Oxidative Stress in Neurodegenerative Diseases

Domanskyi, Andrii; Parlato, Rosanna

doi:10.3390/antiox11030504

Cited by 26 publications

(13 citation statements)

References 9 publications

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“…Oxidative stress develops when the production of ROS overwhelms the endogenous capabilities of the antioxidative defense provided by diverse enzymatic and non-enzymatic mechanisms. Non-enzymatic antioxidants (e.g., GSH and vitamins) and antioxidant enzymes (catalase, SOD, glutathione peroxidase, and thioredoxin) are critically involved in redox regulation and the maintenance of redox homeostasis [ 155 , 156 , 157 , 158 , 159 , 160 ]. In comparison with other tissues, the brain is particularly vulnerable to oxidative damage due to its high rate of oxygen consumption, limited antioxidative defense, presence of metal ions that are able to initiate redox cycling and the formation of highly dangerous and very reactive hydroxyl radicals via Fenton chemistry, and the high amount of polyunsaturated fatty acids (PUFAs) that are prone to oxidation, together with the post-mitotic nature of neurons [ 161 , 162 ].…”

Section: Antioxidant Capacity Of Cannabinoidsmentioning

confidence: 99%

Intracellular Molecular Targets and Signaling Pathways Involved in Antioxidative and Neuroprotective Effects of Cannabinoids in Neurodegenerative Conditions

et al. 2022

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In the last few decades, endocannabinoids, plant-derived cannabinoids and synthetic cannabinoids have received growing interest as treatment options in neurodegenerative conditions. In various experimental settings, they have displayed antioxidative, anti-inflammatory, antiapoptotic, immunomodulatory, and neuroprotective effects. However, due to numerous targets and downstream effectors of their action, the cellular and molecular mechanisms underlying these effects are rather complex and still under discussion. Cannabinoids are able to neutralize free radicals and modulate the production of reactive oxygen species and the activity of antioxidative systems acting on CB1 and CB2 cannabinoid receptors. The activation of CB1 receptors stimulates signaling pathways involved in antioxidative defense and survival (such as the phosphoinositide 3-kinase (PI3K)/Akt, mitogen-activated protein kinase (MAPK), and Nrf2 pathways) and regulates glutamatergic signaling, the activation of N-methyl-D-aspartate (NMDA) receptors, calcium influx, and the induction of Ca2+-regulated signaling cascades, whereas the neuroprotective effects mediated by CB2 receptors are due to the suppression of microglial activation and the release of prooxidative and proinflammatory mediators. This review summarizes the main molecular mechanisms and new advances in understanding the antioxidative and neuroprotective effects of cannabinoids. Because of the plethora of possible pharmacological interventions related to oxidative stress and cannabinoid-mediated neuroprotection, future research should be directed towards a better understanding of the interplay between activated signal transduction pathways and molecular targets with the aim to improve treatment options and efficacy by targeting the endocannabinoid system.

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Section: Antioxidant Capacity Of Cannabinoidsmentioning

confidence: 99%

Intracellular Molecular Targets and Signaling Pathways Involved in Antioxidative and Neuroprotective Effects of Cannabinoids in Neurodegenerative Conditions

et al. 2022

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“…This study illustrates the dose and time-dependent action of NPY in downregulating the activation of pro-apoptotic proteins involved in the pathogenesis of neurodegeneration. The insults of glutamate excitotoxicity, ER stress, and oxidative damage are known to be the prominent causes of neurodegeneration [ 3 , 63 , 64 ]. Using SH-SY5Y neuroblastoma cells as a model, we induced stress to simulate cellular neurodegeneration and co-treated with NPY to investigate its protective effects.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Neuropeptide Y on Human Neuroblastoma SH-SY5Y Cells in Glutamate Excitotoxicity and ER Stress Conditions

Palanivel

Gupta

Mirshahvaladi

et al. 2022

Cells

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Neuropeptide Y (NPY), a sympathetic neurotransmitter, is involved in various physiological functions, and its dysregulation is implicated in several neurodegenerative diseases. Glutamate excitotoxicity, endoplasmic reticulum (ER) stress, and oxidative stress are the common mechanisms associated with numerous neurodegenerative illnesses. The present study aimed to elucidate the protective effects of NPY against glutamate toxicity and tunicamycin-induced ER stress in the human neuroblastoma SH-SY5Y cell line. We exposed the SH-SY5Y cells to glutamate and tunicamycin for two different time points and analyzed the protective effects of NPY at different concentrations. The protective effects of NPY treatments were assessed by cell viability assay, and the signalling pathway changes were evaluated by biochemical techniques such as Western blotting and immunofluorescence assays. Our results showed that treatment of SH-SY5Y cells with NPY significantly increased the viability of the cells in both glutamate toxicity and ER stress conditions. NPY treatments significantly attenuated the glutamate-induced pro-apoptotic activation of ERK1/2 and JNK/BAD pathways. The protective effects of NPY were further evident against tunicamycin-induced ER stress. NPY treatments significantly suppressed the ER stress activation by downregulating BiP, phospho-eIF2α, and CHOP expression. In addition, NPY alleviated the Akt/FoxO3a pathway in acute oxidative conditions caused by glutamate and tunicamycin in SH-SY5Y cells. Our results demonstrated that NPY is neuroprotective against glutamate-induced cell toxicity and tunicamycin-induced ER stress through anti-apoptotic actions.

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“…Since the brain requires a high level of oxygen and ATP for its neuronal functions, it is extremely sensitive to oxidative damage. 1, 2 Stroke is a clinical condition that occurs due to the interrupted oxygenated blood supply to the brain. Global statistics data report ranks stroke, to be second among mortality-causing diseases.…”

Section: Introductionmentioning

confidence: 99%

Nerolidol Attenuates Cerebral Ischemic Injury in Middle Cerebral Artery Occlusion-Induced Rats via Regulation of Inflammation, Apoptosis, and Oxidative Stress Markers

Zhang

Zhou

2023

Pharmacognosy Magazine

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Background Cerebral ischemia is a syndrome that occurs due to the restricted flow of oxygen-rich blood to the brain, causing damage to the brain cells. Globally, ischemia ranks second in causing mortality and third in causing disability in stroke patients. Nerolidol is a bioactive compound present in the essential oil of plants with a floral odour. It is a natural sesquiterpene alcohol used in cosmetics, perfumes, and as a food flavouring agent. It also possesses antioxidant, antimicrobial, anti-inflammatory, and anticancer properties. Materials and Methods In this study, we assessed the anti-ischemic property of nerolidol in cerebral ischemia-induced mice. Healthy male Wistar rats were induced into cerebral ischemia with middle cerebral artery occlusion (MCAO) and treated with 10 mg and 20 mg nerolidol for 21 days. The brain morphometric, antioxidant, and MMP levels were estimated in the brain tissue of MCAO-performed and nerolidol-treated rats. The cerebral infarct-alleviating potency of nerolidol was analysed by estimating the levels of inflammatory cytokines and apoptotic proteins. It was further confirmed by assessing the levels of COX-2/PGE-2 signalling proteins in brain tissue from MCAO-performed in rats. Results Nerolidol significantly reduced the cerebral infarct volume and brain edema via increased antioxidant levels and decreased MMPs. It also decreased the pro-inflammatory cytokines and proapoptotic proteins in brain tissue. The inflammatory signalling proteins NFκB, COX-2, and PGE-2 were significantly decreased in nerolidol-treated MCAO-performed rats, confirming the antiischemic property of nerolidol. Conclusion Our results prove nerolidol significantly alleviates cerebral ischemia in rats, and it can be subjected to further trials to be formulated as an anti-ischemic drug.

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Oxidative Stress in Neurodegenerative Diseases

Abstract: Oxidative stress is typically reported in neurodegenerative diseases [...]

Cited by 26 publications

References 9 publications

Intracellular Molecular Targets and Signaling Pathways Involved in Antioxidative and Neuroprotective Effects of Cannabinoids in Neurodegenerative Conditions

Intracellular Molecular Targets and Signaling Pathways Involved in Antioxidative and Neuroprotective Effects of Cannabinoids in Neurodegenerative Conditions

Neuroprotective Effects of Neuropeptide Y on Human Neuroblastoma SH-SY5Y Cells in Glutamate Excitotoxicity and ER Stress Conditions

Nerolidol Attenuates Cerebral Ischemic Injury in Middle Cerebral Artery Occlusion-Induced Rats via Regulation of Inflammation, Apoptosis, and Oxidative Stress Markers

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