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目的观察虎杖苷(polydatin,PD)对脂多糖(lipopolysaccharide,LPS)感染大鼠心功能下降的改善效果及心肌纤维电镜下超微结构的改变。方法正常Wistar大鼠18只,随机平均分为3组,分别为正常对照组(0.9%生理盐水),LPS组(10mg/kg LPS)和LPS+PD组(10mg/kg LPS+10mg/kg PD),分别观察其心功能指标(LVSP,LVEDP,±dp/dtmax)的改变,7h后取心脏,透射电镜观察不同处理对心肌微结构的影响。结果LPS作用于大鼠7h左右大鼠心功能指标有显著降低(P<0.05),而LPS+PD组心功能指标此时尚维持在正常水平。电镜观察发现LPS刺激7h后心肌微结构较正常组有显著的破坏,而LPS+PD组破坏程度较轻。结论LPS对大鼠心肌纤维有破坏作用并导致心肌功能的下降,PD有保护心肌纤维的作用。
Objective To observe the effect of polydatin (PD) on the reduction of cardiac function in rats infected with lipopolysaccharide (LPS) and the ultrastructural changes under myocardial electron microscope. Methods Eighteen normal Wistar rats were randomly divided into three groups: normal control group (0.9% saline), LPS group (10mg/kg LPS) and LPS+PD group (10mg/kg LPS+10mg/kg PD. ), Observe the change of cardiac function index (LVSP, LVEDP, ±dp/dtmax), take heart after 7h, and observe the effects of different treatments on myocardial microstructure by transmission electron microscopy. RESULTS: LPS exerted a significant decrease in cardiac function in rats at 7 h (P<0.05), while the LPS+PD group maintained a normal level of cardiac function. Electron microscopy showed that myocardial microarchitecture after LPS stimulation significantly damaged the normal group compared to the normal group, while LPS+PD group had less damage. Conclusion LPS has a destructive effect on myocardial fibrosis in rats and leads to a decrease in myocardial function. PD can protect myocardial fibers.