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表型筛选技术解析抗细胞凋亡/铁死亡化合物的化学性质。

Profiling the chemical nature of anti-oxytotic/ferroptotic compounds with phenotypic screening.

机构信息

Cellular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd. La Jolla, CA, 92037, USA.

Cellular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd. La Jolla, CA, 92037, USA.

出版信息

Free Radic Biol Med. 2021 Dec;177:313-325. doi: 10.1016/j.freeradbiomed.2021.11.003. Epub 2021 Nov 5.

Abstract

Because old age is the greatest risk factor for Alzheimer's disease (AD), it is critical to target the pathological events that link aging to AD in order to develop an efficient treatment that acts upon the primary causes of the disease. One such event might be the activation of oxytosis/ferroptosis, a unique cell death mechanism characterized by mitochondrial dysfunction and lethal lipid peroxidation. Here, a comprehensive library of >900 natural compounds was screened for protection against oxytosis/ferroptosis in nerve cells with the goal of better understanding the chemical nature of inhibitors of oxytosis/ferroptosis. Although the compounds tested spanned structurally diverse chemical classes from animal, microbial, plant and synthetic origins, a small set of very potent anti-oxytotic/ferroptotic compounds was identified that was highly enriched in plant quinones. The ability of these compounds to protect against oxytosis/ferroptosis strongly correlated with their ability to protect against in vitro ischemia and intracellular amyloid-beta toxicity in nerve cells, indicating that aspects of oxytosis/ferroptosis also underly other toxicities that are relevant to AD. Importantly, the anti-oxytotic/ferroptotic character of the quinone compounds relied on their capacity to target and directly prevent lipid peroxidation in a manner that required the reducing activity of cellular redox enzymes, such as NAD(P)H:quinone oxidoreductase 1 (NQO1) and ferroptosis suppressor protein 1 (FSP1). Because some of the compounds increased the production of total reactive oxygen species while decreasing lipid peroxidation, it appears that the pro-oxidant character of a compound can coexist with an inhibitory effect on lipid peroxidation and, consequently, still prevent oxytosis/ferroptosis. These findings have significant implications for the understanding of oxytosis/ferroptosis and open new approaches to the development of future neurotherapies.

摘要

由于衰老时阿尔茨海默病(AD)最大的风险因素,因此针对将衰老与 AD 联系起来的病理事件至关重要,以便开发针对疾病主要病因的有效治疗方法。这样的事件之一可能是促凋亡/铁死亡的激活,这是一种独特的细胞死亡机制,其特征是线粒体功能障碍和致命的脂质过氧化。在这里,我们筛选了 >900 种天然化合物库,以寻找对神经细胞中促凋亡/铁死亡的保护作用,目的是更好地了解促凋亡/铁死亡抑制剂的化学性质。虽然测试的化合物跨越了来自动物、微生物、植物和合成来源的结构多样的化学类别,但确定了一组非常有效的抗促凋亡/铁死亡化合物,这些化合物高度富集于植物醌类化合物。这些化合物的抗促凋亡/铁死亡能力与它们在神经细胞中防止体外缺血和细胞内淀粉样β毒性的能力强烈相关,这表明促凋亡/铁死亡的某些方面也构成了与 AD 相关的其他毒性的基础。重要的是,醌类化合物的抗促凋亡/铁死亡特性依赖于它们靶向并直接阻止脂质过氧化的能力,这种能力需要细胞氧化还原酶(如 NAD(P)H:醌氧化还原酶 1(NQO1)和铁死亡抑制蛋白 1(FSP1)的还原活性。由于一些化合物增加了总活性氧的产生,同时减少了脂质过氧化,因此,化合物的促氧化剂特性可以与抑制脂质过氧化的作用共存,并且仍然可以防止促凋亡/铁死亡。这些发现对促凋亡/铁死亡的理解具有重要意义,并为开发未来的神经治疗方法开辟了新途径。

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