机构地区:[1]Medical Research Department,Guangdong Provincial Cardiovascular Institute,Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention,Guangdong General Hospital,Guangdong Academy of Medical Sciences [2]School of Pharmaceutical Sciences,Southern Medical University
出 处:《South China Journal of Cardiology》2016年第2期110-116,共7页岭南心血管病杂志(英文版)
基 金:supported by the National Natural Science Foundation of China(No.81202602/81373486)
摘 要:Background Treatment of rats with the beta-adrenergic agonist Isoprenaline(ISO) results in cardiac hypertrophy and myocardial fibrosis.In the present work,we aimed to study the in vivo effects of ISO on serum levels of monocyte chemoattractant protein- 1 and tissue inhibitor of matrix metalloproteinases type I in Wistar rats.Methods ISO(5 mg·kg-1) or Saline were injected subcutaneously into Wistar rats once a day for 3 or 7 consecutive days.Ventricular remodeling and cardiac function were evaluated by echocardiography.Sections of heart were stained with hematoxylin-eosin(HE) for histopathology or with Massons trichrome for collagen visualization.In addition,heart tissue immunohistochemistry for ɑ-SMA was also analyzed.The serum levels of tissue inhibitor of matrix metalloproteinases type I(TIMP-1) and monocyte chemoattractant protein-1(MCP-1) were determined by Luminex multiplex technology.Results ISO induced cardiac dysfunction in rats after 3 or 7 days of treatment.ISO caused significant increase of myocardial disorder and fibrosis withincreased ɑ-SMA expression.ISO treated aats showed a significant increase in the serum levels of TIMP- 1 and MCP-1.Conclusions Our study suggests that ISO induces profound cardiac remodeling accompanied with increase of serum TIMP-1and MCP-1.Background Treatment of rats with the beta-adrenergic agonist Isoprenaline(ISO) results in cardiac hypertrophy and myocardial fibrosis.In the present work,we aimed to study the in vivo effects of ISO on serum levels of monocyte chemoattractant protein- 1 and tissue inhibitor of matrix metalloproteinases type I in Wistar rats.Methods ISO(5 mg·kg-1) or Saline were injected subcutaneously into Wistar rats once a day for 3 or 7 consecutive days.Ventricular remodeling and cardiac function were evaluated by echocardiography.Sections of heart were stained with hematoxylin-eosin(HE) for histopathology or with Massons trichrome for collagen visualization.In addition,heart tissue immunohistochemistry for ɑ-SMA was also analyzed.The serum levels of tissue inhibitor of matrix metalloproteinases type I(TIMP-1) and monocyte chemoattractant protein-1(MCP-1) were determined by Luminex multiplex technology.Results ISO induced cardiac dysfunction in rats after 3 or 7 days of treatment.ISO caused significant increase of myocardial disorder and fibrosis withincreased ɑ-SMA expression.ISO treated aats showed a significant increase in the serum levels of TIMP- 1 and MCP-1.Conclusions Our study suggests that ISO induces profound cardiac remodeling accompanied with increase of serum TIMP-1and MCP-1.
关 键 词:monocyte TIMP hematoxylin eosin collagen hypertrophy adrenergic injected visualization stained
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...