LXA4诱导HO-1高表达对心肌细胞缺氧/复氧损伤的保护作用
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国家自然科学基金资助(30871180)


Protective role of overexpression of HO-1 induced by lipoxin A4 on hypoxia/reoxygenation lesion of myocardiac cells
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    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-

    Abstract:

    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.

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唐艳荣,吴升华. LXA4诱导HO-1高表达对心肌细胞缺氧/复氧损伤的保护作用[J].南京医科大学学报(自然科学版),2012,(4):458-462

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  • 收稿日期:2011-12-11
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