CAJ | 학술논문

目的观察柿叶黄酮(PLF)对大鼠离体心脏缺血再灌注损伤的干预作用.方法 48只Wistar雄性大鼠随机分为正常对照组,心肌缺血再灌注组,PLF高、中、低剂量组,阳性药对照组.离体大鼠心脏采用Langendorff法灌流,停灌30 min再灌30 min造成心肌缺血再灌注损伤模型.观察PLF各组对冠脉流出液中天门冬氨酸转氨酶(AST)、肌酸激酶(CK)、乳酸脱氢酶(LDH)活性以及心肌组织中超氧化物歧化酶(SOD)、Na~+-K~+-ATP酶、Ca~(2+)-ATP酶活性和丙二醛(MDA)含量的影响.结果 PLF高、中剂量均可显著改善缺血-再灌注所致的心功能损伤,减少AST 、CK和LDH的释放以及心肌组织MDA的产生,增加SOD、Na~+-K~+-ATP酶和Ca~(2+)-ATP酶的活性(P<0.01或P<0.05).结论 PLF对心肌缺血-再灌注损伤具有保护作用, 其机制可能与提高SOD活性、抗氧自由基、减少脂质过氧化反应有关.
목적 관찰시협황동(PLF)대대서리체심장결혈재관주손상적간예작용.방법 48지Wistar웅성대서수궤분위정상대조조,심기결혈재관주조,PLF고、중、저제량조,양성약대조조.리체대서심장채용Langendorff법관류,정관30 min재관30 min조성심기결혈재관주손상모형.관찰PLF각조대관맥류출액중천문동안산전안매(AST)、기산격매(CK)、유산탈경매(LDH)활성이급심기조직중초양화물기화매(SOD)、Na~+-K~+-ATP매、Ca~(2+)-ATP매활성화병이철(MDA)함량적영향.결과 PLF고、중제량균가현저개선결혈-재관주소치적심공능손상,감소AST 、CK화LDH적석방이급심기조직MDA적산생,증가SOD、Na~+-K~+-ATP매화Ca~(2+)-ATP매적활성(P<0.01혹P<0.05).결론 PLF대심기결혈-재관주손상구유보호작용, 기궤제가능여제고SOD활성、항양자유기、감소지질과양화반응유관.
Objective To observe the preventive effect of Persimmon leaf flavones (PLF) on rat myocardial ischemic and reperfu-sion (I/R) injury. Methods 48 Wistar male rats were randomly divided into control, I/R group, high - , medium - and low -dose PLF groups, and verapamil (Ver) group. The isolated perfused rat hearts were set up by Langendorff - perfusion system. Myocardial ischemia reperfusion injury was induced by 30 minutes global ischemia followed by 30 minutes reperfusion. The activities of aspartic transaminase(AST),creatine kinase(CK),lactate dehydrogenase (LDH) in the effluent from aeteria coronaria were measured to evaluate the injury of myocardial cells and the protective effect of PLF. Meanwhile, the activities of superoxide dismutase (SOD) , Na~+ - K~+ - ATPase and Ca~(2+) - ATPase, and the content of malondialdehyde ( MDA) in myocardial tissues were determined. Results High-and medium-dose PLF could obviously recover cardiac function, reduce the releases of AST, CK, LDH from I/R rat hearts, increase the activities of SOD, Na~+-K~+ - ATPase and Ca~(2+) - ATPase, and decrease the MDA product ( P<0.01 or P<0.05). Conclusion PF may offer myocardial protective effect against I/R injury. The mechanism may be related to attenuating free radicals.