The Effect of Sesamin on Motor Asymmetry in Intrastriatal 6-Hydroxydopamine Rat Model of Parkinson's Disease

Authors

  • Farnaz Nikbakht Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  • Monireh Mansouri Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  • Soudabeh Fallah Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  • Tourandokht Baluchnejadmojarad Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
Abstract:

Background and Objective: Parkinson's disease (PD) is an age-related neurodegenerative disease with selective damage of dopaminergic neurons of the mesencephalon. L-dihydroxyphenylamine (L-DOPA) therapy is currently the gold standard maneuver for PD. Due to the protective, anti-inflammatory, and antioxidant effect of sesamin, this study was undertaken to assess dose-dependent effect of this agent on motor asymmetry induced by intrastriatal injection of 6-hydroxydopamine in the rat. Materials and Methods: In this experimental research, male Wistar rats (n=48) were equally divided into sham, sesamin20-treated sham, 6-hydroxydopamine (OHDA)-lesioned, sesamin10 and sesamin20-treated lesion groups, and sesamin20-treated lesion group receiving the estrogenic antagonist fulvestrant. Model of PD was induced by microinjecting 12.5 microgram of 6-OHDA dissolved in normal saline-ascorbate solution into the left striatum. Treated lesion groups received sesamin at doses of 10 or 20 mg/kg/day started one week till 1 h before the surgery. After 1 week, ipsilateral and contralateral rotations induced by apomorphine were counted and net scores were obtained. Results: In the 6-OHDA-lesioned group, the dopaminergic agonist apomorphine induced contralateral rotational behavior (PConclusion: Sesamin administration at doses of 10 and 20 mg/kg could reduce motor asymmetry and attenuate forced biased rotational behavior in 6-OHDA-induced model of PD and part of this effect is possibly via an estrogenic pathway.

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Journal title

volume 3  issue 2

pages  5- 8

publication date 2015-09-10

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