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 mg/2 ml) 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-a (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.

Background and Objective: Lipolysaccharide (LPS) is a large molecule isolated from bacteria such as the enterobacteriaceae family with a negative effect on memory and learning through disturbing the balance of free radicals and creating oxidative stress conditions. In this study, we evaluated the effect of quercetin on oxidative stress and LPS-induced memory impairment in the rat. Materials and Methods: Male rats (n=40) were randomly divided into 5 groups: control, control under treatment with quercetin at a dose of 50 mg/kg, LPS, and LPS groups treated with quercetin at doses of 10 or 50 mg/kg. For induction of inflammation, LPS dissolved in normal saline (500 μ g/kg) was injected intraperitoneally. After one week, the passive avoidance behavior was tested in the shuttle box and hippocampal homogenate was prepared. Acetylcholinesterase (AChE) activity and lipid peroxidation (malondialdehyde, MDA) were measured using specific kits. Data were analyzed by SPSS software (version 16). Results: Step-through latency (STL) in quercetin50-treated LPS group was significantly greater than control group (p<0. 05). In addition, AChE activity and level of MDA was significantly lower in quercetin50-treated LPS group versus LPS group (p<0. 05). Meanwhile, quercetin at a dose of 10 mg/kg did not have such a significant effect. Conclusion: Quercetin at a dose of 50 mg/kg has a protective effect on learning and memory impairment due to LPS and part of its beneficial effect is mediated via attenuation of lipid peroxidation and AChE.

Objective(s): A variety of cytokines are involved in cognitive functioning. Balance restoration between protective and degenerative neuro-inflammation is of great interest in newer therapeutic approaches. In the current study, we investigated the effect of pramipexole (PMX) on memory functions, hippocampal amyloid deposition, serum cytokines, and brain-derived neurotrophic factor (BDNF) levels in lipopolysaccharide (LPS) challenged-rats. Materials and Methods: Male Wistar rats were divided into 5 groups (n=8): control (saline), lipoppolysacharide (LPS 250 mcg/kg bw), and experimental groups (LPS and PMX 0. 5, 1, and 3 mg/ kg bw). Learning and memory were assessed by the novel object recognition test (NORT), Y-maze, and step-through test. Immunological and histological assays were performed. Results: In memory tasks, LPS-challenged rats showed reduction in the observed parameters. In NORT, PMX 1 mg/kg increased recognition index compared with controls, whereas the other two doses increased this index only against the LPS-control. In Y-maze, all doses of PMX significantly had increased alternation when compared with LPS. In the step-through test, only the lowest dose of PMX extended the latency compared with LPS. Histological examination revealed that PMX at doses of 0. 5 and 1 mg/kg reduced amyloid deposition in the hippocampus. Interleukin (IL)-10 serum levels were elevated by 1 mg/kg PMX. Tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β 1 serum levels remained under the detectable minimum in all experimental groups. PMX at all doses significantly decreased BDNF serum concentration. Conclusion: In rats with LPS-induced neuro-inflammation PMX improved hippocampal-dependent memory and exerted immuno-modulatory effects by increasing IL-10.