瑞舒伐他汀对心力衰竭大鼠心功能的改善作用及其机制
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  • 英文篇名:Improving effect of rosuvastatin on the cardiac function of heart failure rats and its underlying mechanism
  • 作者:徐丹 ; 王晓旭
  • 英文作者:XU Dan;WANG Xiao-xu;Department of Cardiology,The First Branch of the First Affiliated Hospital of Chongqing Medical University;
  • 关键词:心力衰竭 ; 瑞舒伐他汀 ; 心功能
  • 英文关键词:heart failure;;rosuvastatin;;cardiac function
  • 中文刊名:GLYZ
  • 英文刊名:The Chinese Journal of Clinical Pharmacology
  • 机构:重庆医科大学附属第一医院第一分院心内科;
  • 出版日期:2019-05-28
  • 出版单位:中国临床药理学杂志
  • 年:2019
  • 期:v.35;No.288
  • 语种:中文;
  • 页:GLYZ201910015
  • 页数:3
  • CN:10
  • ISSN:11-2220/R
  • 分类号:57-59
摘要
目的研究瑞舒伐他汀对心力衰竭大鼠心功能的改善作用及其机制。方法将39只SD大鼠随机分为对照组,模型组及实验组,各13只。模型组及实验组予以皮下注射异丙肾上腺素5 mg·kg~(-1),qd,共7 d,建立心力衰竭大鼠模型,对照组予以皮下注射等量0. 9%NaCl。建模成功后,实验组予以灌胃瑞舒伐他汀5 mg·kg~(-1),模型组及对照组则予以灌胃等量0. 9%Na Cl,qd,共14 d。用超声检测及酶联免疫吸附实验(ELISA)检测大鼠心功能指标;用蛋白免疫印迹法检测大鼠心肌组织有丝分裂原激活的蛋白激酶(MAPK)通路相关蛋白表达。结果对照组,模型组和实验组左心室射血分数(LVEF)分别为(81. 23±5. 46)%,(53. 47±5. 18)%,(59. 09±5. 33)%,血清脑钠肽分别为(123. 11±20. 15),(157. 46±19. 87),(141. 01±19. 08) pg·m L~(-1),肌钙蛋白Ⅰ分别为(33. 57±9. 68),(42. 52±9. 71),(33. 45±9. 56) pg·m L~(-1)。对照组,模型组及实验组大鼠心肌组织p38-MAPK相对表达量分别为0. 56±0. 11,1. 13±0. 05,0. 78±0. 04; P-p44ERK相对表达量分别为0. 26±0. 05,0. 43±0. 04,0. 36±0. 05; P-p42ERK相对表达量分别为1. 56±0. 21,0. 91±0. 04,1. 03±0. 03; P-p54JNK相对表达量分别为0. 19±0. 05,0. 39±0. 02,0. 21±0. 03; P-p46JNK相对表达量分别为0. 75±0. 11,1. 02±0. 01,0. 82±0. 02。模型组与实验组比较,差异均有统计学意义(均P <0. 05)。结论瑞舒伐他汀可改善心力衰竭大鼠心功能,其作用机制与其有效调控MAPK通路相关蛋白表达相关。
        Objective To explore the improving effect of rosuvastatin on the cardiac function of heart failure rats,and analyse the related mechanism. Methods A total of 39 SD rats were randomly assigned to control group,model group and experimental group,each group with 13 rats.The model group and experimental group received subcutaneous injection of 5 mg·kg~(-1) of isoprenaline once daily for 7 d to induce heart failure rat model,while the control group was given subcutaneous injection of0. 9% NaCl. After the heart failure rat model was established,the experimental group received oral administration of 5 mg·kg~(-1) of rosuvastatin once daily,while the model group and control group received 0. 9%NaCl. Each group were given treatment for 2 weeks. Ultrasound technique and enzyme linked immunosorbent assay( ELISA) were used for the measurement of cardiac function indexes; the Western Blot( WB) was used to detect the expression of rats myocardium mitogen-activated protein kinase( MAPK)-associated protein. Results Of the control group,model group and experimental group,the left ventricular ejection fraction( LVEF) were( 81. 23 ± 5. 46) %,( 53. 47 ± 5. 18) %,( 59. 09 ± 5. 33) %, respectively; the levels of serum brain natriuretic peptide were( 123. 11 ± 20. 15),( 157. 46 ± 19. 87),( 141. 01 ± 19. 08) pg · m L~(-1), respectively; cardiac troponin I were( 33. 57 ± 9. 68),( 42. 52 ± 9. 71),( 33. 45 ± 9. 56) pg·m L~(-1),respectively; the relative expression of p38-MAPK in myocardium were0. 56 ± 0. 11,1. 13 ± 0. 05,0. 78 ± 0. 04,respectively; the relative expression of P-p44 ERK were 0. 26 ± 0. 05,0. 43 ± 0. 04,0. 36 ± 0. 05,respectively; the relative expression of P-p42 ERK were 1. 56 ± 0. 21,0. 91 ± 0. 04,1. 03 ± 0. 03,respectively; the relative expression of P-p54 JNK were 0. 19 ± 0. 05,0. 39 ± 0. 02,0. 21 ± 0. 03,respectively; the relative expression of P-p46 JNK were 0. 75 ± 0. 11,1. 02 ± 0. 01,0. 82 ± 0. 02,respectively. There were significant difference between the model group and the control group( P < 0. 05). Conclusion Rosuvastatin can improve cardiac function of the heart failure rats,and the regulation of MAPK-protein expression might be involved in the process.
引文
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