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、CKMB)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。
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,CKMB) 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,CKMB) of the sepsis group were obviously higher than those of the sham operation group,the difference of which was great(t = 4.961,4.798,3.038,P 0.05);after EPO intervention,the serum myocardial injury markers levels for the EPO intervention group were significantly reduced,and its comparison with the sepsis group was significantly different(t = 6.631,5.785,3.931,P 0.05).The serum levels of TNF-α and IL-6 were significantly higher than those of the sham operation group;their comparison were significantly different(t = 6.744,7.883,P 0.05);after EPO intervention,the serum levels of TNF-α and IL-6 for the EPO intervention group were significantly reduced,and its comparison with the sepsis group was significantly different(t = 4.276,7.180,P 0.05).Conclusion EPO can reduce endotoxin-induced myocardial injury through restraining the secretion of TNF-α and IL-6 and the protection of cardiac cells,thus achieving the effects of protection.
出处
《中国现代医生》
2013年第25期4-6,共3页
China Modern Doctor
基金
浙江省台州市科技计划项目(08KY18)