文章摘要
Xiang Gu,Chunzhi Shi,Yibai Feng,Ming Li,Zuolin Fu,Xinping Zhang.[J].南京医科大学学报,2005,19(5):
The antiapoptotic effect of insulin against anoxia/reoxygenation injury in cultured cardiomyocyte of neonatal rat
  
DOI:10.7655
中文关键词: 
英文关键词: insulin  cultured cardiomyocyte  anoxia/reoxygenation  apoptosis
基金项目:
Xiang Gu  Chunzhi Shi  Yibai Feng  Ming Li  Zuolin Fu  Xinping Zhang
Institute of Cardiology,Union Hospital,Tongji Medical College of Huazhong University of Science and Technology,Wuhan 430022,China;Institute of Cardiology,Union Hospital,Tongji Medical College of Huazhong University of Science and Technology,Wuhan 430022,China;Institute of Cardiology,Union Hospital,Tongji Medical College of Huazhong University of Science and Technology,Wuhan 430022,China;Institute of Cardiology,Union Hospital,Tongji Medical College of Huazhong University of Science and Technology,Wuhan 430022,China;Institute of Cardiology,Union Hospital,Tongji Medical College of Huazhong University of Science and Technology,Wuhan 430022,China;Institute of Cardiology,Union Hospital,Tongji Medical College of Huazhong University of Science and Technology,Wuhan 430022,China
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中文摘要:
      
英文摘要:
      Objective: To study protective effect of insulin against cardiomyocyte apoptosis in anoxia/reoxygenation (A/R)injury of neonatal rat. Methods: The model of A/R injury was finished through receiving anoxia for 2 h and reoxygenation for 4 h in cultured cardiomyocytes of neonatal rat. The cardiomyocytes were divided randomly into 3 groups: control group (CON), anoxia/reoxygenation group (A/R) and insulin-treated group (INS). At the end of reoxygenation of 4 hours, activities of lactate dehydrogenase (LDH),contents of malondialdehyde (MDA) were assessed through spectrophotometric procedures, myocyte apoptosis were detected through TUNEL and DNA Ladder. Results: MDA, LDH, and Apoptosis Index were significantly decreased in INS group compared with A/R group (P<0.01). Conclusion: Insulin has a protective effect against A/R injury in cultured cardiomyocyte of neonatal rat; the protective mechanism may contribute to antiapoptosis of insulin.
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