甘草酸二铵对大鼠心肌缺血再灌注损伤脂质过氧化及心肌酶活性的影响

目的: 观察甘草酸二铵(DG)对大鼠心肌缺血再灌注损伤脂质过氧化及心肌酶活性的影响。方法: 雄性wistar大鼠30只,随机分为假手术组、缺血再灌注组和DG20mg·kg^-1组。每组10只。采用在体大鼠心肌缺血30min再灌注60min损伤模型,再灌注60min后分别用比色法测定心肌丙二醛(MDA)含量、超氧化物歧化酶(SOD)、三磷酸腺苷酶(ATP酶)、血清磷酸肌酸激酶(CPK)和乳酸脱氢酶(LDH)水平,并用酶组织化学方法检测心肌组织琥珀酸脱氢酶(SDH)的活性。结果: DG能显著降低心肌组织中MDA含量和SDH的活性(P<0.05,P<0.01),提高SOD和ATP酶活性(P<0.05,P<0.01),并减少心肌CPK和LDH的释放(P<0.05,P<0.01)。结论: DG具有保护大鼠心肌缺血再灌注损伤的作用,其作用机理可能与其降低心肌脂质过氧化,增强心肌细胞SOD、SDH和ATP酶活性有关。

Effects of dammonii glycyrrhizinatis on lipid peroxidation and enzyme activity in ischemia-reperfusion myocardium rats

AIM: To study effects of dammonii glycyrrhizinatis (DG) on lipid peroxidation and enzyme activity in the ischemia-reperfusion myocardium rats. METHODS:30 male Wistar rats were divided into 3 groups:sham group, ischemia-reperfusion group and DG group (20 mg·kg^-1) (n = 10).Myocardial ischemia reperfusion injury model was produced by the 30 min ligation of left descending coronary artery (LAD) and 60 min reperfusion in rats.The content of myocardial malondialdehyde (MDA), the activities of myocardial superoxide dismutase (SOD), adenosinetriphosphatase (ATPase) and plasma lactate dehydrogenase (LDH), creative phosphokinase (CPK) level were measured by colorimetry, and the activities of succinate dehydrogenase (SDH) were measured by histochemical stain after reperfusion.RESULTS: DG significantly reduced myocardium MDA content (P <0.05 or P <0.01), enhanced the activities of SOD, ATPase and SDH (P <0.05, P <0.01) and decreasedmyocardial LDH and CK release (P <0.05 or P <0.01).CONCLUSION: DG can protect myocardium against ischemia-reperfusion injury, and its mechanism may be related to the reduction of myocardial lipid peroxidation, the enhancement of SOD, SDH and ATPase activities.