从p38MAPK途径探讨参附注射液对脓毒症大鼠心功能的影响

【目的】探讨参附注射液对脓毒症大鼠心功能的保护作用及其可能机制。【方法】选用SD雄性大鼠40只,随机分为正常对照组、假手术组、模型组和参附注射液组。采用盲肠结扎穿孔术(CLP)复制脓毒症模型,36 h后取动脉血及左室心肌,检测血清中的肿瘤坏死因子α(TNF-α)和白细胞介素1(IL-1)水平,观察心肌组织匀浆上清液磷酸化p38丝裂原活化蛋白激酶(p-p38MAPK)和p38丝裂原活化蛋白激酶(p38MAPK)变化。【结果】于造模后36 h,模型组大鼠的左心室射血分数(LVEF)及左室短轴缩短率(LVFS)情况较假手术组显著降低(P0.05);参附注射液组大鼠心功能情况较模型组显著升高(P0.05),血清中TNF-α和IL-1水平及心肌组织匀浆上清液p-p38/p38MAPK水平较模型组显著降低(P0.05);假手术组上述指标水平与正常对照组比较差异无统计学意义(P0.05)。【结论】参附注射液对脓毒症心肌损伤具有修复作用,其机制可能与抑制心肌p38MAPK磷酸化,从而减轻该通路的炎症因子释放有关。

Protective Effect of Shen Fu Injection on Cardiac Function in Sepsis Rats Through p38MAPK Pathway

Objective To investigate the protective effect of Shen Fu Injection (SFI) on cardiac function in sepsis rats and to explore the possible mechanism.Methods Forty SD male rats were randomly divided into 4 groups,namely normal control group,sham operation group,model group,SFI group.The sepsis model was established by cecal ligation and puncture (CLP).Thirty-six hours later,the arterial blood and left ventricular myocardium tissues were collected,and then the serum levels of tumor necrosis factor(TNF)-α and interleukin(IL)-1 were detected and the levels ofphosphorylated p38-mitogen-activated protein kinase (p-p38MAPK) and p38-mitogenactivated protein kinase (p38MAPK) in the supernatant of myocardial homogenate were detected.Results Thirty-six hours after modeling,left ventricular ejection fraction (LVEF) and left ventricular fractional shortening(LVFS) of the rats in the model group were significantly lower than those in the sham operation group (P ＜ 0.05).The heart function in SFI group was much improved compared with the model group (P ＜ 0.05).The serum TNF-α and IL-1 levels as well as p-p38/p38MAPK level in the supernatant of myocardial tissue of SFI group were lower than those in the model group (P ＜ 0.05).There were no significant differences of the above indexes between the sham operation group and the normal control group (P ＞ 0.05).Conclusion SFI has protective effect against sepsis myocardial injury.The mechanism may be related with the inhibition of p38MAPK phosphorylation in the myocardium,thereby reducing the release ofinflammatory cytokines in the pathway.