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Reversible inhibition of alpha-ketoglutarate dehydrogenase by hydrogen peroxide: glutathionylation and protection of lipoic acid.过氧化氢对α-酮戊二酸脱氢酶的可逆抑制作用:谷胱甘肽化与硫辛酸的保护
Biochemistry. 2008 Jan 8;47(1):473-8. doi: 10.1021/bi7017464. Epub 2007 Dec 15.
2
The effect of lipoic acid on lipid peroxidation and visual evoked potentials (VEPs) in rats exposed to chronic restraint stress.硫辛酸对慢性束缚应激大鼠脂质过氧化及视觉诱发电位的影响
Int J Neurosci. 2007 Dec;117(12):1691-706. doi: 10.1080/00207450601050287.
3
Alpha-lipoic acid attenuates LPS-induced inflammatory responses by activating the phosphoinositide 3-kinase/Akt signaling pathway.α-硫辛酸通过激活磷脂酰肌醇3-激酶/蛋白激酶B信号通路减轻脂多糖诱导的炎症反应。
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4077-82. doi: 10.1073/pnas.0700305104. Epub 2007 Feb 27.
4
Lipid peroxidation, isoprostanes and vascular damage.脂质过氧化、异前列腺素与血管损伤。
Pharmacol Rep. 2006;58 Suppl:57-68.
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Lipoic acid affects cellular migration into the central nervous system and stabilizes blood-brain barrier integrity.硫辛酸影响细胞向中枢神经系统的迁移,并稳定血脑屏障的完整性。
J Immunol. 2006 Aug 15;177(4):2630-7. doi: 10.4049/jimmunol.177.4.2630.
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Brain cytokine synthesis induced by an intraparenchymal injection of LPS is reduced in MCP-1-deficient mice prior to leucocyte recruitment.在白细胞募集之前,脑实质内注射脂多糖(LPS)诱导的脑内细胞因子合成在单核细胞趋化蛋白-1(MCP-1)缺陷小鼠中减少。
Eur J Neurosci. 2006 Jul;24(1):77-86. doi: 10.1111/j.1460-9568.2006.04891.x.
7
Protective effects of early administration of alpha-lipoic acid against lipopolysaccharide-induced plasma lipid peroxidation.早期给予α-硫辛酸对脂多糖诱导的血浆脂质过氧化的保护作用。
Pharmacol Rep. 2006 May-Jun;58(3):399-404.
8
Oxidative stress and neurodegeneration: where are we now?氧化应激与神经退行性变:我们目前处于什么阶段?
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Oxidative stress-mediated macromolecular damage and dwindle in antioxidant status in aged rat brain regions: role of L-carnitine and DL-alpha-lipoic acid.氧化应激介导的老年大鼠脑区大分子损伤及抗氧化状态下降:左旋肉碱和硫辛酸的作用
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Lipoic acid - the drug of the future?硫辛酸——未来的药物?
Pharmacol Rep. 2005 Sep-Oct;57(5):570-7.

α-硫辛酸对大鼠脂多糖诱导的脑损伤的预防作用

Prophylaxis with alpha-lipoic acid against lipopolysaccharide-induced brain injury in rats.

作者信息

Goraca Anna, Asłanowicz-Antkowiak Katarzyna

机构信息

Chair of Experimental and Clinical Physiology, Department of Cardiovascular Physiology, Medical University of Łódź, Mazowiecka 6/8, Łódź, Poland.

出版信息

Arch Immunol Ther Exp (Warsz). 2009 Mar-Apr;57(2):141-6. doi: 10.1007/s00005-009-0015-z. Epub 2009 Mar 31.

DOI:10.1007/s00005-009-0015-z
PMID:19333732
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2771127/
Abstract

INTRODUCTION

Lipopolysaccharide (LPS) stimulates the synthesis and release of reactive oxygen species that play an important role in the pathogenesis of tissue injuries. In this study the effect of early administration of the antioxidant alpha-lipoic acid (alpha-LA) on brain lipid peroxidation, brain hydrogen peroxide (H(2)O(2)) concentration, and brain total sulfhydryl group (-SH group) content was evaluated in rats with endotoxic shock induced by administration of LPS (Escherichia coli 026:B6, 30 mg/kg i.v.)

MATERIALS AND METHODS

Rats were treated intravenously with normal saline or alpha-LA (60 mg/kg) 30 min after LPS injection. After 5 h of observation, the animals were killed and their brains were isolated for the measurements.

RESULTS

Injection of LPS alone resulted in the development of shock and oxidative stress, the latter indicated by a significant increase in brain concentrations of thiobarbituric acid-reacting substances (TBARS) and H(2)O(2) and a decrease in total brain -SH group content. Administration of alpha-LA after the LPS challenge resulted in an increase in total -SH group content and a decrease in TBARS and H(2)O(2) concentration in the brain tissue compared with the LPS group.

CONCLUSION

The results indicate that alpha-LA treatment effectively protected the brain tissue against endotoxin-induced oxidative stress. Administration of LA could be a useful adjunct to clinical application in the management of septic shock.

摘要

引言

脂多糖(LPS)刺激活性氧的合成与释放,活性氧在组织损伤的发病机制中起重要作用。在本研究中,评估了早期给予抗氧化剂α-硫辛酸(α-LA)对注射LPS(大肠杆菌026:B6,30mg/kg静脉注射)诱导的内毒素休克大鼠脑脂质过氧化、脑过氧化氢(H₂O₂)浓度和脑总巯基(-SH基团)含量的影响。

材料与方法

在注射LPS后30分钟,大鼠静脉注射生理盐水或α-LA(60mg/kg)。观察5小时后,处死动物并分离其大脑进行测量。

结果

单独注射LPS导致休克和氧化应激的发生,后者表现为脑硫代巴比妥酸反应物质(TBARS)和H₂O₂浓度显著增加以及脑总-SH基团含量降低。与LPS组相比,在LPS攻击后给予α-LA导致脑组织中总-SH基团含量增加以及TBARS和H₂O₂浓度降低。

结论

结果表明,α-LA治疗可有效保护脑组织免受内毒素诱导的氧化应激。给予硫辛酸可能是脓毒症休克临床治疗中的一种有用辅助手段。