Department of Anesthesiology, Beijing Anzhen Hospital Capital Medical University, Beijing, 100029, China.
Department of Anesthesiology, Peking University International Hospital, Beijing, 102206, China.
J Nanosci Nanotechnol. 2021 Feb 1;21(2):1397-1402. doi: 10.1166/jnn.2021.18643.
The myocardial I/R damage is very complicated. Apoptosis is considered to its a critical mechanism. During the cardiac muscle I/R process, oxygen-free radicals play a pivotal role. Arrhythmias, as well as enlargement of the area of myocardial infarction after cardiac muscle I/R process, are caused by adequate blast generated O ion free radicals. During the ischemia-reperfusion process, a large amount of O ion free radicals destroyed the cell structure, and it undergoes lipid peroxidation with unsaturated fatty acids that contain a large number of phospholipids in the cell membrane, causing membrane proteins such as ion channels and enzymes on the cell membrane. The activity of cell is reduced, which affects the function of cell membrane and organelle membrane, destroys its integrity and reduces fluidity.We observed the effects of cerium dioxide nanoparticles on glutathione peroxidase as well as superoxide dismutase, also propionate in myocardial tissue of I/R injury in the mouse. Its effects of malondialdehyde and apoptosis were explored to see its protective effect and to provide more preventive measures for ischemia-reperfusion injury.
心肌缺血再灌注损伤非常复杂。细胞凋亡被认为是其关键机制之一。在心肌缺血再灌注过程中，氧自由基起着关键作用。心律失常以及心肌缺血再灌注后心肌梗死面积的扩大，都是由充分产生的 O 离子自由基引起的。在缺血再灌注过程中，大量的 O 离子自由基破坏细胞结构，发生脂质过氧化，细胞膜中含有大量的不饱和脂肪酸磷脂，导致细胞膜上的离子通道和酶等膜蛋白的活性降低，从而影响细胞膜和细胞器膜的功能，破坏其完整性，降低流动性。我们观察了二氧化铈纳米粒子对谷胱甘肽过氧化物酶和超氧化物歧化酶以及丙二醛和细胞凋亡的影响，探讨了其对心肌组织缺血再灌注损伤的保护作用，为缺血再灌注损伤提供了更多的预防措施。
