Naringin Ameliorates Haloperidol-Induced Neurotoxicity and Orofacial Dyskinesia in a Rat Model of Human Tardive Dyskinesia

被引:0
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作者
Mao-Hsien Wang
Chih-Chuan Yang
Hsiang-Chien Tseng
Chih-Hsiang Fang
Yi-Wen Lin
Hung-Sheng Soung
机构
[1] En Chu Kon Hospital,Department of Anesthesia
[2] Mackay Memorial Hospital,Department of Neurosurgery
[3] Mackay Medical College,Department of Medicine
[4] Su Memorial Hospital,Department of Anesthesiology
[5] Fu Jen Catholic University,School of Medicine
[6] National Taiwan University,Institute of Biomedical Engineering
[7] Yuan-Shan Br. of Taipei Veteran General Hospital,Department of Psychiatry
[8] National Defense Medical Center,Department of Biomedical Engineering
来源
Neurotoxicity Research | 2021年 / 39卷
关键词
Naringin; Haloperidol; Orofacial dyskinesia; Striatum;
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摘要
Animal models of haloperidol (HAL)-induced neurotoxicity and orofacial dyskinesia (OD) have long been used to study human tardive dyskinesia (TD). Similar to patients with TD, these models show strong pathophysiological characteristics such as striatal oxidative stress and neural cytoarchitecture alteration. Naringin (NAR), a bioflavonoid commonly found in citrus fruits, has potent antioxidative, anti-inflammatory, antiapoptotic, and neuroprotective properties. The present study evaluated the potential protective effects of NAR against HAL-induced OD in rats and the neuroprotective mechanisms underlying these effects. HAL treatment (1 mg/kg i.p. for 21 successive days) induced OD development, characterized by increased vacuous chewing movement (VCM) and tongue protrusion (TP), which were recorded on the 7th, 14th, and 21st day of drug treatment. NAR (30, 100, and 300 mg/kg) was administered orally 60 min before HAL injection for 21 successive days. On the 21st day, after behavioral testing, the rats were sacrificed, and the nitrosative and oxidative status, antioxidation power, neurotransmitter levels, neuroinflammation, and apoptotic markers in the striatum were measured. HAL induced OD development, with significant increases in the frequency of VCM and TP. NAR treatment (100 and 300 mg/kg) prevented HAL-induced OD significantly. Additionally, NAR treatment reduced the HAL-induced nitric oxide and lipid peroxide production, increased the antioxidation power and neurotransmitter levels in the striatum, and significantly reduced the levels of neuroinflammatory and apoptotic markers. Our results first demonstrate the neuroprotective effects of NAR against HAL-induced OD, suggesting that NAR may help in delaying or treating human TD in clinical settings.
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页码:774 / 786
页数:12
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