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谷氨酰胺对脓毒症模型大鼠心肌细胞的保护作用

柴其翔 韦四喜 王娅婷 方琴 王季石

中国药房2015,Vol.26Issue(31):4378-4380,3.
中国药房2015,Vol.26Issue(31):4378-4380,3.DOI:10.6039/j.issn.1001-0408.2015.31.19

谷氨酰胺对脓毒症模型大鼠心肌细胞的保护作用

Protective Effects of Glutamine on Cardiac Muscle Cell in Septic Model Rats

柴其翔 1韦四喜 1王娅婷 1方琴 2王季石1

作者信息

  • 1. 贵阳医学院附属医院血液科,贵阳 550004
  • 2. 贵阳医学院附属白云医院药剂科,贵阳 550058
  • 折叠

摘要

Abstract

OBJECTIVE:To study protective effects of glutamine (Gln) on cardiac muscle cell in septic model rats. METH-ODS:Rats were randomly divided into sham operation group (normal saline),model group (normal saline) and Gln low-dose, medium-dose and high-dose groups(0.5,0.75,1.0 g/kg)with 10 rats in each group. In these groups,septic rat model was induced by cecal ligation and puncture except sham operation group received sham operation. They were given relevant medicine intrave-nously 10 min after operation,and the characteristics and apoptosis of cardiac muscle cell were observed 12 h after operation. The serum contents of CK,LDH and TnⅠ,and the expression of Bcl-2 and p53 mRNA were all detected. RESULTS:Compared with sham operation group,myocardial necrosis of model group was found,and the serum content of CK,LDH and TnⅠ and apoptotic index increased,and mRNA expression of Bcl-2 in cardiac muscle cell decreased while that of p53 increased,with statistical signifi-cance(P<0.05). Compared with model group,myocardial injury relieved significantly in Gln high-dose and medium-dose groups, and serum contents of CK,LDH and TnⅠ and apoptotic index decreased;mRNA expression of Bcl-2 increased in cardiac muscle cell while that of p53 decreased,with statistical significance (P<0.05). CONCLUSIONS:Gln can improve myocardial injury of septic model rats significantly,by a possible mechanism of down-regulating the expression of p53 gene and up-regulating the ex-pression of Bcl-2 gene.

关键词

脓毒症/谷氨酰胺/心肌细胞/大鼠

Key words

Sepsis/Glutamine/Cardiac muscle cell/Rat

分类

医药卫生

引用本文复制引用

柴其翔,韦四喜,王娅婷,方琴,王季石..谷氨酰胺对脓毒症模型大鼠心肌细胞的保护作用[J].中国药房,2015,26(31):4378-4380,3.

中国药房

OA北大核心CSTPCD

1001-0408

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