龙牙楤木总皂苷对缺氧/再给氧心肌细胞损伤的保护作用  

Protective effects of aralosides on cultured myocardial cells subjected to anoxia/reoxygenation injury

作　　者：孙桂波[1] 徐惠波[1] 温富春[1] 张伟[1] 丁涛[1] 孙晓波[1] 

机构地区：[1]吉林省中医中药研究院新药中心,吉林长春130021

出　　处：《中国药理学通报》2006年第9期1092-1095,共4页Chinese Pharmacological Bulletin

基　　金：国家中医药管理局资助课题(No2000-J-P-23)

摘　　要：目的探讨龙牙楤木总皂苷(As)对培养心肌细胞缺氧/再给氧损伤的保护作用及其机制。方法取体外培养的乳大鼠心肌细胞建立缺氧/再给氧心肌细胞损伤模型,实验分为5组空白对照组;模型组(A/R组),缺氧6h再给氧3h;3个As给药组,缺氧6h再给氧3h,并于缺氧及再给氧开始时分别加入终浓度为1.25、2.5、5.0mg.L-1的As,观察As对细胞上清液中缺氧及再给氧后LDH、CK漏出量、MDA含量、SOD活性的影响。用MTT法检测As对缺氧再给氧损伤心肌细胞线粒体的保护作用。结果As可抑制缺氧及再给氧后LDH、CK漏出量,降低MDA含量,提高SOD活性,升高OD570吸光度值。结论As对培养心肌细胞的缺氧再给氧损伤具有保护作用,提示其作用机制与增强细胞抗氧化作用,减少自由基及脂质过氧化物导致的细胞膜损伤有关。Aim To study the protective mechanism of aralosides （As） on myocardial cells injured by anoxia/reoxygenation （A/R）. Methods An anoxia/reoxygenation model of myocardial cells from neonatal Wistar rats was established. The cells were randomly divided into 5 groups： control, without any treatment; A/R group, preconditional 6 h anoxia followed by 3 h reoxygenation; A/R ＋ As （1.25, 2.5, 5.0 mg·L^-1） groups, preconditioned 6 h anoxia followed by 3 h reoxygenation, and As was added into the culture medium with a final concentration 1.25, 2.5, 5.0 mg·L^-1 before anoxia and reoxygenation. Lactate dehydrogenase（LDH） release, Malondialdehyde （MDA） contents and Superoxide dismutase （SOD） activity in the bathing medium were assayed for the evaluation of myocardial cells injury. The protective role of As on mitochondria of myocardial cells was measured by MTT after A/R injury. Results As could restrain the LDH release hance evidently, decrease the MDA content and enhance the SOD activity and increase OD570 of myocardial cells injured by A/R. Conclusion As has function of protecting the culturing myocardial cells injured by A/R. The mechanism is related to the enhancement of antioxidative effect on cells, and the reduction membrane damage caused by free radical and lipid peroxide.

关 键 词：龙牙楤木总皂苷 心肌细胞培养 超氧化物歧化酶 乳酸脱氢酶 肌酸激酶 

分 类 号：R-332[医药卫生] R284.1