摘要
目的 探讨HSP70对活性氧所致心肌细胞急性损伤的保护作用。方法 用热休克预处理诱导新生大鼠心肌细胞中HSP70的表达 ,采用HSP70反义寡核苷酸阻断HSP70的表达 ,乳酸脱氢酶释放率和细胞总蛋白质合成能力来反映H2 O2 0 .5mM所致心肌细胞损伤程度。结果 H2 O2 引起心肌细胞乳酸脱氢酶释放率明显升高 ,而细胞总蛋白质的合成降低。热休克预处理导致心肌细胞中HSP70表达明显增加 ,并使H2 O2 所致心肌细胞LDH释放率显著降低 ,细胞总蛋白质的合成基本恢复正常水平。HSP70反义寡核苷酸很大程度上阻断了HSP70的表达及热休克预处理的心肌细胞保护作用。结论 在热休克预处理减轻过氧化氢所致乳鼠心肌细胞急性损伤的作用中 ,HSP70发挥了最主要的作用。
Objective:To investigate the protective effect of HSP70 against acute injury of cardiomyocyte induced by H 2O 2.Methods: Neonatal rat cardiomyocytes were treated with heat shock (42 ℃ 30 min, recovery for 12 hrs) to induce expression of HSP70 and HSP70 antisense oligodeoxynucleotides were transfected to block the expression of HSP70. LDH release rate and total protein synthesis were applied to evaluate the injury of neonatal rat cardiomyocyte induced by H 2O 2 (0.5 mmol/L).Results: H 2O 2 could significantly increased LDH release and inhibit total protein synthesis. By inducing the expression of HSPs,heat shock pretreatment significantly reduced LDH release and attenuated the inhibition of total protein synthesis induced by H 2O 2. Moreover, HSP70 antisense oligodeoxynucleotides remarkably blocked the protective effect of heat shock pretreatment against the cellular injuries induced by H 2O 2.Conclusion: HSP70 plays a most important role in cytoprotection of heat shock pretreatment against acute injury of cardiomyocyte mediated by H 2O 2.
出处
《中国现代医学杂志》
CAS
CSCD
2004年第1期12-16,20,共6页
China Journal of Modern Medicine
基金
ThisworkwassupportedbygrantsfromtheSpecialFundsforMajorStateBasicResearchofChina (No .G2 0 0 0 0 5 690 8) ,theNationalNatu ralScienceFoundationofChina (No.3 0 0 0 0 0 69
3 0 3 0 0 177)andtheSpecialFundsoftheMinistryofEducationforPhD (No .2 0 0 2 0
