Farbood Yaghoob, Sarkaki Alireza, Dolatshahi Mojtaba, Taqhi Mansouri Seyed Mohammad, Khodadadi Ali
Physiology Research Center and Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Department of Physiology, School of Medicine, Dezful University of Medical Sciences, Dezful, Iran.
Basic Clin Neurosci. 2015 Apr;6(2):83-9.
Neuroinflammation may play as an important risk factor in progressive degeneration of dopaminergic cells. Antioxidants have protective effects against free radicals-induced neural damage in Parkinson's disease (PD). In the present study, we examined the effects of ellagic acid (EA) on locomotion and neuroinflammatory biomarkers in a rat model of PD induced by 6-hydroxidopamine (6-OHDA).
6-OHDA (16 μg/2 μl) was injected into the right medial forebrain bundle (MFB) in MFB-lesioned rat's brain. Sham group received vehicle instead of 6-OHDA. PD-model was confirmed by rotational test using apomorphine injection. EA (50 mg/kg/2 ml, by gavages) was administered in PD+EA group. One group of MFB-lesioned rats received pramipexole (PPX; 2 mg/kg/2 ml, by gavages) as positive control group (PD+PPX group). Motor activity was assessed by stride length and cylinder tests. The levels of TNF-α and IL-1β were measured in both striatum and hippocampus tissues.
MFB lesion caused significant reduction of stride-length (P<0.001) and also increased the contralateral rotations (P<0.001) and score of the cylinder test (P<0.001). Use of 6-OHDA to induce the PD significantly increased the levels of TNF-α (P<0.001) and IL-1β (P<0.001) in MFB-lesioned rats. EA significantly restored all of the above parameters.
EA can improve the motor impairments in the MFB-lesioned rats via reducing the neuroinflammatory biomarkers and protect the brain against free radicals-induced neural damage. The results suggest that EA can be helpful in management of PD treatment.
神经炎症可能是多巴胺能细胞进行性退化的一个重要危险因素。抗氧化剂对帕金森病（PD）中自由基诱导的神经损伤具有保护作用。在本研究中，我们研究了鞣花酸（EA）对6-羟基多巴胺（6-OHDA）诱导的PD大鼠模型运动能力和神经炎症生物标志物的影响。
将6-OHDA（16μg/2μl）注射到MFB损伤大鼠脑内的右侧内侧前脑束（MFB）。假手术组注射溶剂而非6-OHDA。通过注射阿扑吗啡的旋转试验确认PD模型。PD+EA组给予EA（50mg/kg/2ml，灌胃）。一组MFB损伤大鼠接受普拉克索（PPX；2mg/kg/2ml，灌胃）作为阳性对照组（PD+PPX组）通过步长和圆筒试验评估运动活性。测量纹状体和海马组织中TNF-α和IL-1β的水平。
MFB损伤导致步长显著缩短（P<0.001），对侧旋转增加（P<0.001），圆筒试验评分增加（P<0.001）。使用6-OHDA诱导PD显著增加了MFB损伤大鼠中TNF-α（P<0.001）和IL-1β（P<0.001）的水平。EA显著恢复了上述所有参数。
EA可通过降低神经炎症生物标志物来改善MFB损伤大鼠的运动障碍，并保护大脑免受自由基诱导的神经损伤。结果表明EA有助于PD的治疗。
