OBJECTIVE To investigate the protective effects and mechanisms of costunolide against mousebrain slice injury induced by oxygen-glucose deprivation/reoxygenation(OGD/R).METHODS Mouse brain slice injury was induced by ...OBJECTIVE To investigate the protective effects and mechanisms of costunolide against mousebrain slice injury induced by oxygen-glucose deprivation/reoxygenation(OGD/R).METHODS Mouse brain slice injury was induced by OGD/R in vitro,and the degree ofinjury was evaluated by measuring the release of lactate dehydrogenase(LDH)and 2,3,5-triphenyltetrazolium chloride(TTC)staining.Western blotting was used to analyze the expression of Bax,Bcl-2,Cyt-c,caspase-9,caspase-7 and caspase-3.RESULTS Compared with OGD/R,1,5,and 10μmol·L^-1 costu⁃nolide decreased the LDH levels,increased the TTC staining intensity,inhibited Bax,Cyt-c,caspase-9,caspase-7,caspase-3 expression levels,and enhanced Bcl-2 expression level.CONCLUSION Costunolide has latent neuroprotective activi⁃ties by the regulation of apoptosis via the mitochondrial apoptosis pathway.展开更多
OBJECTIVE TO investigate the neural protection of dehydrocostus lactone(DHL)against neuronal injury induced by oxygen and glucose deprivation/reperfusion(OGD/R)in differentiated PC12 cells.METHODS We used a cellular m...OBJECTIVE TO investigate the neural protection of dehydrocostus lactone(DHL)against neuronal injury induced by oxygen and glucose deprivation/reperfusion(OGD/R)in differentiated PC12 cells.METHODS We used a cellular model of 2 h of OGD and 24 h of reperfusion to mimic cerebral ischemia-reperfusion injury.Cell viability was used to reflect the degree of OGD/R-induced injury.Cells were treated with DHL during the reperfusion phase.Cell Counting Kit(CCK-8)and LDH assays were performed to determine the optimal dose of DHL and cell viability.Flow cytometry analysis and Monodansylcadaverine(MDC)staining were then conducted to detect apoptosis rate and autophagosome formation after OGD/R in PC12 cells.Immunofluorescence and Western blotting analyses were used to detect the expres⁃sion of proteins associated with autophagy and apoptosis.RESULTS OGD/R significantly decreased cell viability and increased apoptosis rate.The expression levels of autophagy-related proteins,namely,LC3 and Beclin-1,and apoptosisrelated proteins,namely,Bax and caspase-3 increased,but that of the anti-apoptosis Bcl-2 protein decreased.However,DHL attenuated OGD/R-induced neuronal injury through inhibition of apoptosis and autophagy properties by modulating au⁃tophagy-associated proteins(LC3 and Beclin-1)and apoptosis-modulating proteins(caspase-3 and Bcl-2/Bax).CONCLU⁃SION Our data provide an evidence for the neuroprotective effect of DHL against ischemic neuronal injury.Hence,DHL could be a promising candidate for treatment of ischemic stroke.展开更多
基金National Natural Science Foundation of China(8166070081260679)Ningxia College FirstClass Discipline Construction Project(Chinese Medicine)Funded Project(NXYLXK2017A06)
文摘OBJECTIVE To investigate the protective effects and mechanisms of costunolide against mousebrain slice injury induced by oxygen-glucose deprivation/reoxygenation(OGD/R).METHODS Mouse brain slice injury was induced by OGD/R in vitro,and the degree ofinjury was evaluated by measuring the release of lactate dehydrogenase(LDH)and 2,3,5-triphenyltetrazolium chloride(TTC)staining.Western blotting was used to analyze the expression of Bax,Bcl-2,Cyt-c,caspase-9,caspase-7 and caspase-3.RESULTS Compared with OGD/R,1,5,and 10μmol·L^-1 costu⁃nolide decreased the LDH levels,increased the TTC staining intensity,inhibited Bax,Cyt-c,caspase-9,caspase-7,caspase-3 expression levels,and enhanced Bcl-2 expression level.CONCLUSION Costunolide has latent neuroprotective activi⁃ties by the regulation of apoptosis via the mitochondrial apoptosis pathway.
基金National Natural Science Foundation of China(8166070081260679)Ningxia Col ege First-Class Discipline Construction Project(Chinese Medicine)Funded Project(NXYLXK2017A06)
文摘OBJECTIVE TO investigate the neural protection of dehydrocostus lactone(DHL)against neuronal injury induced by oxygen and glucose deprivation/reperfusion(OGD/R)in differentiated PC12 cells.METHODS We used a cellular model of 2 h of OGD and 24 h of reperfusion to mimic cerebral ischemia-reperfusion injury.Cell viability was used to reflect the degree of OGD/R-induced injury.Cells were treated with DHL during the reperfusion phase.Cell Counting Kit(CCK-8)and LDH assays were performed to determine the optimal dose of DHL and cell viability.Flow cytometry analysis and Monodansylcadaverine(MDC)staining were then conducted to detect apoptosis rate and autophagosome formation after OGD/R in PC12 cells.Immunofluorescence and Western blotting analyses were used to detect the expres⁃sion of proteins associated with autophagy and apoptosis.RESULTS OGD/R significantly decreased cell viability and increased apoptosis rate.The expression levels of autophagy-related proteins,namely,LC3 and Beclin-1,and apoptosisrelated proteins,namely,Bax and caspase-3 increased,but that of the anti-apoptosis Bcl-2 protein decreased.However,DHL attenuated OGD/R-induced neuronal injury through inhibition of apoptosis and autophagy properties by modulating au⁃tophagy-associated proteins(LC3 and Beclin-1)and apoptosis-modulating proteins(caspase-3 and Bcl-2/Bax).CONCLU⁃SION Our data provide an evidence for the neuroprotective effect of DHL against ischemic neuronal injury.Hence,DHL could be a promising candidate for treatment of ischemic stroke.
