H Li1, G Klein, P Sun, A M Buchan. 1. Alberta Stroke Program, Department of Clinical Neurosciences, Foothills Hospital, University of Calgary, Alberta, Calgary, Canada.
Abstract
OBJECTIVE: Release of oxygen free radicals occurs following cerebral ischemia. Studies show that oxygen free radicals mediate ischemic brain injury. CoQ10 is a potent free radical scavenger and may offset brain injury associated with reperfusion. We tested exogeneous CoQ10 as a neuroprotectant in rats following both global and focal ischemic insults. METHODS: Rats were subjected to either 4-vessel occlusion ischemia (4-VO, 10 min occlusion, 7-day survival) or middle cerebral artery occlusion (MCAO, 120 min-occlusion, 22.5 h survival). Regional cerebral blood flows (rCBF) and physiological variables such as blood pressure, pO2, pCO2, plasma glucose and hematocrit were monitored and measured in focal ischemia. The animals were randomized to receive treatments of either phosphate buffered saline (PBS) vehicle or CoQ10 following global or focal ischemia. Injection times were at the end of ischemia and 3 h later for both models of ischemia. Histological outcomes are expressed as a percentage of hippocampal CA(1) cell injury in global ischemia or percentage of cortical infarct over that of non-ischemic hemisphere in focal ischemia. RESULTS: In global ischemia, animals treated with PBS vehicle and CoQ10 had 86+/-5% (n=8) and 83+/-10% (n=8), respectively, of hippocampal CA(1) cell injury (P>0.05). The percentage of infarct volumes in animals following focal ischemia were 23+/-9% (control, n=10) and 25+/-9% (CoQ10, n=10). There were no temperature or physiological differences between the two treatment groups. CONCLUSION: Acute treatment with CoQ10 via intraperitoneal injection does not prevent neuronal injuries following global and focal ischemia.
OBJECTIVE: Release of oxygen free radicals occurs following cerebral ischemia. Studies show that oxygen free radicals mediate ischemic brain injury. CoQ10 is a potent free radical scavenger and may offset brain injury associated with reperfusion. We tested exogeneous CoQ10 as a neuroprotectant in rats following both global and focal ischemic insults. METHODS:Rats were subjected to either 4-vessel occlusion ischemia (4-VO, 10 min occlusion, 7-day survival) or middle cerebral artery occlusion (MCAO, 120 min-occlusion, 22.5 h survival). Regional cerebral blood flows (rCBF) and physiological variables such as blood pressure, pO2, pCO2, plasma glucose and hematocrit were monitored and measured in focal ischemia. The animals were randomized to receive treatments of either phosphate buffered saline (PBS) vehicle or CoQ10 following global or focal ischemia. Injection times were at the end of ischemia and 3 h later for both models of ischemia. Histological outcomes are expressed as a percentage of hippocampal CA(1) cell injury in global ischemia or percentage of cortical infarct over that of non-ischemic hemisphere in focal ischemia. RESULTS: In global ischemia, animals treated with PBS vehicle and CoQ10 had 86+/-5% (n=8) and 83+/-10% (n=8), respectively, of hippocampal CA(1) cell injury (P>0.05). The percentage of infarct volumes in animals following focal ischemia were 23+/-9% (control, n=10) and 25+/-9% (CoQ10, n=10). There were no temperature or physiological differences between the two treatment groups. CONCLUSION: Acute treatment with CoQ10 via intraperitoneal injection does not prevent neuronal injuries following global and focal ischemia.
Authors: B K Binukumar; Nidhi Gupta; Aditya Sunkaria; Ramesh Kandimalla; W Y Wani; D R Sharma; Amanjit Bal; Kiran Dip Gill Journal: Neurotox Res Date: 2011-11-15 Impact factor: 3.911
Authors: Frank Haberman; Sung-Chun Tang; Thiruma V Arumugam; Dong-Hoon Hyun; Qian-Sheng Yu; Roy G Cutler; Zhihong Guo; Harold W Holloway; Nigel H Greig; Mark P Mattson Journal: Neuromolecular Med Date: 2007-08-10 Impact factor: 3.843