以硝酸铜、硝酸锌、硝酸铝为原料,碳酸钠为沉淀剂,采用共沉淀法制备CuZnAl催化剂,并通过浸渍法引入钾元素制备钾改性CuZnAl催化剂。利用XRD、XPS对该催化剂进行表征。结果表明,钾元素可以成功引入到CuZnAl催化剂中,活性中心Cu以2种形态...以硝酸铜、硝酸锌、硝酸铝为原料,碳酸钠为沉淀剂,采用共沉淀法制备CuZnAl催化剂,并通过浸渍法引入钾元素制备钾改性CuZnAl催化剂。利用XRD、XPS对该催化剂进行表征。结果表明,钾元素可以成功引入到CuZnAl催化剂中,活性中心Cu以2种形态表现。将该催化剂用于仲丁醇(SBA)脱氢生成甲乙酮(MEK)的反应中,在常压、仲丁醇流速为0.1 m L/min、温度为220~250℃的条件下,仲丁醇的转化率为84%,甲乙酮的选择性为95%。运用matlab分析软件并采用双曲线及幂函数动力学模型对反应过程进行最小二乘法参数拟合,通过双曲线动力学模型得出表观活化能为45.51 kJ/mol;通过幂函数动力学模型得出该反应的反应级数为1.37,表观活化能为58.36 kJ/mol。展开更多
OBJECTIVE Mu-Xiang-You-Fang(MXYF)is a classic prescription of Hui medicine,composed of five herbs,which has been used to treat ischemic stroke for many years.However,the potential pharmacological mecha⁃nisms of MXYF r...OBJECTIVE Mu-Xiang-You-Fang(MXYF)is a classic prescription of Hui medicine,composed of five herbs,which has been used to treat ischemic stroke for many years.However,the potential pharmacological mecha⁃nisms of MXYF remain unclear.The present research is to investigate the neuroprotective effect of MXYF and its role in modulating autophagy via AMPK/mTOR signaling pathway in the PC12 oxygen-glucose deprivation and reperfusion(OGD/R)injury model.METHODS MXYF was extracted by supercritical CO2 fluid extraction apparatus.PC12 OGD/R injury model was established by oxygen-glucose deprivation for 2 h and reperfusion for 24 h.The effects of MXYF on the viability and cytotoxicity of PC12 cells were determined through cell counting kit(CCK-8)assay.Colorimetric method was performed to determine the LDH leakage rate.The calcium concentration was determined by chemical fluorescence method and the mitochondrial membrane potential was determined through flow cytometry.Monodansylcadaverine(MDC)staining was conducted to detect autophagosome formation.The expression of LC3,Beclin1,p62,p-AMPK,ULK1,p-mTOR and p-p70s6k proteins were determined by immunofluorescence and Western blotting analyses.RESULTS MXYF(1,2 and 4 mg·L^-1)could significantly increase the cell viability and mitochondrial membrane potential,while decreased the release of lactate dehydrogenase(LDH)and calcium concentration in PC12 cells.Mechanistic studies showed that MXYF reduced the LC3-II/LC3-I ratio and inhibited the expression of beclin1,p-AMPK and ULK1.In comparison,the expres⁃sion of p-mTOR,p-p70s6k and p62 were significantly enhanced.CONCLUSION MXYF inhibits autophagy after OGD/Rinduced PC12 cell injury through AMPK-mTOR pathway,thus MXYF might have therapeutic potential for treating the ischemic stroke.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
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
文摘以硝酸铜、硝酸锌、硝酸铝为原料,碳酸钠为沉淀剂,采用共沉淀法制备CuZnAl催化剂,并通过浸渍法引入钾元素制备钾改性CuZnAl催化剂。利用XRD、XPS对该催化剂进行表征。结果表明,钾元素可以成功引入到CuZnAl催化剂中,活性中心Cu以2种形态表现。将该催化剂用于仲丁醇(SBA)脱氢生成甲乙酮(MEK)的反应中,在常压、仲丁醇流速为0.1 m L/min、温度为220~250℃的条件下,仲丁醇的转化率为84%,甲乙酮的选择性为95%。运用matlab分析软件并采用双曲线及幂函数动力学模型对反应过程进行最小二乘法参数拟合,通过双曲线动力学模型得出表观活化能为45.51 kJ/mol;通过幂函数动力学模型得出该反应的反应级数为1.37,表观活化能为58.36 kJ/mol。
基金National Natural Science Foundation of China(8166070081260679)Ningxia College FirstClass Discipline Construction Project(Chinese Medicine)Funded Project(NXYLXK2017A06)
文摘OBJECTIVE Mu-Xiang-You-Fang(MXYF)is a classic prescription of Hui medicine,composed of five herbs,which has been used to treat ischemic stroke for many years.However,the potential pharmacological mecha⁃nisms of MXYF remain unclear.The present research is to investigate the neuroprotective effect of MXYF and its role in modulating autophagy via AMPK/mTOR signaling pathway in the PC12 oxygen-glucose deprivation and reperfusion(OGD/R)injury model.METHODS MXYF was extracted by supercritical CO2 fluid extraction apparatus.PC12 OGD/R injury model was established by oxygen-glucose deprivation for 2 h and reperfusion for 24 h.The effects of MXYF on the viability and cytotoxicity of PC12 cells were determined through cell counting kit(CCK-8)assay.Colorimetric method was performed to determine the LDH leakage rate.The calcium concentration was determined by chemical fluorescence method and the mitochondrial membrane potential was determined through flow cytometry.Monodansylcadaverine(MDC)staining was conducted to detect autophagosome formation.The expression of LC3,Beclin1,p62,p-AMPK,ULK1,p-mTOR and p-p70s6k proteins were determined by immunofluorescence and Western blotting analyses.RESULTS MXYF(1,2 and 4 mg·L^-1)could significantly increase the cell viability and mitochondrial membrane potential,while decreased the release of lactate dehydrogenase(LDH)and calcium concentration in PC12 cells.Mechanistic studies showed that MXYF reduced the LC3-II/LC3-I ratio and inhibited the expression of beclin1,p-AMPK and ULK1.In comparison,the expres⁃sion of p-mTOR,p-p70s6k and p62 were significantly enhanced.CONCLUSION MXYF inhibits autophagy after OGD/Rinduced PC12 cell injury through AMPK-mTOR pathway,thus MXYF might have therapeutic potential for treating the ischemic stroke.
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.
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.
