Protective effect of luteolin on neurons against cerebral ischemia/reperfusion injury via regulating the activity of ATPase

Abstract

The aim of this study was to determine whether luteolin protects neurons against cerebral ischemia/reperfusion injury and its underlying mechanism. We cultivated hippocampal neurons from new‐born Sprague‐Dawley rats, and established the model of oxygen‐glucose deprivation/reperfusion (2 h/24 h). Neuronal viability was assessed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, and cell injury was evaluated by lactate dehydrogenase (LDH) leakage rate. The percentage of apoptotic cells was measured by using Hoechst 33258 staining. Adult male Sprague‐Dawley rats were subjected to four‐vessel‐occlusion for 10 min followed by reperfusion for 24 h, and the activities of Na+, K+‐ATPase and Ca2+, Mg2+‐ATPase were measured by spectrophotometry. Oxygen‐glucose deprivation/reperfusion decreased the cell viability and increased LDH leakage rate and percentage of apoptotic cells. Compared with oxygen‐glucose deprivation/reperfusion group, luteolin (1‐100 μmol/L) treatment significantly increased the cell viability, decreased LDH leakage rate and the percentage of apoptotic cells in a dose‐dependent manner. Luteolin (200 mg·kg−1, i.p.) markedly inhibited the decrease of ATPase activities induced by global cerebral ischemia/reperfusion. These results demonstrate that luteolin protects neurons against ischemia/reperfusion‐induced cell injury via, at least partly, regulating the activity of ATPase.