摘要
目的探讨氧化苦参碱(Oxymatrine,OMT)对感染性休克大鼠心肌组织损伤的保护作用。方法采用大鼠盲肠结扎穿孔法(cecal ligation and puncture,CLP)复制大鼠感染性休克模型,将SD大鼠随机分成7组,每组8只,分别为假手术(CON)组、OMT对照组、模型(CLP)组、CLP+OMT 52、26、13 mg·kg-1三剂量组、阳性对照(CLP+地塞米松10 mg·kg-1)组。观察OMT对感染性休克大鼠心肌组织结构及超微结构改变的影响。采用放射免疫分析法测定血清中肿瘤坏死因子-a(tumour necrosis factor-α,TNF-α)含量,比色法测定各组大鼠血浆乳酸脱氢酶(lactic dehydrogenase,LDH)的活性改变。结果不同剂量的OMT能明显降低感染性休克大鼠血浆中LDH活性(P<0.01)及血清TNF-α的含量(P<0.05或P<0.01),改善感染性休克所致的心肌组织结构及超微结构损伤,并且该作用在OMT 52、26 mg.kg-1剂量组与阳性对照组的结果相一致。结论 OMT(52、26、13 mg·kg-1)能对抗大鼠感染性休克引起的心肌损伤。
Objective To explore the protective effects of oxymatrine(OMT) on cardiac muscle in rats with septic shock.Methods 56 male SD rats were randomly divided into 7 groups:sham operation group,OMT control group,model(CLP)group,CLP+OMT(52,26,13 mg·kg-1) group,positive control group.The effects of oxymatrine on cardiac pathological and ultramicrostructure changes were observed in rat with septic shock.Serum tumour necrosis factor-a(TNF-a)and plasma lactic dehydrogenase(PLDH)were determined by radioimmunoassay and colorimetric method,respectively.Results OMT could decrease significantly the PLDH(P0.01)and TNF-a(P0.05 or P0.01)levels.OMT could improve the cardiac pathological and ultramicrostructure injury in the CLP+OMT high and middle group as well as in the OMT+DEX group.Conclusion OMT could antagonize the cardiac muscle injury in rats with septic shock.
出处
《宁夏医科大学学报》
2010年第8期876-878,882,F0003,共5页
Journal of Ningxia Medical University
基金
宁夏医科大学2009年面上项目(XM200902)