摘要
目的:探讨S-烯丙基-L-半胱氨酸(SAC)预处理对心肌缺血/再灌(I/R)损伤的保护作用及其机制。方法:采用离体大鼠心脏Langendorff灌流模型,全心停灌30 min,再灌120 min建立I/R模型。测定血流动力学指标和再灌各时间点冠脉流出液中乳酸脱氢酶(LDH)含量。实验结束测心肌组织中甲月赞(formazan),超氧歧化酶(SOD)及活性氧(ROS)量的变化。结果:与对照组比,SAC明显改善左室血流动力学指标,提高心肌组织的formazan含量,降低再灌期间冠脉流出液中LDH含量,提高心肌组织中SOD的活性,降低心肌组织中ROS的水平。苏氨酸明显减弱SAC的保护作用。结论:SAC对离体大鼠I/R心肌损伤有保护作用,其机制可能与SAC通过心肌细胞膜上的氨基酸转运体ASCT-1进入心肌细胞,增加心肌SOD活性,减少活性氧的损伤有关。
Objective： To investigate the effect of S-allyl-L-cysteine（SAC） on isolated rat heart subject to ischemia/reperfusion（I/R） injury and the mechanisms. Methods： The isolated perfused rat hearts on a langendorff apparatus were subjected to global ischemia for 30 min and followed by 120 min of reperfusion.Hemodynamic index,the production of formazan and the level of lactate dehydrogenase（LDH） in the coronary effluent were determined.Superoxide dismutase（SOD） and reactive oxygen species（ROS） in myocardial homogenates were measured.Results： Compared with I/R group,the hemodynamics were greatly improved,the production of formazan was increased,and LDH level in effluent was reduced in SAC group.SAC improved the SOD activity and significantly decreased the level of ROS.In addition,threonine（Thr） attenuated the protective effect of SAC significantly.Conclusion： SAC has protective effect against myocardial ischemia/reperfusion injury on rats.The possible mechanism is that SAC be transported into the cell through alanine-serine-cysteine-transporter1（ASCT-1） improves SOD activity and reduces the level of ROS.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2011年第1期13-17,共5页
Chinese Journal of Applied Physiology
基金
浙江大学第十二届SRTP资助项目
