Morin ameliorates rotenone-induced Parkinson disease in mice through antioxidation and anti-neuroinflammation: gut-brain axis involvement

Ishola, Ismail O.; Awogbindin, Ifeoluwa O.; Olubodun-Obadun, Taiwo G.; Oluwafemi, O.A.; Onuelu, J.E.; Adeyemi, Olufunmilayo O.

doi:10.1016/j.brainres.2022.147958

Cited by 20 publications

(10 citation statements)

References 88 publications

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“…In PD, morin treatment or pretreatment has been associated with improved motor function, protection against dopaminergic neuron loss in the substantia nigra and striatum in an MPTP‐induced mouse model and mitigated ROS production, mitochondrial membrane potential disruption, and apoptosis in primary neuron cultures and PC12 cells exposed to MPP + (Lee et al, 2016; Zhang, Cao, et al, 2010). Consistent with these findings, a study by Ishola et al indicated that morin reversed behavioral deficits induced by rotenone by reducing MDA levels and enhancing GSH and SOD activities (Ishola et al, 2022). Furthermore, recent research has highlighted morin's ability to protect DA neurons from MPTP‐induced neurotoxicity and improve behavioral deficits by promoting the nuclear translocation of the transcription factor EB (TFEB), a mediator of mitophagy, and activating the AMPK/ULK1 pathway (Wang, Cui, et al, 2023).…”

Section: Therapeutic Effects Of Natural Compounds On Pd By Modulating...mentioning

confidence: 62%

Regulation of mitophagy and mitochondrial function: Natural compounds as potential therapeutic strategies for Parkinson's disease

Liang,

Ma,

Zhong

et al. 2024

Phytotherapy Research

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Mitochondrial damage is associated with the development of Parkinson's disease (PD), indicating that mitochondrial‐targeted treatments could hold promise as disease‐modifying approaches for PD. Notably, natural compounds have demonstrated the ability to modulate mitochondrial‐related processes. In this review article, we discussed the possible neuroprotective mechanisms of natural compounds against PD in modulating mitophagy and mitochondrial function. A comprehensive literature search on natural compounds related to the treatment of PD by regulating mitophagy and mitochondrial function was conducted from PubMed, Web of Science and Chinese National Knowledge Infrastructure databases from their inception until April 2023. We summarize recent advancements in mitophagy's molecular mechanisms, including upstream and downstream processes, and its relationship with PD‐related genes or proteins. Importantly, we highlight how natural compounds can therapeutically regulate various mitochondrial processes through multiple targets and pathways to alleviate oxidative stress, neuroinflammation, Lewy's body aggregation and apoptosis, which are key contributors to PD pathogenesis. Unlike the single‐target strategy of modern medicine, natural compounds provide neuroprotection against PD by modulating various mitochondrial‐related processes, including ameliorating mitophagy by targeting the PINK1/parkin pathway, the NIX/BNIP3 pathway, and autophagosome formation (i.e., LC3 and p62). Given the prevalence of mitochondrial damage in various neurodegenerative diseases, exploring the exact mechanism of natural compounds on mitophagy and mitochondrial dysfunction could shed light on the development of highly effective disease‐modifying or adjuvant therapies targeting PD and other neurodegenerative disorders.

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Section: Therapeutic Effects Of Natural Compounds On Pd By Modulating...mentioning

confidence: 62%

Regulation of mitophagy and mitochondrial function: Natural compounds as potential therapeutic strategies for Parkinson's disease

Liang,

Ma,

Zhong

et al. 2024

Phytotherapy Research

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“…The spontaneous alteration assay has been performed to evaluate the improvement in cognitive impairment by our nanoformulation. The report has shown rotenone’s impact on the impairment of cognitive function in PD progression. , In the result, the rotenone exhibited ∼30% reduction in the alteration movement from the A–B-C arm and FCsnps has shown improvement in the cognitive function by restoring ∼25% alteration movement. (Figure d) Herein, the FCsnps has shown a similar pattern of improvement in the behavioral activity that has been reported by existing literature on FTY720 formulation .…”

Section: Resultsmentioning

confidence: 94%

“…The report has shown rotenone's impact on the impairment of cognitive function in PD progression. 19,20 In the result, the rotenone exhibited ∼30% reduction in the alteration movement from the A−B-C arm and FCsnps has shown improvement in the cognitive function by restoring ∼25% alteration movement.…”

Section: ■ Introductionmentioning

confidence: 88%

FTY720 Nanoformulation Induces O-GlcNacylation of Synuclein to Alleviate Synucleinopathy

Sardoiwala,

Boddu,

Biswal

et al. 2023

ACS Chem. Neurosci.

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The post-translational modification and aggregation of alpha-synuclein are one of the major causes of Parkinson's disease (PD) regulation. In that, the phosphorylation and nitration of synuclein elevate the aggregation, while O-GlcNacylation prevents the aggregation of synuclein. The inhibition of synuclein aggregation directs the development of PD therapy. The endowed O-GlcNacylation of synuclein could be a promising strategy to inhibit synucleinopathy. Therefore, the neuroprotective chitosanbased FTY720 nanoformulation, PP2A (Protein phosphatase 2) activator has been employed to evaluate the PP2A role in the O-GlcNacylation of synuclein in an in vivo PD model. The neuroprotective effect of our nanoformulation is attributed to the upregulation of tyrosine hydroxylase (TH), the PD therapeutic target, with behavioral improvement in animals against rotenone-induced PD deficits. The neuroprotective molecular insights revealed the camouflaged role of PP2A by endowing the OGT activity that induces O-GlcNacylation of synuclein in the reduction of synucleinopathy.

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“…Cytokines and chemokines can also act directly on neurons to alter plasticity and promote depression-like behaviors (Koo et al 2010 ) by directly acting on serotonergic neurons and glutamatergic neurons in frontal cortex and hippocampus to alter synaptic plasticity (Beattie et al 2002 ; Garcia-Oscos et al 2012 ). The relationship between depression and PD has been investigated in various rodent models, by administration of MPTP in mice causing changes in depression and motor function (Ren et al 2021 ) or by rotenone-induced PD in mice, in all of which metformin or fluoxetin showed anti-inflammatory neurogenic and neuroplasticity-inducing effects to improve depressive-like behavior (Ishola et al 2022 ; Mendonça et al 2022 ; Zhao et al 2021 ).…”

Section: Other Pathogenic Factors In Dpdmentioning

confidence: 99%

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

Ka¹

2022

J Neural Transm

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Depression, with an estimated prevalence of about 40% is a most common neuropsychiatric disorder in Parkinson disease (PD), with a negative impact on quality of life, cognitive impairment and functional disability, yet the underlying neurobiology is poorly understood. Depression in PD (DPD), one of its most common non-motor symptoms, can precede the onset of motor symptoms but can occur at any stage of the disease. Although its diagnosis is based on standard criteria, due to overlap with other symptoms related to PD or to side effects of treatment, depression is frequently underdiagnosed and undertreated. DPD has been related to a variety of pathogenic mechanisms associated with the underlying neurodegenerative process, in particular dysfunction of neurotransmitter systems (dopaminergic, serotonergic and noradrenergic), as well as to disturbances of cortico-limbic, striato-thalamic-prefrontal, mediotemporal-limbic networks, with disruption in the topological organization of functional mood-related, motor and other essential brain network connections due to alterations in the blood–oxygen-level-dependent (BOLD) fluctuations in multiple brain areas. Other hypothetic mechanisms involve neuroinflammation, neuroimmune dysregulation, stress hormones, neurotrophic, toxic or metabolic factors. The pathophysiology and pathogenesis of DPD are multifactorial and complex, and its interactions with genetic factors, age-related changes, cognitive disposition and other co-morbidities awaits further elucidation.

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Morin ameliorates rotenone-induced Parkinson disease in mice through antioxidation and anti-neuroinflammation: gut-brain axis involvement

Cited by 20 publications

References 88 publications

Regulation of mitophagy and mitochondrial function: Natural compounds as potential therapeutic strategies for Parkinson's disease

Regulation of mitophagy and mitochondrial function: Natural compounds as potential therapeutic strategies for Parkinson's disease

FTY720 Nanoformulation Induces O-GlcNacylation of Synuclein to Alleviate Synucleinopathy

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

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