摘要
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 roles of lipoxin A4（LXA4） in attenuating myocardial hypoxia/reoxygenation（H/R） lesion and the possible mechanisms.Methods：The cells were randomly divided into five groups：control group,H/R group,LXA4 ＋ H/R group,ZnPP ＋ H/R group,LXA4 ＋ ZnPP ＋ H/R group.Pathological changes of cells was observed.The levels of LDH and CK in cellular supernatants were measured,and activity of HO-1 was measured.HO-1 mRNA expression was analyzed by RT-PCR.Results：Pretreatment of the cells undergoing hypoxia/reoxygenation lesion with LXA4 significantly reduced the LDH and CK levels of cells,protected cells from necrosis,and increased the HO-1 activity and the HO-1 mRNA expression as compared with those in the cells without LXA4 pretreatment.However,HO-1 inhibition by ZnPP abolished the protective role of LXA4 on the cells undergoing hypoxia/reoxygenation lesion.Conclusion：LXA4 can induce HO-1 overexpression which provide the protective role on myocardiac cells undergoing hypoxia/reoxygenation lesion.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2012年第4期458-462,共5页
Journal of Nanjing Medical University(Natural Sciences)
基金
国家自然科学基金资助(30871180)
