Protective effect of apigenin on neurons against oxygen‐glucose deprivation/reperfusion induced injury

Abstract

Apigenin, a flavone, has considerable neuroprotective effects by its anti‐oxidative mechanism. However, it is still unclear whether apigenin can protect neurons against oxygen‐glucose deprivation/reperfusion (OGD/R) induced injury. After two hours oxygen‐glucose deprivation and 24 hours reperfusion treatment in primary cultured hippocampal neurons, or ten minutes global cerebral ischemia and followed 24 hours reperfusion induced by Pulsinelli's 4‐vessel occlusion in male Sprague‐Dawley rats, the neuron viability, survival rate and apoptosis rate were evaluated by MTT assay, lactate dehydrogenase (LDH) leakage assay and hoechst staining, respectively. Treatment by OGD/R markedly reduced neuronal viability to 67.60±3.40% of control, increased LDH leakage rate from 17.00±6.25% to 50.49±9.00%, increased apoptosis rate from 7.60±3.56% to 28.90±8.42%. Application of apigenin (10–100 μmol·L−1) during OGD inhibited OGD/R induced neuron injury and apoptosis in a dose‐dependent manner. Besides, the activity of Na+/K+‐ATPase was significantly suppressed in both OGD/R group and global ischemia/reperfusion group. And application of apigenin during ischemia preserved the Na+/K+‐ATPase activity in the both groups. Furthermore, inhibition of Na+/K+‐ATPase with ouabain attenuated the protective effect afforded by apigenin. These data provide the evidence that apigenin has neuroprotective effect against OGD/R induced injury and the protective effect may be associated with its ability to improve Na+/K+‐ATPase activity after OGD/R.