Alpha-lipoic acid protects against 6-hydroxydopamine-induced neurotoxicity in a rat model of hemi-parkinsonism

Peripheral neuropathies are heterogeneous disorders presenting often with hyperalgesia and allodynia. This study has assessed if chronic constriction injury (CCI) of sciatic nerve is accompanied by increased oxidative stress and central nervous system (CNS) changes and if these changes are sensitive to treatment with thioctic acid. Thioctic acid is a naturally occurring antioxidant existing in two optical isomers (+)- and (−)-thioctic acid and in the racemic form. It has been proposed for treating disorders associated with increased oxidative stress. Sciatic nerve CCI was made in spontaneously hypertensive rats (SHRs) and in normotensive reference cohorts. Rats were untreated or treated intraperitoneally for 14 days with (+/−)-, (+)-, or (−)-thioctic acid. Oxidative stress, astrogliosis, myelin sheets status, and neuronal injury in motor and sensory cerebrocortical areas were assessed. Increase of oxidative stress markers, astrogliosis, and neuronal damage accompanied by a decreased expression of neurofilament were observed in SHR. This phenomenon was more pronounced after CCI. Thioctic acid countered astrogliosis and neuronal damage, (+)-thioctic acid being more active than (+/−)- or (−)-enantiomers. These findings suggest a neuroprotective activity of thioctic acid on CNS lesions consequent to CCI and that the compound may represent a therapeutic option for entrapment neuropathies.

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“…These findings are consistent with the demonstration of neuroprotective properties of thioctic acid in animal models of brain injury [52, 53]. …”

Section: Discussionsupporting

confidence: 91%

Neuroprotective Activity of Thioctic Acid in Central Nervous System Lesions Consequent to Peripheral Nerve Injury

Tomassoni

Amenta

Mannelli

et al. 2013

BioMed Research International

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“…Pretreatment with CA decreased the apomorphine-induced rotation and attenuated the degeneration of substantia nigra dopaminergic neurons induced by 6-OHDA in rats. Other studies have shown that pretreatment with alpha lipoic acid at a dose of 100 mg/kg significantly attenuates rotations, prevents the loss of substantia nigra pars compacta neurons, and lowers the levels of malondialdehyde [23]. In addition, magnolol reduces apomorphine-induced rotation and has protective neuronal activity against 6-OHDA-induced toxicity in a PD model [24].…”

Section: Discussionmentioning

confidence: 97%

Carnosic acid protects against 6-hydroxydopamine-induced neurotoxicity in in vivo and in vitro model of Parkinson’s disease: Involvement of antioxidative enzymes induction

Chang

Lin

et al. 2015

Chemico-Biological Interactions

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“…Studies performed using in vivo and in vitro showed that ALA can prevent stress oxidative by inducing of enzymatic antioxidant activity (SOD, catalase and GSH) as well as enhancing the capacity of free radical scavenging and by blocking lipid peroxidation (Abdou and Abdel-Daim 2014;Castro et al 2014;Gorąca et al 2013;Xia et al 2014). Because of its antioxidant activity, ALA acts as a neuroprotective agent in various neurodegenerative diseases related to stress oxidative stress (Boyaci et al 2014;Dalazen et al 2014;Demir et al 2014;Jalali-Nadoushan and Roghani 2013;Li et al 2013;Veskovic et al 2014).…”

Section: Discussionmentioning

confidence: 97%

Protective effects of alpha lipoic acid on high glucose-induced neurotoxicity in PC12 cells

2014

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Hyperglycemia plays an important role in the development of diabetic neuropathy. In this study, we investigated the protective effects of alpha lipoic acid (ALA) against high glucose-induced neurotoxicity in PC12 cells as a suitable in vitro model for studying neuronal functions. PC12 cells were treated with high glucose (25 mg/ml for 24 h) in the absence and presence of ALA (100 μM for 24 h). The viability of PC12 cells was estimated by using MTT assay. The expression of pro- apoptotic Bax, anti- apoptotic Bcl-2 and caspase 3 protein were evaluated by western blotting. The reactive oxygen species (ROS) levels were determined with 2,7-dichlorodihydro- fluorescein diacetate (H2DCFDA). Biochemical markers of oxidative stress were assessed by using the total antioxidant power (TAP), lipid peroxidation (LPO), ADP/ATP ratio, activity of antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD). Pretreatment of PC12 cells with ALA, significantly improved high glucose-induced toxicity by increasing activity of antioxidant enzymes CAT and SOD in the PC12 cell. It also increased the concentrations of TAP. An elevated level of cell death and ROS in high glucose conditions, diminished with ALA treatment. Over expression of Bax and caspase 3 protein, elevation of ADP/ATP ratio and LPO level in high glucose- treated PC12 cells, were significantly reduced by ALA. It was concluded that ALA attenuates neurotoxicity induced by high glucose in PC12 cells.

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Alpha-lipoic acid protects against 6-hydroxydopamine-induced neurotoxicity in a rat model of hemi-parkinsonism

Cited by 56 publications

References 37 publications

Neuroprotective Activity of Thioctic Acid in Central Nervous System Lesions Consequent to Peripheral Nerve Injury

Neuroprotective Activity of Thioctic Acid in Central Nervous System Lesions Consequent to Peripheral Nerve Injury

Carnosic acid protects against 6-hydroxydopamine-induced neurotoxicity in in vivo and in vitro model of Parkinson’s disease: Involvement of antioxidative enzymes induction

Protective effects of alpha lipoic acid on high glucose-induced neurotoxicity in PC12 cells

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