You Position: Home > Paper
Adenosine protects cardiomyocytes from hypoxia/reoxygenation injury
( views:272, downloads:14 )
- Author:
- No author available
- Journal Title:
- ACTA PHYSIOLOGICA SINICA
- Issue:
- 1
- DOI:
- 10.3321/j.issn:0371-0874.2003.01.011
- Key Word:
- 腺苷;缺氧/复氧损伤;心肌细胞
Abstract： 本研究旨在探讨腺苷(adenosine, ADO)对缺氧/复氧(hypoxia/reoxygenation, H/R)心肌细胞的保护作用及其分子机制.将原代培养的新生大鼠心肌细胞分成H/R对照组和ADO (1.0 μmol/L)保护组.用倒置相差显微镜观察心肌细胞的生长状态.检测两组培养基质乳酸脱氢酶(LDH)活性和心肌细胞Ca2+和丙二醛(MDA)浓度.用ELISA法检测肿瘤坏死因子(TNF-α)的表达, 并用凝胶电泳迁移率改变法(EMSA)测定核因子(NF-κB)结合活性.所得结果如下: (1) 心肌细胞H/R培养后皱缩、变圆, 伪足减少, ADO组心肌细胞的形态变化小于对照组; (2) ADO减少缺氧和复氧期间心肌细胞LDH的漏出(both P<0.01); (3)ADO降低缺氧和复氧期间心肌细胞内的Ca2+浓度(both P<0.01); (4) ADO降低缺氧和复氧期间心肌细胞MDA浓度(both P<0.01); (5) ADO抑制缺氧和复氧期间TNF-α的表达(both P<0.01); (6)ADO抑制缺氧和复氧期间心肌细胞NF-κB结合活性(both P<0.01).以上结果提示: (1) 外源性ADO可减轻心肌细胞的H/R损伤; (2) 外源性ADO抑制H/R期间心肌细胞TNF-α的表达; (3) 外源性ADO可能通过抑制心肌细胞NF-κB结合活性下调TNF-α的表达.
- [1]Li C,Browder W,Kao RL.Early activation of transcription factor NF-kappaB during ischemia in perfused rat heart.[J].1999,276(2 Pt.2).
- [2]Kao RL,Ha T,Li C,etc.Early activation of IKKbeta during in vivo myocardial ischemia.[J].2001,280(3).
- [3]Wagner D. R.,Combes A.,McTiernan C.,etc.Adenosine Inhibits Lipopolysaccharide-Induced Cardiac Expression of Tumor Necrosis Factor-\u00a0[J].1998.
- [4]ROBERT K. WINN,CHANDRA RAMAMOORTHY,NICHOLAS B. VEDDER,etc.Leukocyte-Endothelial Cell Interactions in Ischemia-Reperfusion Injury[J].1997,832(1).
- [5]Meldrum DR,Meng X,Banerjee A,etc.Adenosine reduces cardiac TNF-alpha production and human myocardial injury following ischemia-reperfusion.[J].1998,76(2).
- [6]Wada H,Kanda T,Fujiwara H,etc.Improved myocardial ischemia/reperfusion injury in mice lacking tumor necrosis factor-alpha.[J].2002,39(7).
- [7]Meldrum, D. R.,Cain, B. S.,Cleveland, J. C.,etc.Adenosine decreases post-isochaemic cardiac TNF-α production: anti-inflammatory implications for preconditioning and transplantation.[J].1997,92(4).
- [8]Liu L,Kao RL,Li C,etc.Adenosine prevents activation of transcription factor NF-kappa B and enhances activator protein-1 binding activity in ischemic rat heart.[J].2000,127(2).