摘要
目的:研究阿魏酸钠(SF)预处理对心肌细胞缺氧/复氧(A/R)损伤的延迟保护作用。方法:以细胞存活率、LDH活性、SOD活性、GSH-Px活性、MDA含量、细胞超微结构改变等为观察指标,用终浓度分别为0.84、1.68、3.36、6.72 mmol/L的SF预处理原代培养的大鼠乳鼠心肌细胞3 h、24 h后观察其对A/R损伤的保护作用及其特异性NO合成酶抑制剂L-NAME、MAPK抑制剂PD98059的影响。结果:SF预处理能显著提高细胞存活率,降低LDH活性,且呈剂量依赖性;SOD活性、GSH-Px活性增加,MDA含量减少,细胞超微结构显著改善。L-NAME和PD98059能部分取消SF预处理的上述延迟保护作用。结论:SF预处理对心肌细胞A/R损伤有明显的延迟保护作用,其机制可能与NO生成、MAPK活化有关。
Objective： To investigate the delayed protection of sodium ferulate （SF） on the primary cultured rat＇s cardiomyocytes subjected to anoxi- a- reoxygenation （A/R） injury. Methods： The primary cultured neonatal rat cardiomyocytes were pretreated with SF （0.84, 1.68, 3.36, 6.72 mmol/L） or SF （3.36 mmol/L） and L- NAME （0.1 mmol/L）, PI）98059 （50 μmol/L） respectively for 3 hours, and subjected to A/R injury after 24 hours. Viability, the activities of SOD and GSH - Px, MDA contents, ultrastructure of cardiomyocytes, LDH activity in medium were measured. Results： Pretreatment with SF decreased LDH activity and MDA contents, and increased cell viability, the activities of SOD and GSH -Px in a concentration - dependent manner, protected ultrastructure of cardiomyocytes. The delayed protective effects of SF were partly abolished by L - NAME or PD98059. Conclusion： SF has a potent delayed cardioprotection against A/R injury, and its mechanism appears to be related to production of NO, activation of MAPK pathway.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2007年第5期57-60,共4页
Pharmacology and Clinics of Chinese Materia Medica
基金
江西省科技厅
教育厅
卫生厅中医处科研基金联合资助项目
关键词
阿魏酸钠
延迟保护作用
心肌细胞
sodium ferulate, delayed protection, cardiomyocyte
