Aim:To investigate the influence of resveratrol (Res),a nutritional antioxidant,onthe inhibition of apoptosis in rat primary neuron cultures.Methods:The culturedcortical neurons of neonatal Sprague-Dawley rats were pretreated with Res (0.1,1.0,and 10.0 μmol/L) and oxygen-glucose deprivation/reperfusion (OGD/RP) withoxygen and glucose were initiated at d 10 in vitro.Neuronal apoptosis wasdetermined by flow cytometry,and morphological changes of neurons wereobserved by an electron microscope.For the mechanism studies,the intracellularfree calcium concentration ([Ca~(2+)]_i) and the transcription of caspases-3 and-12 inneurons were detected by Fura 2/AM loading and real-time RT-PCR,respectively.Results:OGD/RP insult could induce an increase in the apoptotic rate of neurons(from 11.1% to 49.0%),and elicit an obvious morphological change in neurons;pretreatments with Res (0.1,1.0,and 10.0 μmol/L,respectively) significantlyreduced the elevated rate of apoptosis to 41.7%,40.8%,and 37.4%,respectively,and ameliorated the neuronal morphological injury.Similarly,the OGD/RP insultobviously elicited the elevated levels of the [Ca~(2+)]_i and the expressions of caspases-3and-12 mRNA in neurons.Res pretreatments markedly depressed the neuronalabnormal elevation of [Ca~(2+)]_i and the overexpression of caspases-3 and-12 mRNAin a concentration-dependent manner.Conclusion:Res can attenuate the ratcortical neuronal apoptosis induced by OGD/RP.The mechanisms are,at leastpartly,due to the inhibition of the calcium overload and the overexpression ofcaspases-3 and-12 mRNA. Aim: To investigate the influence of resveratrol (Res), a viral antioxidant, on the inhibition of apoptosis in rat primary neuron cultures. Methods: The culturedcortical neurons of neonatal Sprague-Dawley rats were pretreated with Res (0.1, 1.0, and 10.0 μmol/L L) and oxygen-glucose deprivation/reperfusion (OGD/RP) withoxygen and glucose were initiated at d 10 in vitro. Neuronal apoptosis was determined by flow cytometry, and morphological changes of neurons wereobserved by an electron microscope. For the mechanism studies, the intracellularfree Calcium concentration ([Ca~(2+)]_i) and the transcription of caspases-3 and-12 inneurons were detected by Fura 2/AM loading and real-time RT-PCR, respectively.Results:OGD/RP insult can induce An increase in the apoptotic rate of neurons(from 11.1% to 49.0%), and elicit an obvious morphological change in neurons;pretreatments with Res (0.1,1.0,and 10.0 μmol/L,respectively) significantlyreduced the elevated rate of apoptosis to 41.7 %, 40.8%, and 37.4%, res Pectively, and ameliorated the neuronal morphological injury.Similarly, the OGD/RP insultobviously elicited the elevated levels of the [Ca 2+ ]_i and the expressions of caspases-3and-12 mRNA in neurons. Res pretreatments markedly depressed the neuronalabnormal Elevation of [Ca~(2+)]_i and the overexpression of caspases-3 and-12 mRNA in a concentration-dependent manner.Conclusion: Res can attenuate the ratcortical neuronal apoptosis induced by OGD/RP.The mechanisms are, at leastpartly, Due to the inhibition of the calcium overload and the overexpression of caspases-3 and-12 mRNA.