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Ellagic acid improves hyperalgesia and cognitive deficiency in ۶-hydroxidopamine induced rat model of Parkinson’s disease

عنوان مقاله: Ellagic acid improves hyperalgesia and cognitive deficiency in ۶-hydroxidopamine induced rat model of Parkinson’s disease
شناسه ملی مقاله: JR_IJBMS-18-1_006
منتشر شده در در سال 1394
مشخصات نویسندگان مقاله:

Mojtaba Dolatshahi - Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Yaghoob Farbood - Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Alireza Sarkaki - Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Seyed Mohammad Taqhi Mansouri - Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran Department of Pharmacology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Ali Khodadadi - Petroleum and Environmental Pollutants Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

خلاصه مقاله:
Objective(s):Parkinson's disease (PD) is known for motor impairments. But often, there are non-motor symptoms such as cognitive deficiency and pain misperception, owing to possible role of nigrostriatal pathway. Antioxidants have protective effect on free radical-induced neuronal damage in PD. To further address, we examined the effects of ellagic acid (EA) in a rat model of PD induced by ۶-hydroxidopamine (۶-OHDA). Materials and Methods: Right medial forebrain bundle (MFB) was lesioned by injecting ۶-OHDA (۱۶ µg/۲ µl), in PD–animals.Sham operated animals received vehicle instead of ۶-OHDA. PD was approved by apomorphine-induced contralateral rotation. EA (۵۰ mg/kg/۲ ml, PO, for ۱۰ days) was administered to PD-EA group. Some PD-animals received pramipexole (PPX; ۲ mg/kg/۲ ml, PO) as a positive control group. Analgesia was measured by tail-flick and hot-plate tests. Passive avoidance task was measured by shuttle box apparatus to record the initial and step-through latency. Spatial cognition task was evaluated by Morris water maze test, measuring the escape latency time, path length, swimming speed and time spent in target quadrant. Results: MFB-lesioned rats showed hyperalgesic responses to the stimulus in tail-flick and hot-plate tests. Also they showed memory and learning deficit in cognitive tests. These effects reversed by EA treatment. Conclusion: ۶-OHDA can induce oxidative stress and can disrupt the neural mechanisms underlying proper integration of painful stimuli and cognitive processes in MFB-lesioned rats. Consequently, nigrostriatal pathway can play possible role in nociception and cognition. EA, a natural antioxidant, has neuroprotective effect on this pathway and can ameliorate this defect and be considered in PD management.

کلمات کلیدی:
۶-OHDA, Cognition, Ellagic acid, Pain, Parkinson's disease, Rat

صفحه اختصاصی مقاله و دریافت فایل کامل: https://civilica.com/doc/1297702/