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松果菊苷通过调控JAK1/STAT3信号通路改善老年心肌梗死大鼠的免疫功能 被引量:4

Echinacoside improves immune function of aged myocardial infarction rats by regulating JAK1/STAT3 signaling pathway
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摘要 目的探讨松果菊苷通过调控JAK1/STAT3信号通路改善老年心肌梗死大鼠免疫功能紊乱的机制。方法以SD大鼠为研究对象,分为假手术组(sham组)、心肌梗死组(MI组)、松果菊苷低剂量组(ECH-L组,25 mg/kg)和松果菊苷高剂量组(ECH-H组,50 mg/kg),通过永久性结扎冠状动脉左前降支建立心肌梗死(MI)模型,松果菊苷经过腹腔注射给药;HE染色观察大鼠心肌组织病理变化;Masson染色观察大鼠心肌组织梗死面积;流式细胞术检测大鼠外周血中T淋巴细胞亚群水平;ELISA检测大鼠血清中TNF-α、IL-1β和IL-6表达水平;半自动化分析仪测定大鼠血清心肌酶谱的表达情况;Western blot法检测pJAK1、p-STAT3蛋白表达水平。结果松果菊苷能明显减少大鼠心肌中的中性粒细胞数量,减少大鼠心肌组织梗死面积(P<0.05);MI组中CD4^+的水平、CD4^+/CD8^+比值高于sham组(均P<0.01),CD8^+的水平低于sham组(P<0.01);ECH-L组和ECH-H组中CD4^+的水平、CD4^+/CD8^+比值低于MI组(均P<0.05),CD8^+的水平高于MI组(P<0.05);与sham组比较,MI组大鼠血清中心肌酶(AST、LDH、CK-MB)和炎症因子(TNF-α、IL-1β、IL-6)的表达水平显著上调(均P<0.001),ECH-L组和ECH-H组大鼠血清中心肌酶和炎症因子的表达水平下调(均P<0.05);与sham组比较,MI组大鼠心肌组织中p-JAK1、p-STAT3蛋白表达上调(均P<0.001),ECH-L组和ECH-H组大鼠心肌组织中p-JAK1、p-STAT3蛋白表达较MI组下调(P<0.05,P<0.01)。结论松果菊苷通过调控JAK1/STAT3信号通路减少大鼠心肌组织梗死区炎性细胞浸润、梗死面积,减轻炎症反应,改善免疫功能紊乱、心肌受损情况,从而维护心功能正常。 To investigate the effect of echinacoside on the immune dysfunction in aged rats with myocardial infarction,SD rats were recruited and divided into sham operation group(sham group),myocardial infarction group(MI group),echinacoside low-dose group(ECH-L group,25 mg/kg)and echinacoside high-dose group(ECH-H group,50 mg/kg).Myocardial infarction(MI)model was established by permanently ligating the left anterior descending coronary artery,and echinacoside was administered by intraperitoneal injection.HE staining was used to observe the pathological changes of rat myocardium;masson staining was used to observe myocardial infarct size in rats.Flow cytometry was used to detect the levels of T lymphocyte subsets in peripheral blood of rats,while ELISA was used to detect the expression levels of TNF-α,IL-1βand IL-6 in rat serum;the semi-automated analyzer was used to measure the expression of serum myocardial zymogram in rats.The expression levels of p-JAK1 and p-STAT3 proteins were detected by Western blotting.Data showed that echinacoside could significantly reduce the number of neutrophils in the myocardium of rats,and reduce the infarcted area of rat myocardial tissues(P<0.05).The levels of CD4^+T cells and the ratio of CD4^+/CD8^+in the MI group were higher than those in the sham group(both P<0.01),while the level of CD8^+T cells was lower than that in the sham group(P<0.01);the level of CD4^+and the ratio of CD4^+/CD8^+in ECH-L group and ECH-H group were lower than those in MI group(both P<0.05),while the level of CD8^+was higher than that in MI group(P<0.05).Compared with the sham group,the expression levels of myocardial enzymes(AST,LDH,CK-MB)and inflammatory factors(TNF-α,IL-1β,IL-6)were significantly up-regulated in the MI group(all P<0.001),while down-regulated in serum of ECH-L group and ECH-H group(all P<0.05).Compared with the sham group,the expression of p-JAK1 and p-STAT3 proteins were up-regulated in the myocardial tissue of the MI group(all P<0.001);The expression of p-JAK1 and pSTAT3 proteins in ECH
作者 霍艳萍 焦安德 刘玉梅 张孝丽 HUO Yanping;JIAO Ande;LIU Yumei;ZHANG Xiaoli(Department of Cardiovascular Medicine,Third Affiliated Hospital,Qiqihar Medical College,Qiqihar 161000,China;Department of Cardiovascular Medicine,Qiqihar No.1 Hospital,Qiqihar 161000,China;Department of Endocrinology,Third Affiliated Hospital,Qiqihar Medical College,Qiqihar 161000,China)
出处 《免疫学杂志》 CAS CSCD 北大核心 2020年第8期676-682,共7页 Immunological Journal
关键词 松果菊苷 心肌梗死 T淋巴细胞亚群 炎症因子 JAK1/STAT3信号通路 Echinacoside Myocardial infarction T lymphocyte subset Inflammatory factor JAK1/STAT3 signaling pathway
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  • 1Kawiya Sintara,Duangporn Thong-Ngam,Suthiluk Patumraj,Naruemon Klaikeaw,Tanittha Chatsuwan.Curcumin suppresses gastric NF-κB activation and macromolecular leakage in Helicobacter pylori-infected rats[J].World Journal of Gastroenterology,2010,16(32):4039-4046. 被引量:28
  • 2李贻奎,宁可永,梁嵘,李连达.大鼠冠状动脉结扎心肌缺血模型方法的改进[J].中国新药杂志,2005,14(4):427-428. 被引量:51
  • 3张微微.脑出血及其并发症的内科治疗[J].内科急危重症杂志,2005,11(5):233-235. 被引量:22
  • 4国际心脏病学会和协会及世界卫生组织临床命名标准化联合专题组.缺血性心脏病的命名及诊断标准[J].中华心血管病杂志,1981,9(2):75-75. 被引量:1111
  • 5Nakajima T, Schuhe S, Warrington KJ. T-cell-mediated lysis of endothelial cells in acute coronary syndromes[ J]. Circulation, 2002, 105 (4) : 570 -575. 被引量:1
  • 6Widmer A, Linka AZ, Attenhofer CH. Mechanical complications after myocardial infarction reliably predicted using C-reactive protein levels and lymphocytopenia[ J ]. Cardiology, 2003, 99 (4) : 25 - 31. 被引量:1
  • 7Terashima M, Akita H, Kanazawa K. Circulating T-lymphocyte activation in patients with variant angina[J]. Coron Artery Dis, 2002, 13 (3) : 161 -168. 被引量:1
  • 8Nabel E G, Braunwald E. A tale of coronary artery disease and myocardial infarction[J]. N Engl J Med, 2012,366( 1 ) :54 -63. 被引量:1
  • 9Stary H C. Atlas of Atherosclerosis : Progression and Regres- sion[ M ]. New York :CRC Press, 1999:23. 被引量:1
  • 10Spann N J, Garmire L X, McDonald J G, et al. Regulated accumulation of desmosterol integrates macrophage lipid me- tabolism and iinflammatory responses [ J ]. Cell, 2012, 151 ( 1 ) : 138-152. 被引量:1

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