The possible transduction mechanisms involved in ischemic preconditioning were reviewed briefly,Nitric oxide from the endothelium (and possible also from cardiac myocytes)by the action of bradykinin stimulates soluble...The possible transduction mechanisms involved in ischemic preconditioning were reviewed briefly,Nitric oxide from the endothelium (and possible also from cardiac myocytes)by the action of bradykinin stimulates soluble guanylate cyclase in the cytosol resulting in an elevation of cGMP. This may inhibit the inward slow Ca2+ current by stimulating a cGMP-dependent PDE’ to decrease cGMP levels. The translocation of PKC to membrane by DAG formation resulting from the activation of PLC phosphorylates a membrane protein that may link to the ATP-dependent K+ channel. The pathway may be stimulated by the adenosine A, receptors,muscarine acetylcholine M1, M3 and M5 receptors and a-adrenoceptors as well. The possible approaches for pharmacological exploitation are to minic the endogenous myocardial protective mediators by more selective and long acting analogues, to enhence these mediators by modulating their release, transport and uptake, to modulate myocardial cAMP and cGMP levels,to target guanine-nucleotide binding regulatory proteins and etc.展开更多
在一种仿G蛋白耦合型信号转导的人工超分子系统中引入类似光化学开关的偶氮苯化合物,用来模拟跨膜受体。合成了三种人工受体的中间体4,4′-二氨基酸酯偶氮苯:Azo-PheOMe(6a)、Azo-ValOMe(6b)、Azo-GluOMe(6c)、Azo-SerOMe(6d)、Azo-ThrO...在一种仿G蛋白耦合型信号转导的人工超分子系统中引入类似光化学开关的偶氮苯化合物,用来模拟跨膜受体。合成了三种人工受体的中间体4,4′-二氨基酸酯偶氮苯:Azo-PheOMe(6a)、Azo-ValOMe(6b)、Azo-GluOMe(6c)、Azo-SerOMe(6d)、Azo-ThrOMe(6e)及Azo-PheOEt(6a′)、Azo-ValOEt(6b′)、Azo-GluOEt(6c′)、Azo-SerOEt(6d′)、Azo-ThrOEt(6e′)并采用1 H NMR谱、紫外可见光谱、元素分析以及红外光谱进行了表征。以6a为主要研究对象,分别在两种不同介质(三氯甲烷和甲醇)中,在365nm的紫外光下进行照射不同时间后,发现6a从反式变为顺式,再置于427nm的可见光下,又从顺式变回反式,所需时间不同,并且其最大吸收波长发生了红移,为模拟信号转导体系中受体之构象的变化作初步研究。展开更多
It is vital process for oxidative stress to respond exterior and interior environment, to regulate stress signal transduction. Since tension surgical trauma not only intensifies the stress by generating reactive oxyge...It is vital process for oxidative stress to respond exterior and interior environment, to regulate stress signal transduction. Since tension surgical trauma not only intensifies the stress by generating reactive oxygen species (ROS) endlessly,whether produced endogenously as a consequence of normal cell functions or derived from external sources,but also weakens the biological protective system against ROS attack, these conditions lead to injury to the normal biological oxide-reductive balance, resulting in a condition termed oxidative stress. In a state of oxidative stress, ROS can react with the ingredients of cell such as cellular membrane、protein、nucleic acid to evoke oxidative damage. The result is that oxidative stress induces apoptosis. In this review, we discuss the various stress signal transduction pathways known to be activated in response to oxidative stress, and their effects in influencing cell apoptosis. These pathways constitute important ways for therapeutic interventions aimed at inhibiting oxidative damage or lessening its consequences.展开更多
文摘The possible transduction mechanisms involved in ischemic preconditioning were reviewed briefly,Nitric oxide from the endothelium (and possible also from cardiac myocytes)by the action of bradykinin stimulates soluble guanylate cyclase in the cytosol resulting in an elevation of cGMP. This may inhibit the inward slow Ca2+ current by stimulating a cGMP-dependent PDE’ to decrease cGMP levels. The translocation of PKC to membrane by DAG formation resulting from the activation of PLC phosphorylates a membrane protein that may link to the ATP-dependent K+ channel. The pathway may be stimulated by the adenosine A, receptors,muscarine acetylcholine M1, M3 and M5 receptors and a-adrenoceptors as well. The possible approaches for pharmacological exploitation are to minic the endogenous myocardial protective mediators by more selective and long acting analogues, to enhence these mediators by modulating their release, transport and uptake, to modulate myocardial cAMP and cGMP levels,to target guanine-nucleotide binding regulatory proteins and etc.
文摘在一种仿G蛋白耦合型信号转导的人工超分子系统中引入类似光化学开关的偶氮苯化合物,用来模拟跨膜受体。合成了三种人工受体的中间体4,4′-二氨基酸酯偶氮苯:Azo-PheOMe(6a)、Azo-ValOMe(6b)、Azo-GluOMe(6c)、Azo-SerOMe(6d)、Azo-ThrOMe(6e)及Azo-PheOEt(6a′)、Azo-ValOEt(6b′)、Azo-GluOEt(6c′)、Azo-SerOEt(6d′)、Azo-ThrOEt(6e′)并采用1 H NMR谱、紫外可见光谱、元素分析以及红外光谱进行了表征。以6a为主要研究对象,分别在两种不同介质(三氯甲烷和甲醇)中,在365nm的紫外光下进行照射不同时间后,发现6a从反式变为顺式,再置于427nm的可见光下,又从顺式变回反式,所需时间不同,并且其最大吸收波长发生了红移,为模拟信号转导体系中受体之构象的变化作初步研究。
文摘It is vital process for oxidative stress to respond exterior and interior environment, to regulate stress signal transduction. Since tension surgical trauma not only intensifies the stress by generating reactive oxygen species (ROS) endlessly,whether produced endogenously as a consequence of normal cell functions or derived from external sources,but also weakens the biological protective system against ROS attack, these conditions lead to injury to the normal biological oxide-reductive balance, resulting in a condition termed oxidative stress. In a state of oxidative stress, ROS can react with the ingredients of cell such as cellular membrane、protein、nucleic acid to evoke oxidative damage. The result is that oxidative stress induces apoptosis. In this review, we discuss the various stress signal transduction pathways known to be activated in response to oxidative stress, and their effects in influencing cell apoptosis. These pathways constitute important ways for therapeutic interventions aimed at inhibiting oxidative damage or lessening its consequences.
