Mesh : Animals Quinones / pharmacology therapeutic use Chalcone / analogs & derivatives pharmacology therapeutic use Male Mice Brain-Derived Neurotrophic Factor / metabolism Depression / drug therapy metabolism Hippocampus / drug effects metabolism pathology Behavior, Animal / drug effects Serotonin / metabolism Dopamine / metabolism Rotenone / pharmacology Disease Models, Animal Disks Large Homolog 4 Protein / metabolism Parkinson Disease / drug therapy metabolism psychology

来  源:   DOI:

Abstract:
Depression is a common non-motor symptom of Parkinson\'s disease. Previous studies demonstrated that hydroxysafflor yellow A had properties of improving motor symptoms of Parkinson\'s disease. The effect of hydroxysafflor yellow A on depression in Parkinson\'s disease mice is investigated in this study. To induce Parkinson\'s disease model, male Swiss mice were exposed to rotenone (30 mg/kg) for 6 weeks. The chronic unpredictable mild stress was employed to induce depression from week 3 to week 6. Sucrose preference, tail suspension, and forced swimming tests were conducted. Golgi and Nissl staining of hippocampus were carried out. The levels of dopamine, 5-hydroxytryptamine and the expression of postsynaptic density protein 95, brain-derived neurotrophic factor in hippocampus were assayed. It showed that HSYA improved the depression-like behaviors of Parkinson\'s disease mice. Hydroxysafflor yellow A attenuated the injury of nerve and elevated contents of dopamine, 5-hydroxytryptamine in hippocampus. Treatment with hydroxysafflor yellow A also augmented the expression of postsynaptic density protein 95 and brain-derived neurotrophic factor. These findings suggest that hydroxysafflor yellow A ameliorates depression-like behavior in Parkinson\'s disease mice through regulating the contents of postsynaptic density protein 95 and brain-derived neurotrophic factor, therefore protecting neurons and neuronal dendrites of the hippocampus.
摘要:
抑郁症是帕金森病常见的非运动症状。先前的研究表明,羟基红花黄色素A具有改善帕金森病运动症状的特性。本研究探讨了羟基红花黄色素A对帕金森病小鼠抑郁的影响。建立帕金森病模型,雄性瑞士小鼠暴露于鱼藤酮(30mg/kg)6周。从第3周到第6周,采用慢性不可预测的轻度压力诱发抑郁症。蔗糖偏好,尾部悬挂,并进行了强迫游泳测试。对海马体进行高尔基体和Nissl染色。多巴胺的水平,检测海马组织中5-羟色胺和突触后密度蛋白95、脑源性神经营养因子的表达。表明HSYA改善了帕金森病小鼠的抑郁样行为。羟基红花黄色素A减轻神经损伤,多巴胺含量升高,海马中的5-羟色胺。用羟基红花黄色素A治疗也增加了突触后密度蛋白95和脑源性神经营养因子的表达。这些发现表明,羟基红花黄色素A通过调节突触后密度蛋白95和脑源性神经营养因子的含量来改善帕金森病小鼠的抑郁样行为。因此保护海马的神经元和神经元树突。
公众号