[1]向飞,张琼,褚志刚,等.蛋白激酶C在腺苷A1受体调控缺氧心肌细胞线粒体通透性转换孔开放中的表达和作用[J].第三军医大学学报,2007,29(12):1135-1138.
 XIANG Fei,ZHANG Qiong,CHU Zhi-gang,et al.Role of protein kinase C in adenosine A1 receptor regulating opening of mitochondria permeability transition pore in hypoxic cardiac myocytes[J].J Third Mil Med Univ,2007,29(12):1135-1138.
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蛋白激酶C在腺苷A1受体调控缺氧心肌细胞线粒体通透性转换孔开放中的表达和作用(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
29卷
期数:
2007年第12期
页码:
1135-1138
栏目:
论著
出版日期:
2007-06-30

文章信息/Info

Title:
Role of protein kinase C in adenosine A1 receptor regulating opening of mitochondria permeability transition pore in hypoxic cardiac myocytes
作者:
向飞张琼褚志刚黄跃生
第三军医大学西南医院全军烧伤研究所,创伤、烧伤与复合伤国家重点实验室
Author(s):
XIANG Fei ZHANG Qiong CHU Zhi-gang HUANG Yue-sheng
State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Burns, Southwest Hospital, Third Military Medical University, Chongqing 400038, China
关键词:
心肌细胞缺氧腺苷A1受体蛋白激酶C
Keywords:
cardiac myocyte hypoxia adenosine A1 receptor protein kinase C
分类号:
R322.11;R329.25;R345.69
文献标志码:
A
摘要:
目的    观察腺苷A1受体的活化能否影响缺氧心肌细胞线粒体通透性转换孔的开放及蛋白激酶C(protein kinase C, PKC)在其中的作用。    方法    将原代培养的SD大鼠乳鼠心肌细胞分为5组:对照(常氧)组(A组),缺氧组(B组),缺氧+腺苷A1受体激动剂组(C组),缺氧+腺苷A1受体阻断剂组(D组),缺氧+腺苷A1受体激动剂+PKC阻断剂组(E组)。缺氧6 h后以免疫荧光和免疫印迹法分析A、B、C、D 4组PKC的表达变化,用酯化钙黄绿素和氯化钴共孵育法检测5组线粒体通透性转换孔(MPTP)开放,用CCK-8法检测细胞活力。    结果    缺氧6 h后,B、D、E 3组MPTP显著开放,细胞活力降低,而C组能明显减少MPTP的开放,减轻细胞损害,并能使PKC的表达量增加。    结论    缺氧可引起MPTP开放增加,腺苷A1受体激动剂可上调PKC表达,减少缺氧导致的MPTP开放,维持细胞活力。PKC通路可能是腺苷A1受体调控缺氧心肌细胞MPTP开放的重要途径。
Abstract:
Objective    To investigate whether adenosine A1 receptor (A1R) activation can affect the opening of mitochondria permeability transition pore (MPTP) in hypoxic cardiac myocytes and the effects of protein kinase C (PKC) in this process.     Methods    Neonatal rat cardiac myocytes in primary culture were randomized as normoxic group (A), hypoxic group (B), hypoxia and A1R agonist 2-chloro-N6-cyclopentyladenosine (CCPA, 500 nmol/L)(C), hypoxia and A1R antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 500 nmol/L) (D), hypoxia treated with CCPA (500 nmol/L) and PKC inhibitor chelerythine (CHE, 2 μmol/L) (E). After hypoxia for 6 h, the expression of PKC, the opening of MPTP and the activity of cells were detected.     Results    The opening of MPTP increased and the activity of cardiac myocytes decreased in groups B, D and E. However, these phenomena in group C were opposite and PKC increased.     Conclusion    Hypoxia can increase the opening of MPTP and decrease the activity of cardiac cells, while A1R agonist abolishes these bad effects and increases the expression of PKC. Whereas, the PKC inhibitor prevents this protective role. PKC maybe is the key way that A1R regulates the opening of MPTP in hypoxic cardiac myocytes.

参考文献/References:

向飞,张琼,褚志刚,等. 蛋白激酶C在腺苷A1受体调控缺氧心肌细胞线粒体通透性转换孔开放中的表达和作用[J]. 第三军医大学学报, 2007, 29(12):1135-1138.

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更新日期/Last Update: 2008-10-23