To investigate the protective mechanism of irisflorentin on Na2S2O4-induced injury in an in vitro stroke model,the PC12 cells were divided into blank group(no drug administration,replaced with normal culture medium for 24 h),model group(cultured in nor-mal culture medium for 24 h after adding 10 μg/mL Na2S2O4 for 2 h),positive control group(cultured in 10 μg/mL edaravone for 24 h after adding 10 μg/mL Na2S2O4 for 2 h),and drug-protected group(after the induction of hypoxia by adding 10 μg/mL Na2S2O4 for 2 h,and then replacing the incubation with 3.13,6.25 and 12.5 μg/mL subnormal irisflorentin for 24 h).And the morphology of the cells was observed,cell viability was examined;and the amount of LDH released,intracellular Caspase-3 enzyme activity,Ca2+level,and apoptosis were detected.The expression level of apoptotic protein Caspase-3 was detected by immunoblotting.The results showed that secondary wild irisflorentin in Belamcanda chinensis significantly reduced the degree of damage caused by oxygen glucose depriva-tion/reoxygenation to PC12 cells,enhanced cell survival,decreased intracellular LDH release,Ca2+level,as well as Caspase-3 enzyme activity,and decreased the expression level of Caspase-3 protein.The results showed that Irisflorentin had a significant protective effect(P＜0.01)on oxygen-glucose deprivation/reoxygenation-injured PC12 cells,and its mechanism might be related to the inhibition of apoptosis of neuronal cells in the brain.
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