NF-κB-Mediated Neuroinflammation in Parkinson’s Disease and Potential Therapeutic Effect of Polyphenols

Singh, Sangeeta; Nand, Sachchida; Birla, Hareram; Zahra, Walia; Rathore, Aaina Singh; Singh, Surya Pratap

doi:10.1007/s12640-019-00147-2

Cited by 134 publications

(94 citation statements)

References 213 publications

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“…Akt and ERK signalling pathways play crucial parts in neuroprotection via cell differentiation, proliferation, survival, and apoptosis [18,19]. Numerous recent researches have highlighted the neuroprotective role of plant-based compounds and polyphenols in PD against neurotoxins and neuroinflammation, by promoting cell survival through their antioxidative, anti-inflammatory, and immunomodulatory effects [20][21][22]. Evidences prove the pivotal role of polyphenols in replenishing the neurons via increased activity of ETC, regulating the effects on redox potential, and restraining the apoptosis as a result of increased mitochondrial biogenesis [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effect of Chlorogenic Acid on Mitochondrial Dysfunction-Mediated Apoptotic Death of DA Neurons in a Parkinsonian Mouse Model

Singh

Nand

Birla

et al. 2020

Oxidative Medicine and Cellular Longevity

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106

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Mitochondrial dysfunction and oxidative stress characterize major factors involved in the activation of complex processes corresponding to apoptosis-mediated neuronal senescence of dopaminergic neurons (DA) in Parkinson’s disease (PD). Here, we evaluated the molecular mechanisms participating in the treatment of a 1-methyl-4-phenyl-1,2,3,6-tetrahydopyridine- (MPTP-) intoxicated PD mouse model in response to chlorogenic acid (CGA). The results indicate that CGA treatment significantly improved the motor coordination of the MPTP-intoxicated mice. CGA also alleviated the fall in activity of mitochondrial complexes I, IV, and V in accordance with ameliorating the level of superoxide dismutase and mitochondrial glutathione in the midbrain of MPTP-induced mice. CGA inhibited the activation of proapoptotic proteins including Bax and caspase-3, while elevating the expression of antiapoptotic protein like Bcl-2 consequently preventing the MPTP-mediated apoptotic cascade. The study also revealed the improved phosphorylation state of Akt, ERK1/2, and GSK3β which was downregulated as an effect of MPTP toxicity. Our findings signify that CGA may possess pharmacological properties and contribute to neuroprotection against MPTP induced toxicity in a PD mouse model associated with phosphorylation of GSK3β via activating Akt/ERK signalling in the mitochondrial intrinsic apoptotic pathway. Thus, CGA treatment may arise as a potential therapeutic candidate for mitochondrial-mediated apoptotic senescence of DA neurons in PD.

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Section: Introductionmentioning

confidence: 99%

Neuroprotective Effect of Chlorogenic Acid on Mitochondrial Dysfunction-Mediated Apoptotic Death of DA Neurons in a Parkinsonian Mouse Model

Singh

Nand

Birla

et al. 2020

Oxidative Medicine and Cellular Longevity

Self Cite

106

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“…[40][41][42][43] NF-B pathway activation has been linked to neuroinflammatory responses in Parkinson's Disease, Alzheimer's Disease and other insults to the brain such as TBI and ischemic brain disorders. [44][45][46] Furthermore, inhibition of NF-B was shown to slow than the speed of progression of neurodegenerative disorders. [47] Activation of astrocytes and microglia results in secretion of cytokines (IL-1β, TNF-, and IL-6), α-chemokines (MCP-1, MIP-1, and RANTES), and other inflammatory mediators such as cyclooxygenase-2 and MMP-9.…”

Section: Discussionmentioning

confidence: 99%

Daily Low Dose of Erythropoietin and Neuroinflammation

Nejat¹,

As²,

Ebrahimi³

et al. 2020

Preprint

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Neuroinflammation, defined as inflammatory reactions mediated by cytokines, chemokines, reactive oxygen species, and secondary messengers in the central nervous system (CNS) including the brain and spinal cord is the basis of many neurological disorders [1] Recently, erythropoietin (EPO) has been considered and studied as a modulator of neuroinflammation.[2-4] On this article minireview of pathophysiology of neuroinflammation and the neuroprotective effects of EPO is discussed and a case of subacute huge subdural hematoma with double mydriasis operated urgently, treated with low daily dose (vs high dose once or twice a month in the literature) of EPO and recovered fully and discharged home with good consciousness is reported. In addition, the probable outcome of erythropoietin administration in patients with neuroinflammation in COVID19 is considered.

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“…ROS, such as H 2 O 2 , are also potent NF-κB activators, leading to pro-inflammatory conditions [ 206 , 207 ]. Taken together, NF-κB is an essential contributor to neuroinflammation, plaque progression, and neuronal death in AD and PD [ 208 , 209 , 210 ]…”

Section: Oxidative Stress and Intracellular Signaling Pathwaymentioning

confidence: 99%

A Mechanistic Evaluation of Antioxidant Nutraceuticals on Their Potential against Age-Associated Neurodegenerative Diseases

et al. 2020

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Nutraceuticals have been extensively studied worldwide due to its neuroprotective effects in in vivo and in vitro studies, attributed by the antioxidative properties. Alzheimer (AD) and Parkinson disease (PD) are the two main neurodegenerative disorders that are discussed in this review. Both AD and PD share the similar involvement of oxidative stress in their pathophysiology. Nutraceuticals exert their antioxidative effects via direct scavenging of free radicals, prevent damage to biomolecules, indirectly stimulate the endogenous antioxidative enzymes and gene expressions, inhibit activation of pro-oxidant enzymes, and chelate metals. In addition, nutraceuticals can act as modulators of pro-survival, pro-apoptotic, and inflammatory signaling pathways. They have been shown to be effective particularly in preclinical stages, due to their multiple mechanisms of action in attenuating oxidative stress underlying AD and PD. Natural antioxidants from food sources and natural products such as resveratrol, curcumin, green tea polyphenols, and vitamin E are promising therapeutic agents in oxidative stress-mediated neurodegenerative disease as they have fewer adverse effects, more tolerable, cheaper, and sustainable for long term consumption.

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NF-κB-Mediated Neuroinflammation in Parkinson’s Disease and Potential Therapeutic Effect of Polyphenols

Cited by 134 publications

References 213 publications

Neuroprotective Effect of Chlorogenic Acid on Mitochondrial Dysfunction-Mediated Apoptotic Death of DA Neurons in a Parkinsonian Mouse Model

Neuroprotective Effect of Chlorogenic Acid on Mitochondrial Dysfunction-Mediated Apoptotic Death of DA Neurons in a Parkinsonian Mouse Model

Daily Low Dose of Erythropoietin and Neuroinflammation

A Mechanistic Evaluation of Antioxidant Nutraceuticals on Their Potential against Age-Associated Neurodegenerative Diseases

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