Protective Effect of Shen Fu Injection on Cardiac Function in Sepsis Rats Through p38MAPK Pathway
10.13359/j.cnki.gzxbtcm.2017.03.023
- VernacularTitle:从p38MAPK途径探讨参附注射液对脓毒症大鼠心功能的影响
- Author:
Yuanyuan LUO
;
Xinfeng LIN
;
Jinfang YUE
;
Li YANG
- Keywords:
sepsis/TCD therapy;
Shen Fu Injection;
myocardial dysfunction;
myocardial inhibitors;
p38-mitogen-activated protein kinase(p38MAPK);
cecal ligation and puncture;
disease models,animal;
rats
- From:
Journal of Guangzhou University of Traditional Chinese Medicine
2017;34(3):394-397
- CountryChina
- Language:Chinese
-
Abstract:
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.
