Lipoic acid helps clear iron accumulation in PD model

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Lipoic acid helps clear iron accumulation in PD model

Post by NHE » Thu Aug 27, 2020 2:38 am

Alpha-Lipoic Acid Mediates Clearance of Iron Accumulation by Regulating Iron Metabolism in a Parkinson's Disease Model Induced by 6-OHDA
Front Neurosci. 2020 Jun 25;14:612.

The disruption of neuronal iron homeostasis and oxidative stress are related to the pathogenesis of Parkinson's disease (PD). Alpha-lipoic acid (ALA) is a naturally occurring enzyme cofactor with antioxidant and iron chelator properties and has many known effects. ALA has neuroprotective effects on PD. However, its underlying mechanism remains unclear. In the present study, we established PD models induced by 6-hydroxydopamine (6-OHDA) to explore the neuroprotective ability of ALA and its underlying mechanism in vivo and in vitro. Our results showed that ALA could provide significant protection from 6-OHDA-induced cell damage in vitro by decreasing the levels of intracellular reactive oxygen species and iron. ALA significantly promoted the survival of the dopaminergic neuron in the 6-OHDA-induced PD rat model and remarkably ameliorated motor deficits by dramatically inhibiting the decrease in tyrosine hydroxylase expression and superoxide dismutase activity in the substantia nigra. Interestingly, ALA attenuated 6-OHDA-induced iron accumulation both in vivo and in vitro by antagonizing the 6-OHDA-induced upregulation of iron regulatory protein 2 and divalent metal transporter 1. These results indicated that the neuroprotective mechanism of ALA against neurological injury induced by 6-OHDA may be related to the regulation of iron homeostasis and reduced oxidative stress levels. Therefore, ALA may provide neuroprotective therapy for PD and other diseases related to iron metabolism disorder.

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Re: Lipoic acid helps clear iron accumulation in PD model

Post by Petr75 » Thu Aug 27, 2020 6:12 am

2020 Aug 6
Portland Health Care System, Research and Development Service, Veterans' Hospital Rd, Portland
Lipoic acid modulates inflammatory responses of monocytes and monocyte-derived macrophages from healthy and relapsing-remitting multiple sclerosis subjects


Multiple Sclerosis (MS) is a disabling neuro-inflammatory disease. Its etiology is unknown, but both oxidative stress and inflammation appear to be involved in disease pathology. Macrophages are the predominant cell type in acute inflammatory brain lesions in MS. Macrophages produce pro-inflammatory and toxic molecules that promote demyelination and are key players in phagocytosis/degradation of myelin sheathes. Lipoic acid (LA) is an inexpensive, endogenously-produced small molecule that exhibits antioxidant and anti-inflammatory effects. Treatment with LA is protective in MS and other inflammatory diseases. To examine the mechanism(s) by which LA may attenuate inflammatory lesion activity in MS, we used healthy control and MS cells to evaluate the effects of LA on levels of inflammatory cytokines, phagocytosis, and the immunomodulator cyclic AMP (cAMP) in monocytes and monocyte-derived macrophages (MDM). LA treatment resulted in a generally less inflammatory phenotype of monocytes and MDM from HC, and (to a lesser degree) MS donors. LA inhibited monocyte secretion of cytokines relevant to MS in monocytes, including TNF-α, IL-6 and IL-1β; LA effects on secretion of these cytokines in MDM was mixed with inhibition of TNF-α and IL-6, but stimulation of IL-1β, the latter perhaps due to altered macrophage polarization. LA inhibited phagocytosis in both monocytes and MDM, and increased cAMP levels in monocytes. LA may modulate inflammatory cytokine secretion and phagocytosis via a cAMP-mediated mechanism.

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