1 گروه فیزیولوژی، دانشکده پزشکی، دانشگاه شاهد، تهران، ایران
2 مرکز تحقیقات نوروفیزیولوژی، دانشگاه شاهد، تهران، ایران
3 گروه علوم تشریح و پاتولوژی، دانشکده پزشکی، دانشگاه شاهد، تهران، ایران
عنوان مقاله [English]
Background and Objective: Parkinson's disease is one the most common neurodegenerative diseases clinically diagnosed by movement disorders such as slowness of movement, muscle stiffness, tremor at rest and personality disorder. The goal of this study was to examine the impact of diosgenin with antioxidant and neuroprotective effects on a rat model of Parkinson's disease induced by 6-hydroxydopamine.
Materials and Methods: Forty male Wistar rats were divided into four groups. 1-sham, 2-sham treated with diosgenin (100 mg/kg) 3- The group microinjected with 6-hydroxydopamine (6-OHDA) and 4- 6-OHDA group treated with diosgenin. Rats received diosgenin by gavage before surgery for 1 week. At the end of this period, the experimental model of Parkinson's disease was induced by unilateral injection of 6-OHDA into the striatum. Rotational behavior was studied after the surgery. Malondialdehyde (MDA), glutathione (GSH), catalase, nitrite and glial fibirally acidic protein (GFAP) were measured in the homogenate. Also, nigral neurons were counted and compared using Nissl staining.
Results: There was a significant reduction of rotations in diosgenin-pretreated 6-OHDA-lesioned rats as compared to untreated 6-OHDA group. In addition, pretreatment with diosgenin in 6-OHDA-lesioned group significantly prevented the reduction of neurons in the substantia nigra pars compacta as compared to the untreated group (P<0.05). Also, diosgenin pretreatment decreased the level of GFAP and MDA in the brain homogenate (P<0.01) and increased level of glutathione (GSH) (P<0.05). There was also no significant change regarding nitrite and catalase.
Conclusion: Diosgenin pretreatment improved motor behavior and asymmetry in 6-OHDA-lesioned rats and protected substantia nigra pars compacta neurons and its effect is mediated via attenuation of oxidative stress and astrogliosis.