Lig-8, a Highly Bioactive Lignophenol Derivative from Bamboo Lignin, Exhibits Multifaceted Neuroprotective Activity

Yasushi Ito, Yukihiro Akao, Masamitsu Shimazawa, Norio Seki, Yoshinori Nozawa, Hideaki Hara
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引用次数: 20

Abstract

Lignin is a durable aromatic network polymer that is second only to cellulose in natural abundance. Lig-8, a lignophenol derivative from bamboo lignin, is a highly potent neuroprotectant. It protects human neuroblastoma cells (SH-SY5Y) from hydrogen peroxide (H2O2)–induced apoptosis by preventing caspase-3 activation via either caspase-8 or caspase-9. It exerts this antiapoptotic effect by protecting mitochondrial membrane permeability from damage by H2O2 or the peripheral benzodiazepine receptor ligand PK11195. Lig-8 has been also shown to scavenge the reactive oxygen or nitrogen species in vitro. Furthermore, lig-8 suppresses apoptosis induced by oxygen-glucose deprivation, tunicamycin (endoplasmic reticulum [ER]–stress inducer), or proteasome inhibitor in pheochromocytoma cells. In addition, in vivo, lig-8 reduced intravitreal N-methyl-d-aspartate–induced retinal damage (decreases in retinal ganglion cells and inner plexiform layer thickness) in mice. Lig-8 prevents neuronal damage partly by inhibiting excessive endoplasmic reticulum stress. In this article, we review the protective effects of lig-8 against apoptosis induced by various stimuli. Apoptosis is an active, energy-dependent process through which living cells initiate their own death. It can be induced by a variety of physiological and pharmacological stimuli. Apoptotic cell death is associated with neurodegenerative disorders such as Alzheimer, Parkinson, or Huntington disease as well as glaucoma. We believe that the elucidation of the mechanism of antiapoptotic action of lig-8 may help in finding new approaches to the treatment of neurodegenerative disorders.

Abstract Image

从竹木质素中提取的高生物活性木质素酚衍生物,具有多方面的神经保护作用
木质素是一种耐用的芳香网状聚合物,其天然丰度仅次于纤维素。从竹木质素中提取的木质素酚衍生物,是一种高效的神经保护剂。它通过caspase-8或caspase-9阻止caspase-3激活,从而保护人神经母细胞瘤细胞(SH-SY5Y)免受过氧化氢(H2O2)诱导的凋亡。它通过保护线粒体膜通透性免受H2O2或外周苯二氮卓受体配体PK11195的损伤而发挥抗凋亡作用。li -8也被证明在体外清除活性氧或活性氮。此外,在嗜铬细胞瘤细胞中,lig8可抑制氧-葡萄糖剥夺、tunicamycin(内质网应激诱导剂)或蛋白酶体抑制剂诱导的细胞凋亡。此外,在体内,lit -8可减轻小鼠玻璃体内n -甲基-d-天冬氨酸引起的视网膜损伤(视网膜神经节细胞和内丛状层厚度减少)。li -8部分通过抑制过度内质网应激来防止神经元损伤。本文就lig8对各种刺激诱导的细胞凋亡的保护作用进行综述。细胞凋亡是一种活跃的、能量依赖性的过程,通过这种过程,活细胞开始了自己的死亡。它可由多种生理和药理刺激引起。凋亡细胞死亡与神经退行性疾病如阿尔茨海默病、帕金森病或亨廷顿病以及青光眼有关。我们相信,阐明li -8抗凋亡作用的机制可能有助于找到治疗神经退行性疾病的新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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