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阿魏酸钠对心肌细胞缺氧/复氧损伤的保护作用及其机制

Protective effect and mechanism of pharmacologic preconditioning induced by sodium ferulate on primary cultured myocardial cell injury by anoxia/reoxygenation

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【作者】 傅颖君何明

【Author】 FU Ying-jun, HE Ming (Department of Pharmacology, Jiangxi Medical College, Nanchang 330006, China )

【机构】 江西医学院药理教研室江西医学院药理教研室 江西 南昌 330006江西 南昌 330006

【摘要】 目的 研究阿魏酸钠(SF)预适应对心肌细胞缺氧/复氧损伤的保护作用及其机制。方法 采用1~3d新生SD大鼠,常规方法培养心肌细胞,给予模拟缺氧(缺血)液、模拟复氧(再灌注)液以及药理性预适应药物阿魏酸钠以分析KATP+通道、NO及PKC的影响。结果 与对照组比,单纯缺氧/复氧使LDH,CK,MDA及LD水平显著升高,细胞搏动频率、细胞存活率和SOD,GSH-Px活力显著下降。SF预适应后明显减轻上述变化。Glib,L-NAME和Ploy B均部分取消SF预适应的减轻作用。结论 SF预适应对心肌细胞缺氧/复氧损伤有显著的保护作用;此保护心肌过程是多种因素综合作用的结果。

【Abstract】 Aim To study the preconditioning effects and mechanism of action of sodium ferulate (SF) onprimary cultured myocardial cell injury induced by anoxia/reoxygenation. Methods Cultured myocardial cellsof neonatal SD rats were randomly divided into ten groups: control group: without any treatment; anoxia/reoxygenation group (A/R), reoxygenation of 1 h following anoxia of 3 h; anoxia preconditioning group (AP),reoxygenation of 30 mins following anoxia of 30 mins, three times before the same procedure as group A/R; SFpreconditioning groups, 20 rains of SF (1.68, 0.42, 0.105 mmol·L-1 in final concentration) preconditioningfollowed by 10 mins wash out before A/R; KATP+ channel blocker group, NOS inhibitor group and PKC inhibitorgroup, adding gliberclamide, L-NAME, ploymyxin B at final concentration of 12 g·mL-1, 50 μmol·L-1, 50μtmol·L-1, to culture medium respectively 10 min before the same procedures as SF preconditioning group(1.68 mmol·L-1). Myocardial cells pulse rate and rhythm, myocyte viability, the activity of LDH and CK inculture, the contents of intracelluar MDA, LD in myocardial cells, the activity of SOD and GSH-Px of thecultured myocardial cell were measured at the end of experiment. Results Compared with control group,anoxia/reoxygenation caused great increases of levels of LDH, CK, MDA and LD (P<0.01), decreases ofmyocardial cells pulse rate, cell viability, SOD and GSH-Px(P<0.01);SF preconditioning significantlyattenualed these increases and decreases. Glib, L-NAME, and Ploy B partly abolished the effects of SFpreconditioning. Conclusion SF preconditioning is effective in protecting myocardial cells from anoxia injury.The cardioprotective effect of SF preconditioning is produced by multiple factors.

  • 【文献出处】 药学学报 ,Acta Pharmaceutica Sinica , 编辑部邮箱 ,2004年05期
  • 【分类号】R285
  • 【被引频次】30
  • 【下载频次】243
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