摘要
目的 观察维生素E(Vit E)对迟发性运动障碍(TD)大鼠的影响,探讨TD可能的病理生理机制。方法 将24只雄性Sprague-Dawley(SD)大鼠随机分为空白对照组(腹腔注射生理盐水2ml/kg+第5周始灌胃5ml/kg生理盐水)、TD组(腹腔注射氟哌啶醇2 mg/kg+第5周始灌胃5 ml/kg生理盐水)、TD+Vit E组(腹腔注射氟哌啶醇2 mg/kg+第5周始灌胃5 ml/kg Vit E溶液),每组8只,共观察9周。每周第7天评定大鼠口周异常运动,第9周末测定血清超氧化物歧化酶(SOD)活力、脂质过氧化代谢产物丙二醛(MDA)浓度。结果 (1)第2周末TD组和TD+vit E组大鼠口周异常运动评分增加(P<0.05),第5周达峰值;第9周末,TD+Vit E组减分[(9.1±8.9)分]大于TD组[(0.6±4.2)分],差异有显著性(P<0.05);(2)第9周末,TD组大鼠血清SOD活力[(340±43)U/ml]低于空白对照组[(393±32)U/ml],MDA水平[(20±6)nmol/ml]高于空白对照组[(9±4)nmol/ml],TD+Vit E组可缓解这一改变[SOD为(403±17)U/ml,MDA为(6±4)nmol/ml],差异有非常显著性(P<0.01)。结论 Vit E能有效缓解TD模型大鼠口周异常运动症状;氧化应激在TD发生过程中起重要作用。
Objective To investigate pathophysiological mechanism of tardive dyskinesia (TD) by treating the TD model rats with Vitamin E (Vit E). Methods Twenty-four male Sprague-Dawley (SD) rats were randomly assigned into the control, TD and TD + Vit E group, processed with saline, haloperidol + saline, haloperidol + Vit E respectively. Orofacial dyskinesia [Vacuous chewing movements (VCMs) and tongue protrusions] was evaluated at each weekend. Venous blood was collected at the end of 9-week research and the serum superoxide dismutase ( SOD) activity and malondialdehydescid ( MDA) were assayed. Results Haloperidol could cause orofacial dyskinesia in rats; Vit E might relieve these symptoms (decreased score:9. 1 ±8. 9) ,it was significant difference to compare with the TD rats (decreased score:0.6 ±4. 2;P <0. 05). Serum SOD activity [ (340±43) U/ml] was increased and MDA level [(20±6) nmol/ ml] was decreased significantly in the TD rats. These changes could be returned by Vit E treatment [SOD: (403±17) U/ml,MDA:(6±4) nmol/ml]. Conclusions Vit E can relieve orofacial dyskinesia of TD model rats effectively, oxidative damages might be the key factors of TD.
出处
《中华精神科杂志》
CAS
CSCD
北大核心
2004年第3期179-181,共3页
Chinese Journal of Psychiatry
基金
首都医学发展科研基金资助项目(2002-3095)
关键词
维生素E
迟发性运动障碍
动物模型
大鼠
病理生理机制
Dyskinesia, drug-induced
Vitamin E
Free radicals
Superoxide dismutase
Malondialdehyde
Oxidative stress