北五味子总木脂素对高脂血症大鼠心肌缺血再灌注损伤的保护作用及其机制

Protective effect of Schizandrae Lignanoid on myocardial ischemia-reperfusion injury in hyperlipidemic rats and its mechanism

目的:探讨北五味子总木脂素(SCL)对高脂血症大鼠心肌缺血再灌注损伤的保护作用及其机制,为SCL将来用于治疗高脂血症并发心肌缺血等疾病提供理论依据和实验基础。方法:建立大鼠高脂血症模型,分为对照组、假手术组、模型组及SCL60、20和5mg·kg-1组以及200mg·kg-1复方丹参片组(CDT)。再灌注后,测定心肌梗死面积、血脂及心肌髓过氧化物酶(MPO)含量,观察心肌病理变化。结果:与模型组比较SCL60、20和5mg·kg-1组随着剂量增加心肌梗死面积与左心室面积比值及MPO活性降低(P<0.01);SCL60及20mg·kg-1组缺血区心肌纤维断裂及坏死减少,灶性出血及炎性细胞浸润减轻;SCL60和20mg·kg-1组血清TC、TG、LDL-c及ApoB降低(P<0.05或P<0.01),HDL-c及ApoA1升高(P<0.05或P<0.01)。结论:SCL对高脂血症大鼠心肌缺血再灌注损伤有一定的保护作用,其机制可能与抑制中性粒细胞浸润、影响血脂代谢有关。

Objective To investigate the protective effect of Schizandrae Lignanoid （SCL） on myocardial ischemia reperfusion injury in hyperlipidemic rats and its mechanisms and provide theoretical basis and experiment foundation for treatment of myocardial ischemia complicated with hyperlipidemic disease with SCL in the future. Methods After hyperlipidemic rat models were set up by oral administration of high lipid emulsion, the rats were divided into seven groups： control group, sham group, model group, SCL 60, 20, 5mg·kg^-1 groups and 200mg·kg^-1 CDT group. After reperfusion, the blood samples taken from the ventricles were assayed for blood lipid ; MPO activities of ischemic myocardium were measured; Infarct area of left ventricles was measured by Evens blue-TTC staining, and myocardial pathological changes were also observed. Results Compared with model group, the myocardial infarct area/ventricle area ratios and MPO activities in SCL 60, 20, 5mg·kg^-1 groups decreased （P〈0.01） with the raise of SCL dose; In SCL 60 and 20mg·kg^-1 groups myocardial fiber rupture and necrosis in isehemic area with less focal hemorrhage and inflammatory cell infiltration decreased; In SCL 60 and 20mg·kg^-1 groups the levels of serum TC, TG, LDL-c, ApoB decreased and HDL-c, ApoA1 increased （P〈0.05 or P〈0.01）. Conclusion SCL has protective effects on myocardial ischemia reperfusion injury in hyperlipidemic rats and the mechanisms involved may be related to its reJzulation of blood tinid and inhibition of neutronhil infiltration.