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首页> 外文期刊>Life sciences >Water extract of propolis and its main constituents, caffeoylquinic acid derivatives, exert neuroprotective effects via antioxidant actions
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Water extract of propolis and its main constituents, caffeoylquinic acid derivatives, exert neuroprotective effects via antioxidant actions

机译:蜂胶的水提取物及其主要成分咖啡酰奎尼酸衍生物通过抗氧化作用发挥神经保护作用

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摘要

We investigated whether water extract of Brazilian green propolis (WEP) and its main constituents [caffeoylquinic acid derivatives (3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoylquinic acid, chlorogenic acid) and cinnamic acid derivatives (p-coumaric acid, artepillin C, drupanin, baccharin)] exert neuroprotective effects against the retinal damage induced by oxidative stress. Additionally, their neuroprotective effects were compared with their antioxidant effects. WEP, 3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoyIquinic acid, chlorogenic acid, and p-coumaric acid (but not artepillin C, baccharin, or drupanin) concentration-dependently inhibited oxidative stress-induced neurotoxicity [achieved using L-buthionme-(S^)-sulfoxirnine (BSO) to deplete glutathione in combination with glutamate to inhibit cystine uptake] in cultured retinal ganglion cells (RGC-5, a rat ganglion cell line transformed using El A virus). At their effective concentrations against oxidative stress-induced retinal damage, WEP, 3,4-di-caffeoylquinic acid, 3,5-di-cafieoylquinic acid, and chlorogenic acid (but not cinnamic acid derivatives) inhibited lipid peroxidation (LPO) in mouse forebrain homogenates. Thus, the neuroprotective effects of WEP and caffeoylquinic acid derivatives paralleled those against LPO. These findings indicate that WEP and caffeoylquinic acid derivatives have neuroprotective effects against retinal damage in vitro, and that these effects may be partly mediated via antioxidanteffects.
机译:我们调查了巴西绿色蜂胶(WEP)的水提取物及其主要成分[咖啡酰奎尼酸衍生物(3,4-二-O-咖啡酰奎尼酸,3,5-二-O-咖啡酰奎尼酸,绿原酸)和肉桂酸衍生物(对香豆酸,青蒿素C,Drupanin,baccharin)对氧化应激引起的视网膜损伤具有神经保护作用。另外,将它们的神经保护作用与抗氧化作用进行了比较。 WEP,3,4-二-O-咖啡酰奎尼酸,3,5-二-O-咖啡酰奎尼酸,绿原酸和对香豆酸(但不包括青霉素C,baccharin或drupanin)浓度依赖性地抑制氧化应激,在培养的视网膜神经节细胞(RGC-5,一种用El A病毒转化的大鼠神经节细胞系)中诱导的神经毒性[通过使用L-buthionme-(S ^)-亚磺酰氧胺(BSO)与谷氨酸结合消耗谷胱甘肽来抑制胱氨酸的摄取而达到] )。在抗氧化应激引起的视网膜损伤的有效浓度下,WEP,3,4-二咖啡酰奎尼酸,3,5-二咖啡酰奎尼酸和绿原酸(但不是肉桂酸衍生物)抑制小鼠脂质过氧化(LPO)前脑匀浆。因此,WEP和咖啡酰奎尼酸衍生物的神经保护作用与针对LPO的神经保护作用平行。这些发现表明,WEP和咖啡酰奎尼酸衍生物在体外具有针对视网膜损害的神经保护作用,并且这些作用可能是通过抗氧化作用部分介导的。

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