title: The beneficial effects of 18β-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model.
abstract: This study investigated the effects of 18β-glycyrrhetinic acid (GA) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. All subjects (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) I/R, (3) GA, and (4) GA+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with the vehicle for 10 days. In the GA group, mice were given GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the GA+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with the same dose of GA for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidaitons and a decrease in elements of the antioxidant defense systems. However, GA treatment was protective against the oxidative effects of I/R by inducing significant increases in antioxidant defense systems and a significant decrease of lipid peroxidations. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by GA treatment. Therefore, the current study demonstrated that GA treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, GA may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, it may be a viable and safe alternative treatment for ischemic stroke in humans.
authors.affiliation: Department of Brain and Neurosurgery, Faculty of Medicine, University of Inonu, 44280, Malatya, Turkey, mustafa.oztanir@inonu.edu.tr.
authors.forename: M Namik
authors.initials: MN
authors.lastname: Oztanir
authors.forename: Osman
authors.initials: O
authors.lastname: Ciftci
authors.forename: Aslı
authors.initials: A
authors.lastname: Cetin
authors.forename: M Akif
authors.initials: MA
authors.lastname: Durak
authors.forename: Nese
authors.initials: N
authors.lastname: Basak
authors.forename: Yener
authors.initials: Y
authors.lastname: Akyuva
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000473:pathology; D001923:Brain Chemistry / Q000187:drug effects; D002545:Brain Ischemia / Q000188:drug therapy* / Q000473:pathology; D017536:Carotid Artery, Common; D053148:Caspase 3 / Q000032:analysis; D002374:Catalase / Q000032:analysis; D003250:Constriction; D004353:Drug Evaluation, Preclinical; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D005978:Glutathione / Q000032:analysis; D005979:Glutathione Peroxidase / Q000032:analysis; D006034:Glycyrrhetinic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000473:pathology / Q000517:prevention & control; D013482:Superoxide Dismutase / Q000032:analysis; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D000975:Antioxidants; D004365:Drugs, Chinese Herbal; D018696:Neuroprotective Agents; D017392:Thiobarbituric Acid Reactive Substances; C119129:18alpha-glycyrrhetinic acid; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; C505410:Casp3 protein, rat; D053148:Caspase 3; D005978:Glutathione; D006034:Glycyrrhetinic Acid