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目的:探讨脂氧素A4(lipoxinA4,LXA4)在大鼠心肌细胞缺氧/复氧损伤中的保护作用及可能机制。方法:将细胞随机分为5组,每组6孔,分别为对照组(con组)、缺氧/复氧组(H/R组)、LXA4预处理的缺氧/复氧组(LXA4+H/R组)、HO-1抑制剂锌原卟啉(ZnPP)预处理的缺氧/复氧组(ZnPP+H/R组)、LXA4+ZnPP预处理的缺氧/复氧组(LXA4+ZnPP+H/R组)。观察细胞形态改变,测定细胞上清液中乳酸脱氢酶(lactate dehydrogenase,LDH)、肌酸激酶(creatine kinase,CK)水平以反映细胞损伤,并检测心肌细胞HO-1活性和HO-1的mRNA表达水平。结果:与H/R组比较,LXA4+H/R组细胞形态较规整,LDH、CK水平较低,而HO-1的活性及mRNA表达水平明显增加;LXA4+ZnPP+H/R组终止了LXA4对缺氧/复氧细胞的保护作用,细胞形态明显改变,细胞死亡较多,HO-1的活性及mRNA水平受到抑制。结论:LXA4预处理可诱导大鼠心肌细胞HO-1高表达,具有抗心肌细胞缺氧/复氧损伤的保护作用。
Objective: To investigate the protective effect of lipoxin A4 (LXA4) on hypoxia / reoxygenation injury in rat cardiomyocytes and its possible mechanism. Methods: The cells were randomly divided into 5 groups with 6 wells in each group, which were control group (con group), hypoxia / reoxygenation group (H / R group), LXA4 pretreatment hypoxia / reoxygenation group H / R group, ZnPP + H / R group, LXA4 + ZnPP preconditioning hypoxia / reoxygenation group (LXA4 + ZnPP + H / R group). The morphological changes of the cells were observed. The level of lactate dehydrogenase (LDH) and creatine kinase (CK) in the supernatant of the cells was measured to reflect the cell injury and to detect the activity of HO-1 and HO-1 mRNA expression level. Results: Compared with H / R group, the cell morphology of LXA4 + H / R group was more regular, the level of LDH and CK was lower, and the activity and mRNA expression of HO-1 were significantly increased; LXA4 + ZnPP + H / R group was terminated The protective effect of LXA4 on hypoxia / reoxygenation cells significantly changed the cell morphology and cell death, and the activity and mRNA level of HO-1 were inhibited. CONCLUSION: LXA4 preconditioning can induce high HO-1 expression in rat cardiomyocytes and protect against cardiomyocyte hypoxia / reoxygenation injury.