Assessment of reactive oxygen species (ROS) status in chronic cerebral hypoperfusion-induced neurodegeneration

Abstract

Aging is a major risk factor for neurodegenerative disorders, such as Alzheimer`s disease, dementia, and the number of people with these conditions is increasing rapidly. It has been well established that aging and dementia are accompanied by a reduced cerebral blood flow (CBF). Chronic cerebral hypoperfusion-induced neurodegeneration was produced by bilateral, common carotid artery occlusion (2VO) in the rats. 2VO rats have long been employed to examine the role of cerebral hypoperfusion in neurodegenerative processes. Neurodegeneration is associated with the generation of reactive oxygen species which is lethal to neuronal cell at high concentration. Increased levels of oxidative damage to DNA, lipids and proteins have been detected by a range of assays in post-mortem tissues from patients with neurodegenerative diseases. The aim of this study was to evaluate the status of reactive oxygen species (ROS) in chronic cerebral hypoperfusion-induced neurodegeneration in 2VO rats. Rats were randomly divided into 2 groups, each group (n=7). Group A rats served as a control. And group B rats were subjected to 2VO. After 8 weeks of 2VO, antioxidant enzymes activity, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase and lipid peroxidation marker (malondialdehyde (MDA) concentration) were estimated in the brain tissue and compared with control. 2VO caused significant (P< 0.001) mean increase in GPx, SOD, and catalase activities as well as MDA levels as compared to the control. The present study revealed that chronic cerebral hypoperfusion in 2VO rats increase the production of ROS, which is reflected in increased level of GPx, SOD, catalase and MDA in the brain.