文章摘要
雒磊,任晓东,马文兵,姚鸿萍.促红细胞生成素对高脂血症大鼠的降脂作用及机制研究[J].中国药事,2022,36(10):1166-1173
促红细胞生成素对高脂血症大鼠的降脂作用及机制研究
The Lipid-lowering Eff ect and Mechanism of Erythropoietin on Hyperlipidemia Rats
  
DOI:10.16153/j.1002-7777.2022.10.008
中文关键词: 促红细胞生成素  高脂血症  血液黏度  氧化损伤  炎症
英文关键词: erythropoietin  hyperlipidemia  blood viscosity  oxidative damage  infl ammatory response
基金项目:陕西省自然科学基金(编号 2015JM8447)
作者单位
雒磊 西安交通大学第一附属医院,西安 710061 
任晓东 西安交通大学第一附属医院,西安 710061 
马文兵 西安交通大学第一附属医院,西安 710061 
姚鸿萍 西安交通大学第一附属医院,西安 710061 
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中文摘要:
      目的:探讨促红细胞生成素(EPO)对高脂血症大鼠血脂水平的调节及作用机制。方法:将SD 大鼠随机分为正常对照组、高脂血症模型组、EPO组,每组8只。正常对照组大鼠给予基础饲料,模型组及EPO组大鼠给予高脂饲料,连续喂养8周。8周后EPO组按1000 U·kg-1腹腔注射EPO,每周3次,正常对照组和高脂血症模型组大鼠腹腔注射生理盐水。给药4周后,检测血清总胆固醇(TC)、甘油三酯 (TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平及炎症因子白细胞介素-1β(IL-1β)、肿瘤坏死因子α(TNF-α)含量,肝脏组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,血液流变学检测血液黏度相关指标,蛋白免疫印迹(Western Blotting)检测肝脏组织SOD1、IL-1β的蛋白表达。结果:EPO不影响高脂血症大鼠体质量增长,可显著降低高脂血症大鼠TC、TG、LDL-C水平,升高HDL-C水平;EPO可改善高脂血症大鼠血液黏滞性,降低低切变率、 中切变率、高切变率全血黏度和中切变率全血还原黏度、血沉等指标;还可明显降低高脂血症大鼠肝脏组织MDA含量,升高SOD活性,降低血清IL-1β和TNF-α水平,增强肝脏组织SOD1蛋白表达,减弱 IL-1β蛋白表达。结论:EPO可显著改善高脂血症大鼠的血脂水平,其降脂作用机制可能与改善血液黏滞性、减轻肝脏氧化损伤和炎症反应有关。
英文摘要:
      Objective: To investigate the regulation and mechanism of erythropoietin (EPO) on blood lipid level in hyperlipidemia rats. Methods: SD rats were randomly divided into control group, hyperlipidemia model group and EPO group, with 8 rats in each group. Basic diet was provided to the rats in control group, and high-fat diet was provided to the rats in model group and EPO group for 8 weeks. After 8 weeks, the rats in EPO group were intraperitoneally injected with 1000 U∙kg-1 EPO three times per week, and the rats in control group and hyperlipidemia model group were intraperitoneally injected with normal saline. Subsequent to 4 Objective: To investigate the regulation and mechanism of erythropoietin (EPO) on blood lipid level in hyperlipidemia rats. Methods: SD rats were randomly divided into control group, hyperlipidemia model group and EPO group, with 8 rats in each group. Basic diet was provided to the rats in control group, and high-fat diet was provided to the rats in model group and EPO group for 8 weeks. After 8 weeks, the rats in EPO group were intraperitoneally injected with 1000 U∙kg-1 EPO three times per week, and the rats in control group and hyperlipidemia model group were intraperitoneally injected with normal saline. Subsequent to 4
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