Effect of Shuangshen Tongguan Recipe on nuclear factor-kappa B signal pathway and myocardial junction-mediated intercellular communication in acute myocardial ischemia/reperfusion injured model rats.
- Author:
Jian-xun LIU
1
;
Xiao HAN
;
Xiao-bin MA
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Connexin 43; metabolism; Drugs, Chinese Herbal; pharmacology; therapeutic use; Intercellular Adhesion Molecule-1; blood; Male; Myocardial Reperfusion Injury; blood; drug therapy; Myocardium; metabolism; pathology; NF-kappa B; biosynthesis; physiology; Phytotherapy; Rats; Rats, Sprague-Dawley; Signal Transduction
- From: Chinese Journal of Integrated Traditional and Western Medicine 2005;25(3):228-231
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of Shuangshen Tongguan Recipe (SSTG) on myocardial nuclear factor-kappa B (NF-kappaB) signal pathway, expression of myocardial junction intercellular communication (MJIC) connexin 43 (Cx43), and infarcted myocardial size and weight of the rats' heart after acute myocardial ischemia/reperfusion (I/R) damage.
METHODSModel rat of I/R injury was established by coronary arterial ligating/ releasing. The infarcted myocardial size and weight were determined by N-BT staining, expression of NF-kappaB p65 in myocardial tissue and Cx43 were determined by immunohistochemical method, contents of serum tumor necrosis factor-alpha(TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) were measured by ABC-ELISA.
RESULTSThe myocardial infarcted size and weight, expression of NF-kappaB p65, contents of serum TNF-alpha and ICAM-1 of I/R injured rats in the model group were significantly increased (P<0.05), while Cx43 degraded markedly after modeling. These changes were restored after treated with SSTG (P <0.05).
CONCLUSIONSerious myocardial infarction occurs after ischemia/reperfusion injury, combined with NF-kappaB signal pathway activation and severe Cx43 degradation. SSTG could inhibit the activation of NF-kappaB, the over-excretion of TNF-alpha and ICAM-1 in serum, and the degradation of Cx43 to decrease the myocardial infarcted size and weight.
