Volume 11, Issue 1 (January & February 2020)                   BCN 2020, 11(1): 41-48 | Back to browse issues page

DOI: 10.32598/bcn.9.10.340


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1- Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
2- Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.; Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
3- Neurophysiology Research Center, Shahed University, Tehran, Iran.
Abstract:  
Introduction: Kainic Acid (KA) is an ionotropic glutamate receptor agonist. KA can induce neuronal overactivity and excitotoxicity. Rosmarinic Acid (RA) is a natural polyphenolic compound with antioxidant, anti-apoptotic, anti-neurodegenerative, and anti-inflammatory properties. This study aimed to assess the effect of RA on apoptosis, nNOS-positive neurons number, as well as Mitogen-Activated Protein Kinase (MAPK) and Cyclooxygenase-2 (COX-2) immunoreactivity, following intrahippocampal Kainic acid injection in rats. 
Methods: The study rats were randomly assigned to three groups of sham, KA (KA was injected into the right side of the hippocampus) and KA+RA (a dose of 10 mg/kg/day through a gavage needle for one week before KA injection). Then, histopathological changes, including apoptosis [Terminal Deoxynucleotidyl Transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay], nNOS-positive neurons number, as well as COX-2 and MAPK immunoreactivity were evaluated in the hippocampus. 
Results: In the RA pretreated group, nNOS-positive neurons and TUNEL- positive cells were significantly reduced compared to the KA group (P<0.05). COX-2and MAPK immunoreactivity demonstrated no significant changes compared to the KA group. They indicated a significant higher reactivity for COX-2 (P<0.01) and MAPK (P<0.005) versus the sham group. 
Conclusion: RA had neuroprotective effects, compared to KA, through reduced apoptosis and nNOS-positive neurons, but not MAPK and COX-2. 
Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2016/04/12 | Accepted: 2018/10/27 | Published: 2020/01/1