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辣椒素可损害幼年小鼠神经祖细胞的增殖和海马神经发生。

Capsaicin impairs proliferation of neural progenitor cells and hippocampal neurogenesis in young mice.

机构信息

Department of Pharmacy, College of Pharmacy and Research Institute for Drug Development, Longevity Life Science and Technology Institutes, Pusan National University, Geumjeong-gu, Busan, Korea.

出版信息

J Toxicol Environ Health A. 2010;73(21-22):1490-501. doi: 10.1080/15287394.2010.511572.

Abstract

Capsaicin (N-vanillyl-8-methyl-1-nonenamide) is a major pungent ingredient in hot peppers and induces apoptosis in malignant carcinoma cell lines. However, the adverse effects of capsaicin on neuronal development have not been fully explored. The aim of this study was to determine whether capsaicin affected murine-derived cerebellar multi-potent neural progenitor cells (NPC) or adult hippocampal neurogenesis in vivo. Capsaicin dose-dependently suppressed NPC proliferation, and higher concentrations were cytotoxic. Capsaicin decreased the activation of extracellular signal-regulated kinases (ERK) without markedly affecting p38 kinases. Capsaicin reduced the number of newly generated cells in the dentate gyrus of the hippocampus but did not significantly alter learning and memory performance in young adult mice. Interestingly, capsaicin decreased ERK activation in the hippocampus, suggesting that reduced ERK signaling may be involved in the capsaicin-mediated regulation of hippocampal neurogenesis.

摘要

辣椒素(N-香草基-8-甲基-1-壬酰胺)是辣椒中的主要辛辣成分,可诱导恶性癌细胞系凋亡。然而,辣椒素对神经元发育的不良影响尚未得到充分研究。本研究旨在确定辣椒素是否影响体内鼠源性小脑多潜能神经前体细胞(NPC)或成年海马神经发生。辣椒素呈剂量依赖性抑制 NPC 增殖,较高浓度则具有细胞毒性。辣椒素降低细胞外信号调节激酶(ERK)的激活,而对 p38 激酶影响不大。辣椒素减少了海马齿状回中新生成细胞的数量,但对年轻成年小鼠的学习和记忆能力没有显著影响。有趣的是,辣椒素降低了海马中的 ERK 激活,提示减少的 ERK 信号可能参与了辣椒素介导的海马神经发生调节。

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