Turkmen, Nese BasakYuce, HandeTaslidere, AsliSahin, YaseminAyhan, IdrisUnuvar, SonguelCiftci, Osman2024-08-042024-08-0420221984-82502175-9790https://doi.org/10.1590/s2175-97902022e21219https://hdl.handle.net/11616/101122The aim of the present study is to investigate the cardioprotective effects of 1813-glycyrrhetinic acid (1813-GA) against oxidative and histological damage caused by global cerebral ischemia/ reperfusion (I/R) in C57BL/J6 mice. All male mice (n:40) were randomly divided into four groups: (1) sham-operated (Sham), (2) I/R, (3) 1813-GA, and (4) 1813-GA+I/R. Ischemia was not applied to the sham and 1813-GA groups. In the I/R group, the bilateral carotid arteries were clipped for 15 min to induce ischemia, and the mice were treated with the vehicle for 10 days. In the 1813-GA group, the mice were given 1813-GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the 1813-GA+I/R group, the ischemic procedure performed to the I/R model was applied to the animals and afterwards they were intraperitoneally (i.p.) treated with 1813-GA (100 mg/kg) for 10 days. It was found that global cerebral I/R increased TBARS levels and decreased antioxidant parameters. The 1813-GA treatment decreased the level of TBARS and increased GSH, GPx, CAT, SOD activities. Also, the control group cardiac tissue samples were observed to have a normal histological appearance with the Hematoxylin-Eosin staining method. Histopathological damage was observed in the heart tissue samples belonging to the I/R group. The 1813-GA treatment ameliorates oxidative and histological injury in the heart tissue after global ischemia reperfusion, and may be a beneficial alternative treatment.eninfo:eu-repo/semantics/closedAccessGlobal cerebral IR1813-glycyrrhetinic acidOxidative stressHeart injuryArticle5810.1590/s2175-97902022e212192-s2.0-85146521928Q2WOS:000924004500001Q4