Inhibition of magnesium lithospermate B on the c-Jun N-terminal kinase 3 mRNA expression in cardiomyocytes encountered ischemia/reperfusion injury.
- Author:
Li-min YANG
1
;
Yao-long XIAO
;
Jia-hui OU-YANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cardiotonic Agents; pharmacology; Drugs, Chinese Herbal; pharmacology; JNK Mitogen-Activated Protein Kinases; Male; Mitogen-Activated Protein Kinases; antagonists & inhibitors; genetics; metabolism; Myocardial Ischemia; complications; Myocardial Reperfusion Injury; enzymology; etiology; pathology; Myocytes, Cardiac; drug effects; enzymology; RNA, Messenger; biosynthesis; drug effects; Rats; Rats, Sprague-Dawley
- From: Acta Pharmaceutica Sinica 2003;38(7):487-491
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the function of c-Jun N-terminal kinase 3 (JNK3) in the process of ischemic/reperfused heart injury and the mechanism underlying the protective action of magnesium lithospermate B (MTB), a bioactive compound isolated from Danshen.
METHODSBy in situ hybridization, JNK3 mRNA was detected in the ventricular preparations of the Langendorff ischemic/reperfused rat heart. The inhibitory effect of MTB on the expression of JNK3 mRNA was also investigated.
RESULTSThe purple and blue hybridization signals were located in the cytoplasm of the cardiomyocytes, which were weaker in the non-perfused hearts and stronger in the hearts encountered 30 min of ischemia and 30 min of reperfusion. Image analysis showed that the expression of JNK3 mRNA in the cardiomyocytes increased after 30 min of ischemia and 30 min of reperfusion, which showed significant difference compared with that in the cardiomyocytes of the non-perfused heart and the control heart (P < 0.05). Treatment with of 0.1, 1 and 10 mumol.L-1 MTB abolished the elevation of JNK3 mRNA expression in the ischemic/reperfused heart (P < 0.05).
CONCLUSIONJNK3 may be another component in the signal transduction pathway of ischemia/reperfusion induced cardiomyocyte apoptosis. MTB may protect the heart from ischemia/reperfusion injury by reducing apoptosis through inhibition of the JNK3 activity.
