢(H₂O₂)诱导培养的小脑颗粒细胞凋亡。在这些细胞中,多糖显著抑制H₂O₂诱导的凋亡,降低半胱天冬酶-3、Bax和Bim的表达,并增加Bcl-2的表达。这些结果表明,多糖调节凋亡相关蛋白的表达,抑制氧化应激诱导的神经元凋亡,因此具有显著的神经保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73a6/5514871/8055e241a9a8/NRR-12-953-g002.jpg

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