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目的:探讨促红细胞生成素(erythropoietin,EPO)对脂多糖(lipopolysaccharides,LPS)诱导的急性失代偿性心力衰竭(acute decompensated heart hailure,ADHF)的保护机制。方法:50只C57Bl/6小鼠随机分为空白(Nor)组、阿霉素(doxorubicin,Dox)组、阿霉素感染(Dox+LPS,D&L)组、阿霉素治疗(Dox+EPO,D&E)组和阿霉素感染治疗组(Dox+LPS+EPO,DLE),每组10只。前5周,除Nor组外,其他组腹腔注射Dox(每次5 mg.kg-1,1次.周-1,共5周),建立CHF小鼠模型。第7周时,D&L和DLE组腹腔注射单剂LPS 5 mg.kg-1,D&E和DLE组腹腔注射单剂EPO5 000 iu.kg-1。观察1周后,第8周行心脏超声检查、血清中白介素-6(interleukin-6,IL-6)和脑钠肽(brain natriuretic peptide,BNP)含量测定、HWI、心肌组织的免疫组织化学分析P-STAT3,Bcl-2和Bax蛋白的表达。结果:与D&L组相比,DLE组小鼠给予EPO处理后心室壁厚度、射血分数(ejection fraction,EF)也明显增高(P<0.01);P-STAT3和Bcl-2表达增加,Bax表达减少(P<0.05);但IL-6蛋白表达改变不明显。结论:EPO的抗炎作用对LPS诱导的炎症反应影响不明显,但可增强心肌细胞本身对炎症损伤防御机制。
Objective: To investigate the protective mechanism of erythropoietin (EPO) on lipopolysaccharides (LPS) -induced acute decompensated heart hailure (ADHF). Methods: Fifty C57Bl / 6 mice were randomly divided into two groups: Nor group, Dox group, Dox + LPS group, Dox + EPO group, D & E) group and doxorubicin infection treatment group (Dox + LPS + EPO, DLE), 10 rats in each group. In the first 5 weeks, other groups were given intraperitoneal injection of Dox (5 mg.kg-1 and 1-times per week for 5 weeks) except for Nor group, and CHF mice were established. At week 7, D & L and DLE received either intraperitoneal injections of a single dose of LPS 5 mg.kg-1, and D & E and DLE intraperitoneally injected with a single dose of EPO 5000 iu.kg-1. One week later, the hearts were examined by echocardiography at the eighth week, the contents of interleukin-6 (IL-6) and brain natriuretic peptide (BNP), HWI and immunohistochemistry P-STAT3, Bcl-2 and Bax protein expression. Results: Compared with D & L group, the thickness of ventricular wall and the EF of DLE group were significantly increased (P <0.01); the expression of P-STAT3 and Bcl-2 was increased and the expression of Bax (P <0.05), but the change of IL-6 protein was not obvious. Conclusion: The anti-inflammatory effect of EPO has no obvious effect on the inflammatory response induced by LPS, but it can enhance the defense mechanism of cardiomyocytes against inflammatory injury.