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[6]-姜烯酚对过氧化氢诱导的神经元损伤后 HT22 细胞胆碱能信号的影响。

Effects of [6]-shogaol on cholinergic signaling in HT22 cells following neuronal damage induced by hydrogen peroxide.

机构信息

Department of Laboratory Animal Medicine, College of Veterinary Medicine, Chonbuk National University, Jeonju 561 756, Republic of Korea.

出版信息

Food Chem Toxicol. 2012 May;50(5):1454-9. doi: 10.1016/j.fct.2012.02.014. Epub 2012 Feb 22.

DOI:10.1016/j.fct.2012.02.014
PMID:22381256
Abstract

Cholinergic neurons play a major role in memory and attention. The dysfunction and death of these neurons, especially in the hippocampus, are thought to contribute to the pathophysiology of memory deficits associated with Alzheimer's disease (AD). Therefore, studying the cholinergic properties and cell survival may help in treating this disease. We investigated the possible effects of [6]-shogaol on cholinergic signaling in HT22 hippocampal neuronal cells. HT22 cells express essential cholinergic markers, including choline acetyltransferase (ChAT) and choline transporter (ChTp). HT22 cells treated with H(2)O(2) for 3h showed an increase in ROS production (35%). These features were partly recovered by [6]-shogaol. Treating H(2)O(2)-treated HT22 cells with [6]-shogaol markedly increased the expression of ChAT and ChTp, an effect similar to that of brain-derived neurotrophic factor (BDNF). Furthermore, K-252a, an inhibitor of the BDNF receptor Trk B, attenuated the effects of both [6]-shogaol and BDNF. These data suggest that [6]-shogaol protects neurons by increasing ChAT and ChTp expression through a BDNF increase and thus may be useful for treating neurodegenerative diseases.

摘要

胆碱能神经元在记忆和注意力中起着重要作用。这些神经元的功能障碍和死亡,特别是在海马体中,被认为是导致与阿尔茨海默病(AD)相关的记忆缺陷的病理生理学的原因。因此,研究胆碱能特性和细胞存活可能有助于治疗这种疾病。我们研究了[6]-姜烯酚对 HT22 海马神经元细胞中胆碱能信号的可能影响。HT22 细胞表达重要的胆碱能标志物,包括胆碱乙酰转移酶(ChAT)和胆碱转运蛋白(ChTp)。用 H2O2 处理 3 小时的 HT22 细胞显示 ROS 产生增加(35%)。[6]-姜烯酚部分恢复了这些特征。用[6]-姜烯酚处理 H2O2 处理的 HT22 细胞可显著增加 ChAT 和 ChTp 的表达,其作用类似于脑源性神经营养因子(BDNF)。此外,BDNF 受体 Trk B 的抑制剂 K-252a 减弱了[6]-姜烯酚和 BDNF 的作用。这些数据表明,[6]-姜烯酚通过增加 BDNF 来增加 ChAT 和 ChTp 的表达来保护神经元,因此可能对治疗神经退行性疾病有用。

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