外源性EPO对内毒素诱导心肌损伤的保护及其机制研究.docVIP

外源性EPO对内毒素诱导心肌损伤的保护及其机制研究 　　[摘要] 目的 观察促红细胞生成素（EPO）对内毒素诱导心肌损伤的保护作用及可能的机制。 方法 成功复制内毒素心肌损伤模型后采用随机数字表法将30只大鼠分为假手术组、脓毒症组和EPO干预组，每组随机分配10只大鼠。假手术组开腹后找到盲肠后缝合腹壁切口，不穿刺盲肠；脓毒症组行盲肠结扎穿孔术；EPO干预组于模型复制后给予EPO腹腔注射1000 U/kg。采用酶联免疫吸附分析（ELISA）法测定心肌损伤标志物（cTnI、CK、CK-MB）含量和肿瘤坏死因子（TNF-α）、白细胞介素-6（IL-6）水平。 结果 脓毒症组大鼠血清心肌损伤标志物（cTnI、CK、CK-MB）水平显著高于假手术组，相比较有显著性差异（t = 4.961、4.798、3.038，P 0.05）；经EPO干预后，EPO干预组大鼠血清心肌损伤标志物（cTnI、CK、CK-MB）水平显著降低，与脓毒症组比较有显著性差异（t = 6.631、5.785、3.931，P 0.05）。脓毒症组大鼠血清TNF-α、IL-6水平显著高于假手术组，相比较有显著性差异（t = 6.744、7.883，P 0.05）；经EPO干预后，EPO干预组大鼠血清TNF-α、IL-6水平显著降低，与脓毒症组比较有显著性差异（t = 4.276、7.180，P 0.05）。 结论 EPO可能通过抑制TNF-α、IL-6的分泌和对心肌细胞的保护效应来达到减轻大鼠内毒素诱导的心肌损伤，从而起到保护作用。 　　[关键词] 脓毒症；心肌损伤；促红细胞生成素；动物模型 　　[中图分类号] R541 [文献标识码] A [文章编号] 1673-9701（2013）25-0004-03 　　A study on the protection function and mechanism of exogenous EPO on endotoxin-induced myocardial injury 　　JIN Wenyang SUN Wei CHEN Jianping 　　Emergency Department， Taizhou Hospital， Enze Medical Center， Linhai 317000， China 　　[Abstract] Objective To observe the protection function of EPO on endotoxin-induced myocardial injury and its possible mechanism. Methods After successful replication of endotoxin myocardial damage model， 30 rats were divided into sham operation group， sepsis group and EPO intervention group through random numerical table method. 10 rats were randomly distributed to each group. For the sham operation group， the incision was sutured after the cecum was found， and the cecum was not punctured； for the sepsis group， cecum ligation and perforation were carried out； for EPO intervention group， intraperitoneal injection of EPO was carried out by 1000 U/kg. The myocardial injury markers （cTnI， CK， CK-MB） content， tumor necrosis factor （TNF-α） and interleukin-6 （IL-6） level were measured through enzyme-linked immunosorbent assay （ELISA）. Results Rats serum myocardial injury markers levels （cTnI， CK， CK-MB） of the sepsis group were obviously higher than those of the sham operation group， the difference of w