Protection of ultra-filtration extract from Danggui Buxue Decoction on oxidative damage in cardiomyocytes of neonatal rats and its mechanism.
- Author:
Ying-Dong LI
1
,
2
;
Yan-Hua MA
;
Jian-Xiong ZHAO
;
Xin-Ke ZHAO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Caspase 3; genetics; metabolism; Cell Survival; drug effects; Creatine Kinase; metabolism; Cytoprotection; drug effects; Drugs, Chinese Herbal; pharmacology; Gene Expression Regulation; drug effects; HSP70 Heat-Shock Proteins; genetics; metabolism; L-Lactate Dehydrogenase; metabolism; Malondialdehyde; metabolism; Mice; Myocardium; pathology; ultrastructure; Myocytes, Cardiac; drug effects; enzymology; pathology; Oxidative Stress; drug effects; Peroxidase; metabolism; Phytotherapy; Plant Extracts; pharmacology; RNA, Messenger; genetics; metabolism; Rats; Reverse Transcriptase Polymerase Chain Reaction; Superoxide Dismutase; metabolism; Ultrafiltration
- From: Chinese journal of integrative medicine 2011;17(11):854-859
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate whether the administration of the ultra-filtration extract from Danggui Buxue Decoction (EDBD) was able to protect cardiomyocytes from oxidative injury of rats induced by hydrogen peroxide (H(2)O(2)) and its potential mechanism.
METHODSMyocardial cells from 1- to 2-day-old neonatal rats were cultured in Dulbecco's modified Eagle's medium low-glucose and Ham's F12 medium (1:1), and the cellular injury was induced by H(2)O(2). The ultra-filtration extract mixture from Angelica sinensis and Hedysarum polybotrys was given in three doses of 3.75, 7.5, and 15 mg/mL. Morphological changes of cardiomyocytes were observed by microscope. Survival rate of myocardial cells was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The cardiomyocyte damages were estimated by detecting lactate dehydrogenase (LDH) and creatine kinase (CK) releases in the medium, superoxide dismutase (SOD) activities, and intracellular malondialdehyde (MDA) and myeloperoxidase (MPO) contents. The levels of caspase-3 and heat shock protein 70 (hsp70) mRNA expression in cardiomyocytes were measured by reverse transcription polymerase chain reaction.
RESULTSThe EDBD could protect the cardiomyocytes from H(2)O(2) injury in a dosedependent manner (3.75, 7.50, and 15.00 mg/mL). The EDBD could significantly decrease LDH and CK leakages and intracellular MDA and MPO contents, increase SOD activity, up-regulate hsp70 expression, and down-regulate caspase-3 expression.
CONCLUSIONThe EDBD has protection on cardiomyocytes injured by H(2)O(2) through improving cell antioxidant ability, up-regulating hsp70 expression, and inhibiting caspase-3 activity.
