A Review on Natural Antioxidants for Their Role in the Treatment of Parkinson’s Disease

Moteriya, Pooja; Dhankhar, Sanchit; Chauhan, Samrat; Garg, Nitika; Bhattacharya, Tanima; Ali, Mohammed Ashraf; Chaudhary, Anis Ahmad; Rudayni, Hassan Ahmed; Al-Zharani, Mohammed; Ahmad, Wasim; Khan, Shaheen N.; Singh, Thakur Gurjeet; Mujwar, Somdutt

doi:10.3390/ph16070908

Cited by 31 publications

(16 citation statements)

References 230 publications

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“…The situation becomes more vulnerable in metabolically active tissues such as the brain which, apart from being less equipped with innate antioxidant defense, also tend to resist the delivery of drugs due to the blood–brain barrier ( Rinaldi et al, 2016 ). Augmenting the innate antioxidant defense with external antioxidants having the ability to cross the blood–brain barrier could, thus, be beneficial in the treatment of brain tumors ( Mittal et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas

Baba,

Mir,

Mokhdomi

et al. 2024

Front. Pharmacol.

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P66Shc and Rac1 proteins are responsible for tumor-associated inflammation, particularly in brain tumors characterized by elevated oxidative stress and increased reactive oxygen species (ROS) production. Quercetin, a natural polyphenolic flavonoid, is a well-known redox modulator with anticancer properties. It has the capacity to cross the blood–brain barrier and, thus, could be a possible drug against brain tumors. In this study, we explored the effect of quercetin on Rac1/p66Shc-mediated tumor cell inflammation, which is the principal pathway for the generation of ROS in brain cells. Glioma cells transfected with Rac1, p66Shc, or both were treated with varying concentrations of quercetin for different time points. Quercetin significantly reduced the viability and migration of cells in an ROS-dependent manner with the concomitant inhibition of Rac1/p66Shc expression and ROS production in naïve and Rac1/p66Shc-transfected cell lines, suggestive of preventing Rac1 activation. Through molecular docking simulations, we observed that quercetin showed the best binding compared to other known Rac1 inhibitors and specifically blocked the GTP-binding site in the A-loop of Rac1 to prevent GTP binding and, thus, Rac1 activation. We conclude that quercetin exerts its anticancer effects via the modulation of Rac1-p66Shc signaling by specifically inhibiting Rac1 activation, thus restraining the production of ROS and tumor growth.

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Section: Discussionmentioning

confidence: 99%

Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas

Baba,

Mir,

Mokhdomi

et al. 2024

Front. Pharmacol.

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“…At present, the treatment of PD can only alleviate the symptoms of the disease. The development of related drugs is mainly based on oral or injectable dopamine substitutes or their degradation inhibitors [ 41 ]. Finding strategies that can prevent, delay, or reverse the degeneration of dopamine neurons, including the efficacy of phytochemicals in the treatment of PD, has been a hot research focus.…”

Section: Discussionmentioning

confidence: 99%

Chiisanoside Mediates the Parkin/ZNF746/PGC-1α Axis by Downregulating MiR-181a to Improve Mitochondrial Biogenesis in 6-OHDA-Caused Neurotoxicity Models In Vitro and In Vivo: Suggestions for Prevention of Parkinson’s Disease

Hsu,

Chen,

Gao

et al. 2023

Antioxidants

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The degeneration of dopamine (DA) neurons is known to be associated with defects in mitochondrial biogenesis caused by aging, environmental factors, or mutations in genes, leading to Parkinson’s disease (PD). As PD has not yet been successfully cured, the strategy of using small molecule drugs to protect and restore mitochondrial biogenesis is a promising direction. This study evaluated the efficacy of synthetic chiisanoside (CSS) identified in the leaves of Acanthopanax sessiliflorus to prevent PD symptoms. The results show that in the 6-hydroxydopamine (6-OHDA) model, CSS pretreatment can effectively alleviate the reactive oxygen species generation and apoptosis of SH-SY5Y cells, thereby lessening the defects in the C. elegans model including DA neuron degeneration, dopamine-mediated food sensitivity behavioral disorders, and shortened lifespan. Mechanistically, we found that CSS could restore the expression of proliferator-activated receptor gamma coactivator-1-alpha (PGC-1α), a key molecule in mitochondrial biogenesis, and its downstream related genes inhibited by 6-OHDA. We further confirmed that this is due to the enhanced activity of parkin leading to the ubiquitination and degradation of PGC-1α inhibitor protein Zinc finger protein 746 (ZNF746). Parkin siRNA treatment abolished this effect of CSS. Furthermore, we found that CSS inhibited 6-OHDA-induced expression of miR-181a, which targets parkin. The CSS’s ability to reverse the 6-OHDA-induced reduction in mitochondrial biogenesis and activation of apoptosis was abolished after the transfection of anti-miR-181a and miR-181a mimics. Therefore, the neuroprotective effect of CSS mainly promotes mitochondrial biogenesis by regulating the miR-181a/Parkin/ZNF746/PGC-1α axis. CSS potentially has the opportunity to be developed into PD prevention agents.

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“…There are several phytochemicals which have been studied for their potential therapeutic benefits in PD. These substances may have neuroprotective mechanisms targeting mainly oxidative stress and mitochondrial impairment but also neuroinflammation, apoptosis, abnormal protein accumulation, and neurotrophic support [ 116 , 117 , 118 , 119 ]. Among flavonols, quercetin showed a strong protective effect in a 6-OHDA-induced PD model, boosting mitochondrial activity, counteracting oxidative stress, and decreasing synuclein accumulation [ 120 ] ( Table 1 ).…”

Section: Treatments Targeting Oxidative Stress In Pdmentioning

confidence: 99%

Oxidative Stress and Neurodegeneration: Insights and Therapeutic Strategies for Parkinson’s Disease

Bej,

Cesare,

Volpe

et al. 2024

Neurology International

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Parkinson’s disease (PD) is a progressive neurodegenerative condition marked by the gradual deterioration of dopaminergic neurons in the substantia nigra. Oxidative stress has been identified as a key player in the development of PD in recent studies. In the first part, we discuss the sources of oxidative stress in PD, including mitochondrial dysfunction, dopamine metabolism, and neuroinflammation. This paper delves into the possibility of mitigating oxidative stress as a potential treatment approach for PD. In addition, we examine the hurdles and potential of antioxidant therapy, including the challenge of delivering antioxidants to the brain and the requirement for biomarkers to track oxidative stress in PD patients. However, even if antioxidant therapy holds promise, further investigation is needed to determine its efficacy and safety in PD treatment.

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A Review on Natural Antioxidants for Their Role in the Treatment of Parkinson’s Disease

Cited by 31 publications

References 230 publications

Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas

Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas

Chiisanoside Mediates the Parkin/ZNF746/PGC-1α Axis by Downregulating MiR-181a to Improve Mitochondrial Biogenesis in 6-OHDA-Caused Neurotoxicity Models In Vitro and In Vivo: Suggestions for Prevention of Parkinson’s Disease

Oxidative Stress and Neurodegeneration: Insights and Therapeutic Strategies for Parkinson’s Disease

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