ellagic acid protects the brain against 6-hydroxydopamine induced neuroinflammation in a rat model of parkinson’s disease

introduction: neuroinflammation may play as an important risk factor in progressive degeneration of dopaminergic cells. antioxidants have protective effects against free radicalsinduced 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). methods: 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. results: 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. discussion: 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.