Autumn 2012, Volume 3, Number 5 5 Basic and Clinical Coenzyme Q10 Protects Hippocampal Neurons against Ischemia/ Reperfusion Injury via Modulation of BAX/Bcl-2 Expression Mohammad Zamani 1 , Majid Katebi 2,3 , Mehdi Mehdizadeh 1,4 , Farzaneh Mohamadzadeh 1 , Mansooreh Soleimani 1,4 * 1. Cellular and Molecular Research Center of Tehran University of Medical Sciences, Tehran, Iran. 2. Persian Gulf Research Center for Stem Cell Therapy. 3. Dept. of Anatomy, School of Medicine, Hormozgan University of Medical Sciences, Hormozgan, Iran. 4. Dept. of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. * Corresponding Author: Mansaooreh Soleimani, PhD Anatomy Department, Hemat Campus, Tehran University of Medical Sciences, Hemat Highway, Tehran, Iran. E-mail: mansourehsoleimani@gmail.com Introduction: Preliminary studies have confrmed reduction in cell death following treatment with antioxidants. According to this fnding we study the relationship between consumption of CoQ10 and expression of Bax and Bcl2 in hippocampus following ischemia/reperfusion as proteins involved in cell programmed death or apoptosis. Methods: We studied the protective role of CoQ10 against ischemia-reperfusion. Experimental design includes four groups: intact, ischemic control, sham control and treatment group with CoQ10. The mice were pre-treated with CoQ10 for a week, then ischemia was induced by common carotid artery ligation and following the reduction in infammation (a week) the mice was treated with CoQ10. Nissl staining was applied for counting the necrotic cells of hippocampus and the western blot was performed to measure the Bax and Bcl2 expression. Results: Cell death was signifcantly lower when mice were treated with CoQ10. Bax expression was signifcantly high in the ischemic group but low in the treatment group, and the bcl2 expression was lower in the ischemic group than the treatment and the vehicle groups. Discussion: Ischemia for 15 minutes induced cell death in hippocampus with more potent effect on CA1. CoQ10 intake signifcantly reduced cell death and prevented the expression of Bax while inducing an increase in expression of bcl2. A B S T R A C T Article info: Received: 4 December 2012 First Revision: 15 January 2012 Accepted: 31 August 2012 Key Words: CoQ10, Hippocampus, Ischemia-Reperfusion, Neuroprotective Effect. 1. Introduction erebral ischemia is a critical clinical issue with no satisfactory cure that can be fatal and disabling, requiring long-term treat- ment and heavy fnancial expenses (Aliev et al, 2008; Camarata et al, 1994; David et al, 2002). Hippocampus is involved in memory formation and spatial information processing and is among the frst areas of the brain affected by ischemia/reperfusion and hypoxic conditions. C Ischemia and hypoxia can cause cells to have an- aerobic respiration to survive (Zhang et al, 1994), but may also lead to acidosis and lactate accumulation and cell death. During reperfusion, release of oxygen free radicals and other oxidative may cause damage to cells, with even greater intensity than the ischemia. Rapid medical intervention may reduce cell death (Turunen et al, (2004). Antioxidants are substances that remove free radicals, preventing damage to cell membranes, DNA, and cell death. Coenzyme Q10 (CoQ10) is a lipid-soluble cofac- tor found naturally in the inner mitochondrial membrane