七氟醚预处理对心肌缺血再灌注损伤心肌保护作用的研究进展
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摘要
缺血再灌注损伤(IRI)是指部分患者或动物缺血后再灌注,不仅没有使组织器官功能恢复,反而使缺血所致的功能和代谢障碍及结构破坏进一步加剧。它在心外科的手术中经常发生,严重影响手术的成功率及预后。用七氟醚预处理减轻心肌IRI的损伤是近年来的研究热点,本文就其机制进行综述。
心肌IRI的机制主要为：①再灌注时活性氧(ROS)生成增多。ROS使细胞膜脂质过氧化增强,通透性增高,Ca2+大量内流,引起细胞内Ca2+超载,并使得线粒体功能受损；引起DNA断裂和染色体畸变；引起蛋白质变性和酶活性降低；诱导炎症介质产生。②细胞内钙超载。钙超载使得线粒体功能障碍,使ATP生成减少；激活Ca2+依赖性的多种降解酶,引起细胞结构及核酸损害；促进ROS生成；破坏细胞骨架。③再灌注时产生的炎症介质及趋化因子诱导白细胞聚集、粘附,导致机械阻塞和炎症反应失控,引起细胞损伤。④细胞凋亡。七氟醚预处理可以改善心肌的收缩力,减少心率失常,改善心功能和心肌灌注,减少心肌梗死面积,减轻心肌IRI。其主要机制为：①ROS预适应。七氟醚预处理后产生少量ROS,可以作为一种信号分子,通过促进NO合成、增加蛋白激酶C(PKC)的激活、促进谷胱甘肽过氧化物酶(GPx)、过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的生成以及增加谷胱甘肽转移酶(GST)的表达来发挥保护作用。②促进线粒体ATP敏感性钾通道(mito-KATP通道)的开放。Mito-KATP通道开放后,可以减少ROS生成,稳定线粒体跨膜电位(△ψm),调节线粒体基质的容积,降低线粒体钙超载,抑制线粒体通透性转换孔(MPTP)的开放,从而减轻再灌注时线粒体的损伤,保护心肌。③调节凋亡基因的表达。七氟醚预处理可上调Bcl-2基因的表达,下调Bax的表达,使Bcl-2/Bax比例升高；减少Caspase家族蛋白酶中Caspase-3和Caspase-9的活化；抑制Fas、 FasL蛋白的表达,从而减少细胞凋亡。④七氟醚预处理能够抑制中性粒细胞等炎症细胞的激活,并减少IL、 TNF-α等的表达,改变抗炎因子的平衡,参与心肌保护。还能降低核因子-κB (NF-κB)的活性。⑤激活PI3K/Akt信号通路。此通路激活后,可以抑制NF-κB的活性、减少MPTP的开放、促进NO的合成、上调Bcl-2/Bax的比例来发挥心肌保护作用。
最后,以本综述内容及相关文献为背景,设计了下一步的研究方向及方法。
Ischemia-repurfusion injury(IRI) is ischemia injury of tissue and organs after restoration of blood flow after transient ischemia and caused further reversible or irreversible cell damage.It is an important factor to affect the success and prognosis of cardiac surgery.The sevoflurane preconditioning of cardium is a hotpot in recent years for it will reduce myocardial IRI,but the exact pathogenesis is still unclear.Here we summarize and analyze it.
The mechanism of myocardial IRI:①The overproduction of ROS.ROS peroxidates membrane lipid and increases its permeability which enlarges the inflow of Ca+,all these causing intracellular calcium overload and the mitochondria dysfunction;ROS causes destruction of DNA;ROS causes inhibition of protein and enzymes;ROS induces the induction of inflammatory factors.②ntracellular calcium overload. Intracellular calcium overload induces the production of ATP,promotes mitochondria dysfunction and actives a variety of Ca2+dependent degradative enzymes.which finally cause cell damage.Intracellular calcium overload and the generation of ROS are in reciprocal causation,they play an impeotant role in myocardial IRI.③The mediators of inflammation generated in repurfusion induce aggregation and adhesion of leukocytes,resulting in mechanical obstruction and uncontrolled inflammatory reaction.④Apoptosis.
The sevoflurane preconditioning can improve myocardial contractility, reduce arrhythmia, improve cardiac function and myocardial perfusion, reduce infarct size. Its mechanisms are as follows.⑤The role of ROS.The small amount of ROS generated by sevoflurane preconditioning promote the synthesis of NO,increase the activation of PKC, and promote the generation of glutathione peroxidase, CAT and SOD,and increase the expression of GST.It plays a protective effect.②Promote mito-K.ATP channels opening.Mito-KATP channels'open can reduce the generation of ROS.stable mitochondrial transmembrane potentinal,adjust the volume of mitochondrial matrix.reduce mitochondrial calcium overload and suppress the opening of MPTP,thereby reducing the mitochondrial injury in reperfusion.③ Regulate the expression of apoptotic gene.Sevoflurane preconditioning can upregulate the expression of Bcl-2gene while lowering the expression of Bax gene.supress the activation of caspase family,inhibite the expression of Fas and FasL,thereby reducing apoptosis.④The sevoflurane preconditioning can inhibit the activation of neutrophils and other inflammatory cells,and reduce the expression of IL,TNF-a,et al.⑥Reduced NF-κB's activity.⑦Activation of PI3K/Akt signaling pathway.The activation of PI3K/Akt pathway can inhibite the activation of NF-κB, reduce the opening of MPTP, promote the synthesis of NO and increase the ratio of Bcl-2/Bax,thereby to play a positive role in myocardial protection.
The commonly used animal model in myocardial IRI are rats:in vivo models and in vitro models.Here we introduce the most used methods to making these two models.
Finally,with the review and relevant literature as the background,we design the research directions and methods in future.
心肌IRI的机制主要为：①再灌注时活性氧(ROS)生成增多。ROS使细胞膜脂质过氧化增强,通透性增高,Ca2+大量内流,引起细胞内Ca2+超载,并使得线粒体功能受损；引起DNA断裂和染色体畸变；引起蛋白质变性和酶活性降低；诱导炎症介质产生。②细胞内钙超载。钙超载使得线粒体功能障碍,使ATP生成减少；激活Ca2+依赖性的多种降解酶,引起细胞结构及核酸损害；促进ROS生成；破坏细胞骨架。③再灌注时产生的炎症介质及趋化因子诱导白细胞聚集、粘附,导致机械阻塞和炎症反应失控,引起细胞损伤。④细胞凋亡。七氟醚预处理可以改善心肌的收缩力,减少心率失常,改善心功能和心肌灌注,减少心肌梗死面积,减轻心肌IRI。其主要机制为：①ROS预适应。七氟醚预处理后产生少量ROS,可以作为一种信号分子,通过促进NO合成、增加蛋白激酶C(PKC)的激活、促进谷胱甘肽过氧化物酶(GPx)、过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的生成以及增加谷胱甘肽转移酶(GST)的表达来发挥保护作用。②促进线粒体ATP敏感性钾通道(mito-KATP通道)的开放。Mito-KATP通道开放后,可以减少ROS生成,稳定线粒体跨膜电位(△ψm),调节线粒体基质的容积,降低线粒体钙超载,抑制线粒体通透性转换孔(MPTP)的开放,从而减轻再灌注时线粒体的损伤,保护心肌。③调节凋亡基因的表达。七氟醚预处理可上调Bcl-2基因的表达,下调Bax的表达,使Bcl-2/Bax比例升高；减少Caspase家族蛋白酶中Caspase-3和Caspase-9的活化；抑制Fas、 FasL蛋白的表达,从而减少细胞凋亡。④七氟醚预处理能够抑制中性粒细胞等炎症细胞的激活,并减少IL、 TNF-α等的表达,改变抗炎因子的平衡,参与心肌保护。还能降低核因子-κB (NF-κB)的活性。⑤激活PI3K/Akt信号通路。此通路激活后,可以抑制NF-κB的活性、减少MPTP的开放、促进NO的合成、上调Bcl-2/Bax的比例来发挥心肌保护作用。
最后,以本综述内容及相关文献为背景,设计了下一步的研究方向及方法。
Ischemia-repurfusion injury(IRI) is ischemia injury of tissue and organs after restoration of blood flow after transient ischemia and caused further reversible or irreversible cell damage.It is an important factor to affect the success and prognosis of cardiac surgery.The sevoflurane preconditioning of cardium is a hotpot in recent years for it will reduce myocardial IRI,but the exact pathogenesis is still unclear.Here we summarize and analyze it.
The mechanism of myocardial IRI:①The overproduction of ROS.ROS peroxidates membrane lipid and increases its permeability which enlarges the inflow of Ca+,all these causing intracellular calcium overload and the mitochondria dysfunction;ROS causes destruction of DNA;ROS causes inhibition of protein and enzymes;ROS induces the induction of inflammatory factors.②ntracellular calcium overload. Intracellular calcium overload induces the production of ATP,promotes mitochondria dysfunction and actives a variety of Ca2+dependent degradative enzymes.which finally cause cell damage.Intracellular calcium overload and the generation of ROS are in reciprocal causation,they play an impeotant role in myocardial IRI.③The mediators of inflammation generated in repurfusion induce aggregation and adhesion of leukocytes,resulting in mechanical obstruction and uncontrolled inflammatory reaction.④Apoptosis.
The sevoflurane preconditioning can improve myocardial contractility, reduce arrhythmia, improve cardiac function and myocardial perfusion, reduce infarct size. Its mechanisms are as follows.⑤The role of ROS.The small amount of ROS generated by sevoflurane preconditioning promote the synthesis of NO,increase the activation of PKC, and promote the generation of glutathione peroxidase, CAT and SOD,and increase the expression of GST.It plays a protective effect.②Promote mito-K.ATP channels opening.Mito-KATP channels'open can reduce the generation of ROS.stable mitochondrial transmembrane potentinal,adjust the volume of mitochondrial matrix.reduce mitochondrial calcium overload and suppress the opening of MPTP,thereby reducing the mitochondrial injury in reperfusion.③ Regulate the expression of apoptotic gene.Sevoflurane preconditioning can upregulate the expression of Bcl-2gene while lowering the expression of Bax gene.supress the activation of caspase family,inhibite the expression of Fas and FasL,thereby reducing apoptosis.④The sevoflurane preconditioning can inhibit the activation of neutrophils and other inflammatory cells,and reduce the expression of IL,TNF-a,et al.⑥Reduced NF-κB's activity.⑦Activation of PI3K/Akt signaling pathway.The activation of PI3K/Akt pathway can inhibite the activation of NF-κB, reduce the opening of MPTP, promote the synthesis of NO and increase the ratio of Bcl-2/Bax,thereby to play a positive role in myocardial protection.
The commonly used animal model in myocardial IRI are rats:in vivo models and in vitro models.Here we introduce the most used methods to making these two models.
Finally,with the review and relevant literature as the background,we design the research directions and methods in future.
引文
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