欧米伽-3 多不饱和脂肪酸通过组蛋白去乙酰化酶 3/过氧化物酶体增殖体激活受体-γ 辅激活因子途径保护创伤性脊髓损伤,从而缓解内质网应激诱导的神经炎症。

IF 3.2 3区 医学 Q2 CLINICAL NEUROLOGY
Lijiang He, Jingfang Ye, Xunrong Zhuang, Jinnan Shi, Wenhua Wu
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引用次数: 0

摘要

欧米伽-3 多不饱和脂肪酸(ω-3 PUFAs)可减轻中枢神经系统的炎症反应,从而起到神经保护作用。抑制组蛋白去乙酰化酶3(HDAC3)可通过SIRT1途径对脊髓损伤(SCI)后的神经产生保护作用,但SCI的病理生理机制十分复杂,ω-3 PUFA与细胞器之间的相互作用在很大程度上仍是未知的。本研究旨在探讨ω-3 PUFAs通过HDAC3/过氧化物酶体增殖体激活受体-γ辅助激活剂(PGC)-1ɑ途径对SCI后内质网(ER)应激诱导的神经炎症的影响。为此,我们建立了挫伤诱导的 SCI 大鼠模型,以评估 ω-3 PUFA 对 SCI 中 ER 应激介导的炎症的影响。SCI 后脊髓病变迅速诱发 ER 应激,ω-3 PUFA 治疗后ER 应激显著降低。与ER应激降低相一致的是,HDAC3表达水平和炎症反应均降低,而PGC-1ɑ表达水平在SCI后升高。我们发现,ω-3 PUFA 治疗通过抑制 HDAC3 减轻了 ER 应激,从而减少了 SCI 诱导的炎症。综上所述,这些结果表明ω-3 PUFA可通过调节组蛋白去乙酰化酶3/过氧化物酶体增殖激活受体-γ辅助激活剂通路,在防止SCI诱导的神经炎症和促进神经功能恢复方面发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Omega-3 polyunsaturated fatty acids alleviate endoplasmic reticulum stress-induced neuroinflammation by protecting against traumatic spinal cord injury through the histone deacetylase 3/ peroxisome proliferator-activated receptor-γ coactivator pathway.

Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) attenuate inflammatory responses in the central nervous system, leading to neuroprotective effects. Inhibition of histone deacetylase 3 (HDAC3) has neuroprotective effects after spinal cord injury (SCI) through the SIRT1 pathway, but the pathophysiological mechanisms of SCI are complex and the interactions between ω-3 PUFAs and organelles remain largely unknown. This study aimed to investigate the effect of ω-3 PUFAs on endoplasmic reticulum (ER) stress-induced neuroinflammation through the HDAC3/peroxisome proliferator-activated receptor-γ coactivator (PGC)-1ɑ pathway after SCI. To this end, a contusion-induced SCI rat model was established to evaluate the effects of ω-3 PUFAs on ER stress-mediated inflammation in SCI. ER stress was rapidly induced in spinal cord lesions after SCI and was significantly reduced after ω-3 PUFA treatment. Consistent with reduced ER stress, HDAC3 expression levels and inflammatory responses were decreased, and PGC-1ɑ expression levels were increased after SCI. We found that ω-3 PUFA treatment attenuated ER stress through HDAC3 inhibition, thereby reducing SCI-induced inflammation. Taken together, these results suggest a role for ω-3 PUFA in protecting against SCI-induced neuroinflammation and promoting neurological functional recovery by regulating the histone deacetylase 3/ peroxisome proliferator-activated receptor-γ coactivator pathway.

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来源期刊
CiteScore
5.40
自引率
6.20%
发文量
118
审稿时长
6-12 weeks
期刊介绍: Journal of Neuropathology & Experimental Neurology is the official journal of the American Association of Neuropathologists, Inc. (AANP). The journal publishes peer-reviewed studies on neuropathology and experimental neuroscience, book reviews, letters, and Association news, covering a broad spectrum of fields in basic neuroscience with an emphasis on human neurological diseases. It is written by and for neuropathologists, neurologists, neurosurgeons, pathologists, psychiatrists, and basic neuroscientists from around the world. Publication has been continuous since 1942.
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