Effect and mechanism of methyl protodioscin in protecting cardiomyocytes against anoxia/reoxygenation injury.
- Author:
Zong NING
1
;
Yi-kui LI
;
Yan ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Hypoxia; Cells, Cultured; Diosgenin; analogs & derivatives; pharmacology; Myocardial Reperfusion Injury; metabolism; Myocytes, Cardiac; drug effects; metabolism; Oxygen; adverse effects; Rats; Rats, Sprague-Dawley; Saponins; pharmacology
- From: Chinese Journal of Integrated Traditional and Western Medicine 2010;30(4):407-409
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect and mechanism of methyl protodioscin (MPD), an active ingredients of yamogenin, in protecting cardiomyocytes (CMC) against anoxia/reoxygenation (A/R) injury.
METHODSCultured CMCs of neonatal SD rats were randomly divided into three groups, cells in Group A were untreated normal cells, cells in Group B and C were made to injury CMC model by A/R, and only those in Group C were treated with MPD. Levels of ATPase activity and lactate dehydrogenase (LDH) in cell membrane of CMCs were determined. Besides, the mRNA expression of sodium-calcium exchanger (NCX) in MPD treated CMCs was detected.
RESULTSAs compared with Group B, the degree of CMC injury was significantly milder and the activities of Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase were higher in Group C after cells were treated with MPD in concentration of 10 microg/mL and 50 microg/mL. The mRNA expression of NCX in CMCs was down-regulated after MPD treatment (P < 0.05).
CONCLUSIONMPD could maintain the low calcium internal environment in CMCs by way of protecting the membranous function of Na+ -pump and Ca2+ -pump, and influencing the Ca2+ transmembrane transportation in CMCs.
