Effects of Radix Ginseng and Radix Ophiopogonis extract (SMF) on protein S-nitrosylation in ischemic myocardial tissue.
- Author:
Jin-hong FENG
1
;
Qiang SHI
;
Yi WANG
;
Yi-yu CHENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Creatine Kinase; blood; Drugs, Chinese Herbal; pharmacology; L-Lactate Dehydrogenase; blood; Male; Myocardial Ischemia; blood; drug therapy; metabolism; Myocardium; metabolism; Nitric Oxide; blood; Nitric Oxide Synthase Type III; metabolism; Nitrosation; drug effects; Nitroso Compounds; metabolism; Panax; chemistry; Random Allocation; Rats; Rats, Sprague-Dawley
- From: China Journal of Chinese Materia Medica 2008;33(15):1894-1897
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of Radix Ginseng and Radix Ophiopogonis extract (SMF) on protein S-nitrosylation in rats myocardial with ischemia/reperfusion injury (MI/RI).
METHODMyocardial ischemia/reperfusion in rats were produced by occlusion of the left anterior descending coronary artery. To study the cardioprotective effects of SMF on the acute MI/RI rats, the serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), and nitric oxide (NO) were determined. The change of the expression of endothelial nitric oxide synthase (eNOS) was detected by Western blot. The content of related S-nitrosylation proteins in myocardial tissue was measured by Biotin-Switch method.
RESULTSMF significantly decreased the serum levels of CK and LDH as well as increased the serum levels of NO and the expression of eNOS in myocardial tissue. The contents of S-nitrosylation proteins were significantly increased from (4.42 +/- 0.60) micromol x g(-1) to (8.78 +/- 1.37) micromol x g(-1). The molecular weight of the majority S-nitrosylation proteins were in the range of 90 x 10(3)-117 x 10(3).
CONCLUSIONIncreased expression of eNOS and NO induced by SMF may activate S-nitrosylation of many proteins in rat hearts. The change of the activities or functions of those proteins by S-nitrosylation may be an important mechanism for myocardial protective effects of SMF.
