Effect of sevoflurane on adriamycin-induced damage to primary neonatal rat cardiomyocytes
10.3760/cma.j.issn.0254-1416.2012.12.016
- VernacularTitle:七氟烷对阿霉素诱导新生大鼠原代心肌细胞损伤的影响
- Author:
Xin HAN
;
Lihua FAN
;
Xianghong LU
- Publication Type:Journal Article
- Keywords:
Anesthetics,inhalation;
Doxorubicin;
Myocytes,cardiac
- From:
Chinese Journal of Anesthesiology
2012;(12):1474-1476
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of sevoflurane on adriamycin-induced damage to primary neonatal rat cardiomyocytes.Methods Primary neonatal rat cardiomyocytes were isolated from Sprague-Dawley rats (within 24 h after birth) and cultured in DMEM liquid culture medium.The cells were seeded in 96-well plates (200μl/hole) or 6-well plates (2 ml/hole) with a density of 5 × 104/ml and randomly divided into 4 groups (n =24 each):control group (group C),adriamycin group (group A),sevoflurane group (group S) and adriamycin + sevoflurane group (group AS).In groups A and AS,adriamycin 1 μmol/L was added to the cultured medium,the equal volume of PBS was added instead in groups C and S,and the cells were then incubated for 24 h.The cells were exposed to 2.4％ sevoflurane for 2 h starting from 24 h of incubation in groups A and AS.The cell viability,concentrations of cTnI and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in the culture medium,and expression of Bax and Bcl-2 were detected 2 h after the end of exposure to sevoflurane.The Bax/Bcl-2 ratio was calculated.Results Compared with group C,the cell viability and expression of Bcl-2 were significantly decreased,while the concentrations of cTnI and NT-proBNP in the culture medium,expression of Bax and Bax/Bcl-2 ratio were significantly increased in group A,and the cell viability was decreased in group AS (P ＜ 0.05).The expression of Bcl-2 was significantly higher and the concentrations of cTnI and NT-proBNP in the culture medium,expression of Bax and Bax/Bcl-2 ratio were significantly lower in group AS than in group A (P ＜ 0.05).Conclusion Sevoflurane can reduce adriamycin-induced damage to primary neonatal rat cardiomyocytes and inhibition of cell apoptosis is involved in the mechanism.
