ReferenceID 4510
Icaritin Provides Neuroprotection in Parkinson's Disease by Attenuating Neuroinflammation, Oxidative Stress, and Energy Deficiency
Antioxidants (Basel)
Neuroinflammation, oxidative stress, and mitochondrial dysfunction are all important pathogenic mechanisms underlying motor dysfunction and dopaminergic neuronal damage observed in patients with Parkinson's disease (PD).
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- Reference Id
- 4510
- Evidence Id
- 21100
- Core Evidence Id
- 21100
- Source Reference Id
- 2298
- Herb2 Reference Id
- HBREF003095
- Subject Paper Key
- HBIN016163_33805302
- Pubmed Id
- 33805302
- Doi
- 10.3390/antiox10040529
- Paper Title
- Icaritin Provides Neuroprotection in Parkinson's Disease by Attenuating Neuroinflammation, Oxidative Stress, and Energy Deficiency
- Paper Abstract
- Neuroinflammation, oxidative stress, and mitochondrial dysfunction are all important pathogenic mechanisms underlying motor dysfunction and dopaminergic neuronal damage observed in patients with Parkinson's disease (PD). However, despite extensive efforts, targeting inflammation and oxidative stress using various approaches has not led to meaningful clinical outcomes, and mitochondrial enhancers have also failed to convincingly achieve disease-modifying effects. We tested our hypothesis that treatment approaches in PD should simultaneously reduce neuroinflammation, oxidative stress, and improve alterations in neuronal energy metabolism using the flavonoid icaritin in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Using matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI), coupled with biochemical analyses and behavioral tests, we demonstrate that icaritin improves PD by attenuating the the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome activity and stabilizing mitochondrial function, based on our extensive analyses showing the inhibition of NLRP3 inflammasome, reduction of NLRP3-mediated IL-1beta secretion, and improvements in the levels of antioxidant molecules. Our data also indicated that icaritin stabilized the levels of proteins related to mitochondrial function, such as voltage-dependent anion channel (VDAC) and ATP synthase subunit beta (ATP5B), as well as those of molecules related to energy metabolism, such as ATP and ADP, ultimately improving mitochondrial dysfunction. By employing molecular docking, we also discovered that icaritin can interact with NLRP3, VDAC, ATP5B, and several blood-brain barrier (BBB)-related proteins. These data provide insights into the promising therapeutic potential of icaritin in PD.
- Journal
- Antioxidants (Basel)
- Publish Year
- 2021
- Experiment Subject
- mouse; patient
- Experiment Type
- Animal Experiment
- Phenotype Related
- Motor Dysfunction; Neuroinflammation; Parkinson's Disease; Mitochondrial Dysfunction
- Paper Title Cn
- Paper Title En
- Icaritin Provides Neuroprotection in Parkinson's Disease by Attenuating Neuroinflammation, Oxidative Stress, and Energy Deficiency
- Bilingual Status
- semi_complete