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缺血心肌早期恢复血供,这对于防止细胞坏死和加快细胞功能的恢复是至关重要的。然而,研究表明,缺血心肌在再灌流时会产生自由基,造成更严重的损伤。缺血-再灌流导致自由基生成,这一过程涉及多种细胞、细胞器和酶,包括中性粒细胞、黄嘌呤氧化酶、环氧合酶、脂氧合酶、儿茶酚胺的自动氧化作用、线粒体和肌浆网。氧自由基氧分子单价还原(每次加上一个电子),依次产生了超氧阴离子自由基(O(?))、过氧化氢(H_2O_2)、羟自由基(OH·)和水。O(?)和OH·因为都具有未配对电子,所以称为超氧阴离子自由基和羟自由基。H_2O_2产生OH·的反应可被来自铁蛋白、肌红蛋白和血红蛋白的铁催化(图1)。
Early recovery of ischemic myocardium blood supply, which is essential for the prevention of cell necrosis and speed up the recovery of cellular function. However, studies have shown that ischemic myocardium produces free radicals during reperfusion, resulting in more severe damage. Ischemia-reperfusion results in the production of free radicals, a process involving the autoxidation of many cells, organelles and enzymes including neutrophils, xanthine oxidase, cyclooxygenase, lipoxygenase, catecholamines, mitochondria And sarcoplasmic reticulum. Oxygen free radical oxygen molecules monovalent reduction (with one electron at a time), followed by the generation of superoxide anion radicals (O (?)), Hydrogen peroxide (H 2 O 2), hydroxyl radicals (OH ·) and water. O (?) And OH · because they have unpaired electrons, so called superoxide anion radicals and hydroxyl radicals. The reaction of H 2 O 2 to produce OH · can be catalyzed by iron from ferritin, myoglobin and hemoglobin (Figure 1).