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[6]-姜酚通过上调神经营养因子减轻过氧化氢处理星形胶质细胞中的神经元凋亡。

[6]-shogaol attenuates neuronal apoptosis in hydrogen peroxide-treated astrocytes through the up-regulation of neurotrophic factors.

机构信息

Department of Laboratory Animal Medicine, College of Veterinary Medicine, Chonbuk National University of Jeonju, Korea.

出版信息

Phytother Res. 2013 Dec;27(12):1795-9. doi: 10.1002/ptr.4946. Epub 2013 Feb 11.

DOI:10.1002/ptr.4946
PMID:23401228
Abstract

Neuronal apoptosis induced by oxidative stress is a prominent feature of neurodegenerative disorders. [6]-shogaol, a bio-active compound in ginger, possesses potent anti-inflammatory actions and has recently emerged as a potential therapeutic agent for neurodegenerative disorders. However, the effects of [6]-shogaol on astroglial apoptosis following exogenously induced oxidative stress has not yet been investigated. Here, we show that the anti-apoptotic activity of [6]-shogaol in astrocytes following exposure to hydrogen peroxide (H2 O2 ) involves a marked up-regulation of neurotrophic factors such as nerve growth factor, glial cell line-derived neurotrophic factor, and brain-derived neurotrophic factor. Astrocytes co-treated with [6]-shogaol and H2 O2 for 1 h showed decrease in reactive oxygen species production compared with those only treated with H2 O2 . Moreover, [6]-shogaol counteracted the reduced expression of ERK1/2 in H2 O2 -treated astrocytes and protected these cells from oxidative stress and apoptosis by attenuating the impairment of mitochondrial function proteins such as Bcl-2 and Bcl-xL. Additionally, [6]-shogaol inhibits the expression of the apoptotic proteins Bax and caspase-3 in H2 O2 -treated astrocytes. This data suggest that following oxidative stress, [6]-shogaol protects astrocytes from oxidative damage through the up-regulating levels of neurotrophic factors. These findings provide further support for the use of [6]-shogaol as a therapeutic agent in neurodegenerative disorders.

摘要

氧化应激诱导的神经元凋亡是神经退行性疾病的一个显著特征。[6]-姜烯酚,生姜中的一种生物活性化合物,具有强大的抗炎作用,最近已成为神经退行性疾病的潜在治疗药物。然而,[6]-姜烯酚对外源性氧化应激诱导的星形胶质细胞凋亡的影响尚未得到研究。在这里,我们表明,[6]-姜烯酚在暴露于过氧化氢(H2O2)后对星形胶质细胞的抗凋亡活性涉及神经营养因子的显著上调,如神经生长因子、胶质细胞系源性神经营养因子和脑源性神经营养因子。与仅用 H2O2 处理的星形胶质细胞相比,用[6]-姜烯酚和 H2O2 共同处理 1 小时的星形胶质细胞中活性氧的产生减少。此外,[6]-姜烯酚逆转了 H2O2 处理的星形胶质细胞中 ERK1/2 的表达减少,并通过减弱线粒体功能蛋白(如 Bcl-2 和 Bcl-xL)的损伤来保护这些细胞免受氧化应激和凋亡。此外,[6]-姜烯酚抑制了 H2O2 处理的星形胶质细胞中凋亡蛋白 Bax 和 caspase-3 的表达。这些数据表明,在氧化应激后,[6]-姜烯酚通过上调神经营养因子的水平来保护星形胶质细胞免受氧化损伤。这些发现为[6]-姜烯酚在神经退行性疾病中的治疗应用提供了进一步的支持。

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