It is now clear that both endogenous and exogenous sources of nitric oxide(NO) exert important modulatory effects on cardiac mitochondrial function.There is also growing evidence that NO can be produced within the mit...It is now clear that both endogenous and exogenous sources of nitric oxide(NO) exert important modulatory effects on cardiac mitochondrial function.There is also growing evidence that NO can be produced within the mitochondria themselves.NO can influence respiratory activity,both through direct effects on the respiratory chain or indirectly via modulation of mitochondrial calcium accumulation.At pathological concentrations,NO causes irreversible alterations in respiratory function and also interacts with reactive oxygen species(ROS) to form reactive nitrogen species(RNS),which may further impair mitochondrial respiration and even lead to open the mitochondrial permeability transition pore and induce cell death.Diabetes,aging,myocardial ischemia,and heart failure are all associated with altered ROS generation,which can alter the delicate regulatory balance of effects of NO in the mitochondria.展开更多
目的研究人血白蛋白治疗对局灶性脑缺血再灌注小鼠脑组织Toll样受体4(TLR4)和骨髓分化因子88(MyD88)mRNA表达的影响。方法健康雄性成年昆明小鼠54只,随机分为假手术组(14只)、生理盐水组(20只)和白蛋白组(20只),每组又均分为再灌后6、24...目的研究人血白蛋白治疗对局灶性脑缺血再灌注小鼠脑组织Toll样受体4(TLR4)和骨髓分化因子88(MyD88)mRNA表达的影响。方法健康雄性成年昆明小鼠54只,随机分为假手术组(14只)、生理盐水组(20只)和白蛋白组(20只),每组又均分为再灌后6、24 h 2个时间点。采用左侧大脑中动脉线栓法制备小鼠局灶性脑缺血再灌注模型,RT-PCR法检测左侧脑组织TLR4、MyD88 mRNA的表达水平,并进行神经功能缺损评分。结果生理盐水组和白蛋白组脑缺血再灌注后6、24 h TLR4、MyD88 mRNA表达水平明显高于假手术组,且24 h表达水平升高更明显(P<0.05);但白蛋白组6、24 h TLR4、MyD88 mRNA表达量明显低于生理盐水组(P<0.05);24 h白蛋白组小鼠的神经功能缺损评分与生理盐水组比较有明显改善(P<0.05);24 h TLR4、MyD88 mRNA表达水平与神经功能缺损评分呈正相关(r=0.92,r=0.85,P<0.05)。结论白蛋白治疗可以下调脑缺血早期脑组织高表达的TLR4、MyD88 mRNA的水平,改善脑缺血后小鼠神经功能缺损。展开更多
文摘It is now clear that both endogenous and exogenous sources of nitric oxide(NO) exert important modulatory effects on cardiac mitochondrial function.There is also growing evidence that NO can be produced within the mitochondria themselves.NO can influence respiratory activity,both through direct effects on the respiratory chain or indirectly via modulation of mitochondrial calcium accumulation.At pathological concentrations,NO causes irreversible alterations in respiratory function and also interacts with reactive oxygen species(ROS) to form reactive nitrogen species(RNS),which may further impair mitochondrial respiration and even lead to open the mitochondrial permeability transition pore and induce cell death.Diabetes,aging,myocardial ischemia,and heart failure are all associated with altered ROS generation,which can alter the delicate regulatory balance of effects of NO in the mitochondria.
文摘目的研究人血白蛋白治疗对局灶性脑缺血再灌注小鼠脑组织Toll样受体4(TLR4)和骨髓分化因子88(MyD88)mRNA表达的影响。方法健康雄性成年昆明小鼠54只,随机分为假手术组(14只)、生理盐水组(20只)和白蛋白组(20只),每组又均分为再灌后6、24 h 2个时间点。采用左侧大脑中动脉线栓法制备小鼠局灶性脑缺血再灌注模型,RT-PCR法检测左侧脑组织TLR4、MyD88 mRNA的表达水平,并进行神经功能缺损评分。结果生理盐水组和白蛋白组脑缺血再灌注后6、24 h TLR4、MyD88 mRNA表达水平明显高于假手术组,且24 h表达水平升高更明显(P<0.05);但白蛋白组6、24 h TLR4、MyD88 mRNA表达量明显低于生理盐水组(P<0.05);24 h白蛋白组小鼠的神经功能缺损评分与生理盐水组比较有明显改善(P<0.05);24 h TLR4、MyD88 mRNA表达水平与神经功能缺损评分呈正相关(r=0.92,r=0.85,P<0.05)。结论白蛋白治疗可以下调脑缺血早期脑组织高表达的TLR4、MyD88 mRNA的水平,改善脑缺血后小鼠神经功能缺损。
