Neuroprotection of antioxidant enzymes against transient global cerebral ischemia in gerbils

Abstract

Experimentally transient global cerebral ischemia using animal models have been thoroughly studied and numerous reports suggest the involvement of oxidative stress in the pathogenesis of neuronal death in ischemic lesions. In animal models, during the reperfusion period after ischemia, increased oxygen supply results in the overproduction of reactive oxygen species (ROS), which are involved in the process of cell death. ROS, such as superoxide anions, hydroxyl free radicals, hydrogen peroxide and nitric oxide are produced as a consequence of metabolic reactions and central nervous system activity. These reactive species are directly involved in the oxidative damage of cellular macromolecules such as nucleic acids, lipids and proteins in ischemic tissues, which can lead to cell death. Antioxidant enzymes are believed to be among the major mechanisms by which cells counteract the deleterious effect of ROS after cerebral ischemia. Consequently, antioxidant strategies have been long suggested as a therapy for experimental ischemic stroke; however, clinical trials have not yet been able to promote the translation of this concept into patient treatment regimens. This article focuses on the contribution of oxidative stress or antioxidants to the post-ischemic neuronal death following transient global cerebral ischemia by using a gerbil model.

The protective cardiac effects of Β-myrcene after global cerebral ıschemia/reperfusion in C57BL/J6 mouse

“…All mice were kept under a 12-h light/dark cycle at an ambient temperature of 21±2°C and a humidity level of 60±5%. A total of 40 animals were randomly divided into four groups (n = 10): (1) control (sham-operated), (2) global cerebral IR, (3) MYR, and (4) MYR+IR. This experimental design was described in our previous study 15 .…”

Picroside II protects the blood-brain barrier by inhibiting the oxidative signaling pathway in cerebral ischemia-reperfusion injury

“…The antioxidant capacity of brain tissue is very fragile, which makes it difficult to resist the attack of free radicals[9]. Moreover, a large number of ROS mediate tissue damage directly, which results in impaired nerve function[10,11,12,13]. Therefore, ROS are believed to be a key cause of the nerve injury after CI/R.…”

Free Radicals, the Natural Antioxidant Buyang Huanwu Decoction and Ischemic Stroke

“…Neuroprotectants commonly used in clinical treatment include calcium channel blockers, glutamate receptor antagonists and N-methyl-D-aspartic acid receptor (NMDA) antagonists. Research has shown that oxidative stress plays an important role in the pathophysiology of cerebral ischemia and that excessive ROS is produced during cerebral ischemia and reperfusion [1] . Studies have also suggested that oxidative stress and damage caused by free radicals lead are key factors for triggering stroke and other neurodegenerative diseases.…”

“…reperfusion [1] . Studies have also suggested that oxidative stress and damage caused by free radicals lead are key factors for triggering stroke and other neurodegenerative diseases.…”

“…For instance, the NO free radical plays a key role in the relaxation of blood vessels, blood pressure regulation and during learning and memorization. Nevertheless, excessive free radicals can initiate lipid peroxidation and result in protein oxidation and DNA damage in cells, and are often implicated in diseases with high mortality rates, including cardiovascular and cerebrovascular diseases, cancer and neurodegenerative diseases [1][2][3][4] . …”