中国医科大学学报

中国医科大学学报

中国医科大学学报 ›› 2012, Vol. 41 ›› Issue (5): 422–426.

• 基础医学 • 上一篇    下一篇

p38丝裂原激活蛋白激酶抑制剂对脓毒症早期大鼠心肌中炎性因子和细胞凋亡蛋白表达的影响

苏翠靖1,马志宇1,佟淼2,马涛1,李莹洁1   

  1. 1.中国医科大学附属第一医院急诊科,沈阳 110001;2.沈阳市苏家屯区妇婴医院,沈阳 110101
  • 收稿日期:2012-09-27 修回日期:2012-09-27 出版日期:2012-05-20 发布日期:2012-09-27

Effects of p38MAPK Inhibitor on Inflammatory Factors and Expression of Cell Apoptotic Proteins in Rats’Myocardium at the Early Stage of Sepsis

SU Cui-jing1,MA Zhi-yu1,TONG Miao2,MA Tao1,LI Ying-jie1   

  1. 1.Department of Emergency, The First Hospital, China Medical University, Shenyang 110001, China; 2.The Hospital of Sujiatun District for Women and Children, Shenyang 110101, China
  • Received:2012-09-27 Revised:2012-09-27 Online:2012-05-20 Published:2012-09-27

摘要: 目的 探讨脓毒症时心肌损害的原因及p38丝裂原激活蛋白激酶(MAPK)抑制剂的保护作用。方法 将84只雄性SD大鼠随机分为对照组、实验组和治疗组(n=28)。实验组和治疗组采用腹腔注射内毒素(10 mg/kg)制作脓毒症模型,治疗组同时加p38MAPK抑制剂SB203580予以干预,对照组腹腔注射生理盐水。在不同时间点观察大鼠血清脑钠素(BNP)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)的浓度及心肌组织中TNF-α、IL-6、凋亡蛋白caspase-9的表达情况。 结果 实验组大鼠血清TNF-α、IL-6进行性升高。对照组心肌组织中仅有微量TNF-α、IL-6及caspase-9表达,而实验组心肌组织中则大量表达。血清TNF-α、IL-6浓度及心肌中caspase-9的表达与心肌损害程度呈显著正相关。应用SB203580后,治疗组血清TNF-α、IL-6浓度显著降低,心肌中caspase-9的表达也减少。但各组血清BNP浓度之间差异无统计学意义,均在正常范围之内。结论 TNF-α、IL-6的大量释放及其在心肌中的表达是脓毒症心肌损害的原因之一,p38MAPK抑制剂SB203580可对脓毒症大鼠心肌损害起保护作用。

关键词: 脓毒症, 白细胞介素6, 肿瘤坏死因子α, 心肌损伤, p38丝裂原激活蛋白激酶

Abstract: Objective To investigate the causes of myocardial injury in sepsis and the functions of p38 mitogen-activated protein kinase (MAPK) inhibitor in rats. Methods Eighty-four Male SD rats were randomly divided into control group, experimental group and treatment group (n=28). The control group was administered with saline intraperitoneally. The experimental group and treatment group was injected with endotoxin LPS (10mg/kg) intraperitoneally to establish sepsis models. Besides, the treatment group was also given p38MAPK inhibitor, SB203580. At different time points, the concentrations of serum brain natriuretic peptide (BNP), tumor necrosis factor-aphla (TNF-α), interleukin 6 (IL-6) and expression of cardiac muscle (TNF-α), IL-6, apoptotic protein, caspase-9 were detected. Results In experimental group, the postoperative serum TNF-αand IL-6 progressively increased. In control group, trace expression of TNF-α, IL-6 and caspase-9 was found in myocardial tissues, while in experimental group, overexpression of them was found. The concentrations of serum TNF-α and IL-6 and the expression of caspase9 were significantly correlated with myocardial damage. After the application of p38MAPK inhibitor, SB203580, the concentrations of serum TNF-α and IL-6 decreased significantly, and so did the expression of caspase9 in myocardial tissues. However, the serum BNP had no difference among the groups, all within the normal range. Conclusion The release and expression of a large number of TNF-α, IL-6 in the myocardium is one of the causes of myocardial damage in sepsis. p38MAPK inhibitor, SB203580 may protect myocardiam in rats with sepsis.

Key words: sepsis, interleukin-6, tumor necrosis factor-alpha, myocardial injury, p38MAPK

中图分类号: 

  • R542.2
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