Lipoic acid protects dopaminergic neurons in LPS-induced Parkinson’s disease model

Li, Yanhua; He, Qing; Yu, Jie‐Zhong; Liu, Chunyun; Li, Feng; Chai, Zhi; Wang, Qing; Zhang, Hongzhen; Zhang, Guang‐Xian; Xiao, Bao‐Guo; Ma, Chi

doi:10.1007/s11011-015-9698-5

Cited by 37 publications

(23 citation statements)

References 45 publications

(52 reference statements)

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“…LA is found in both vegetable and animal-based foods, identified as lipoyl-lysine (coupling of LA to specific lysine residues; Ghibu et al, 2009 ; Shay et al, 2009 ; Rochette et al, 2013 ; Li et al, 2015 ). R-LA is most abundantly found in vegetables such as spinach, broccolis, and tomatoes, which contain, respectively, 3.15 ± 1.11, 0.94 ± 0.25, and 0.56 ± 0.23 × 10 −3 g lipoyl-lysine (gram dry weight).…”

Section: Lipoic Acidmentioning

confidence: 99%

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Molz

Schröder

2017

Front. Pharmacol.

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The aging process comprises a series of organic alterations, affecting multiple systems, including the nervous system. Aging has been considered the main risk factor for the advance of neurodegenerative diseases, many of which are accompanied by cognitive impairment. Aged individuals show cognitive decline, which has been associated with oxidative stress, as well as mitochondrial, and consequently energetic failure. Lipoic acid (LA), a natural compound present in food and used as a dietary supplement, has been considered a promising agent for the treatment and/or prevention of neurodegenerative disorders. In spite of a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect, to date only a few studies have examined its effects in humans. Investigations performed in animal models of memory loss associated to aging and neurodegenerative disorders have shown that LA improves memory in a variety of behavioral paradigms. Moreover, cell and molecular mechanisms underlying LA effects have also been investigated. Accordingly, LA displays antioxidant, antiapoptotic, and anti-inflammatory properties in both in vivo and in vitro studies. In addition, it has been shown that LA reverses age-associated loss of neurotransmitters and their receptors, which can underlie its effects on cognitive functions. The present review article aimed at summarizing and discussing the main studies investigating the effects of LA on cognition as well as its cell and molecular effects, in order to improve the understanding of the therapeutic potential of LA on memory loss during aging and in patients suffering from neurodegenerative disorders, supporting the development of clinical trials with LA.

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Section: Lipoic Acidmentioning

confidence: 99%

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Molz

Schröder

2017

Front. Pharmacol.

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“…SCFA HDACi have a profound influence on microglial homeostasis [Erny et al, 2015]. Microglia are implicated in several pathways of importance in neurodegenerative disorders, including AD and PD [Asai et al, 2015;Boison and Aronica, 2015;Chung et al, 2015;Jyothi et al, 2015;Li et al, 2015;Singh et al, 2015;Br€ uck et al, 2016;Choong et al, 2016;Olson and Gendelman, 2016;Villegas-Llerena et al, 2016]. They constitute the primary active immune defense in the central nervous system and are constantly scavenging for plaques, damaged neurons, and infectious agents [Estes and McAllister, 2015;Mhatre et al, 2015;Matt and Johnson, 2016].…”

Section: Apoptotic Priming In Mitochondriamentioning

confidence: 99%

“…Thus, the enhanced cognitive benefit observed when mice are fed AAM [Ames, 2010] may have more to do with ALA and ALCAR each acting as butyrate-like SCFA HDACi [Krishna et al, 2002;van de Mark et al, 2003;Dashwood and Ho, 2007;Jones et al, 2010;Steliou et al, 2012;Nasca et al, 2013;Bassett and Barnett, 2014;Moos et al, 2016] that activate the Nrf2 pathway [Suh et al, 2004;Endo et al, 2013;Gomes and Negrato, 2014;Fern andez-Galilea et al, 2015;Li et al, 2015;Tebay et al, 2015] than their antioxidant properties [Ribas et al, 2014].…”

Section: Apoptotic Priming In Mitochondriamentioning

confidence: 99%

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Irwin

Moos

Faller

et al. 2016

Drug Development Research

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Preclinical Research In this review, we discuss epigenetic-driven methods for treating neurodegenerative disorders associated with mitochondrial dysfunction, focusing on carnitinoid antioxidant-histone deacetylase inhibitors that show an ability to reinvigorate synaptic plasticity and protect against neuromotor decline in vivo. Aging remains a major risk factor in patients who progress to dementia, a clinical syndrome typified by decreased mental capacity, including impairments in memory, language skills, and executive function. Energy metabolism and mitochondrial dysfunction are viewed as determinants in the aging process that may afford therapeutic targets for a host of disease conditions, the brain being primary in such thinking. Mitochondrial dysfunction is a core feature in the pathophysiology of both Alzheimer and Parkinson diseases and rare mitochondrial diseases. The potential of new therapies in this area extends to glaucoma and other ophthalmic disorders, migraine, Creutzfeldt-Jakob disease, post-traumatic stress disorder, systemic exertion intolerance disease, and chemotherapy-induced cognitive impairment. An emerging and hopefully more promising approach to addressing these hard-to-treat diseases leverages their sensitivity to activation of master regulators of antioxidant and cytoprotective genes, antioxidant response elements, and mitophagy. Drug Dev Res 77 : 109-123, 2016. © 2016 Wiley Periodicals, Inc.

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“…Lipoic acid is a natural lipophilic antioxidant that has beneficial effects on heart diseases, diabetes, and neuroinflammatory disorders [29][30][31][32]. Lipoic acid occurs in two forms: α-lipoic acid and DHLA [33].…”

Section: Discussionmentioning

confidence: 99%

Dihydrolipoic acid protects against lipopolysaccharide-induced behavioral deficits and neuroinflammation via regulation of Nrf2/HO-1/ NLRP3 signaling in rat

Bian

Wang

Huang

et al. 2020

Preprint

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Background: Recently, depression has been identified as prevalent and severe mental disorder. However, the mechanisms underlying the depression risk remain elusive. The neuroinflammation and NLRP3 inflammasome activation are known to be involved in the pathology of depression. Dihydrolipoic acid (DHLA) has been reported as a strong antioxidant and exhibits anti-inflammatory properties in various diseases, albeit the direct relevance between DHLA and depression is yet unknown. The present study aimed to investigate the anti-depressant effects and potential mechanism of DHLA in the Lipopolysaccharide (LPS)-induced depression animal model. Methods: Adult male Sprague–Dawley rats were utilized. LPS and DHLA were injected intraperitoneally every 2 days and daily, respectively. Fluoxetine(Flu) was injected intraperitoneally daily. PD98059, an inhibitor of ERK, was injected intraperitoneally one hour before DHLA injection daily. Small interfering ribonucleic acid (siRNA) for nuclear factor erythroid 2-like (Nrf2) was injected into the bilateral hippocampus 14 days before the DHLA injection. Depression-like behavior tests were performed. Western blot and immunofluorescence staining detected the ERK/Nrf2/HO-1/ROS/NLRP3 pathway-related proteins. Results: The DHLA and fluoxetine treatment exerted anti-depressant effects in LPS-induced depression rats. The DHLA treatment increased the expression of ERK, Nrf2, and HO-1 but decreased the ROS generation levels and reduced the expression of NLRP3, caspase-1, and IL-1b in LPS-induced depression rats. PD98059 abolished the effects of DHLA on anti-depression as well as the levels of Nrf2 and HO-1 proteins. Similarly, Nrf2 siRNA reversed the anti-depressant effect of DHLA administration via the decreased expression of HO-1. Conclusions: These findings suggested that DHLA exerted anti-depressant-like effects via ERK/Nrf2/HO-1/ROS/NLRP3 pathway in LPS-induced depression rats. Thus, DHLA may serve as a potential therapeutic strategy for depression.

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Lipoic acid protects dopaminergic neurons in LPS-induced Parkinson’s disease model

Cited by 37 publications

References 45 publications

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Dihydrolipoic acid protects against lipopolysaccharide-induced behavioral deficits and neuroinflammation via regulation of Nrf2/HO-1/ NLRP3 signaling in rat

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