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Hyperoside Stabilizes Redox-Mitochondrial-Inflammatory Networks in a Haloperidol-Induced Tardive Dyskinesia-Like
Hsiang-Chien Tseng1,2, Mao-Hsien Wang3, Kuo-Chi Chang4,5
1Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 11101, Taiwan.
Life (Basel, Switzerland)
|May 27, 2026
Summary
Hyperoside (HS) shows promise in treating tardive dyskinesia (TD) by protecting against haloperidol-induced motor dysfunction. It works by modulating redox-mitochondrial-inflammatory networks and activating Nrf2 pathways.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Tardive dyskinesia (TD) is a movement disorder linked to dopamine D2 receptor blockade.
- TD pathology involves a redox-mitochondrial-inflammatory network in striatal circuits.
- Hyperoside (HS), a flavonol glycoside, has cytoprotective effects but its role in TD is unknown.
Purpose of the Study:
- To investigate the protective effects of Hyperoside (HS) against haloperidol (HP)-induced tardive dyskinesia (TD)-like orofacial dyskinesia (OD) in rats.
- To explore the role of the Nrf2 pathway in HS-mediated protection.
Main Methods:
- Rats received haloperidol (HP) to induce TD-like orofacial dyskinesia (OD).
- Hyperoside (HS) was administered alone or with HP, with or without Nrf2 inhibition (ML385).
- Behavioral abnormalities (VCMs, TPs) and striatal molecular markers (oxidative stress, mitochondrial function, inflammation, apoptosis) were assessed.
Main Results:
- HP induced dyskinetic behavior, oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis.
- HS significantly reduced behavioral abnormalities and restored redox balance, mitochondrial function, and anti-inflammatory/anti-apoptotic signaling.
- Nrf2 inhibition exacerbated molecular pathology and reduced HS-mediated protection.
Conclusions:
- Hyperoside (HS) demonstrates neuroprotective effects against haloperidol-induced TD-like pathology.
- Nrf2-related mechanisms are crucial in mitigating network destabilization in TD.
- Integrated stress-response pathways are important in modulating TD progression.
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