Effects of sarcoplasmic reticulum Ca2+-ATP enzyme in myocardial damage due to daunorubicin in rats
10.3760/cma.j.issn.1008-5734.2014.03.010
- VernacularTitle:肌浆网Ca2﹢-ATP酶在柔红霉素致大鼠心肌损伤中的作用
- Author:
Lingjuan LUO
1
;
Xinmei XIE
1
;
Wenting HE
1
;
Fanye ZENG
1
;
Hongliang ZHANG
1
Author Information
1. 新疆医科大学附属中医医院肿瘤二科,乌鲁木齐,830000
- Publication Type:Journal Article
- Keywords:
Daunorubicin;
Sarcoplasmic reticulum calcium-transporting ATPases;
Rats
- From:
Adverse Drug Reactions Journal
2014;(3):159-162
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of in myocardial damage due to daunorubicin (DNR)in rats. Methods SD rats were divided into the control group and the DNR group using a random-digital table,each group comprised 15 rats. The rats in the DNR group received intraperitoneal injection of daunorubicin 3. 5 mg/kg once a week for 4 weeks. The rats in the control group received intraperitoneal injection of same volume of 0. 9% sodium chloride solution once a week for 4 weeks. The rats′behavior changes in the 2 groups were observed. The electrocardiographic examination,expression of sarcoplasmic reticulum Ca2﹢-ATP enzyme( SERCA2a)and histopathological test were performed at the end of 1,3 and 4 weeks of the experiment on 5 rats in the 2 groups,respectively. Results The subacute myocardial injury rat model could be reproduced by DNR intraperitoneal injection. The rats in the DNR group developed lassitude,drumble and drowsiness from the second week. The control group rats′activity, body weight and feeding were normal. The electrocardiographic examination in DNR group showed the following results:voltage of QRS wave decreased by more than 30% compared with the normal,ST segment elevation,and P wave peaked. Myocardial tissue histopathological examination revealed turbid cytoplasm, vacuolation,disordered arrangement of muscle fiber,and broadened fiber gaps. The expression of SERCA2a were moderately positive in both groups at the end of the first week. The expression of SERCA2a were weakly positive in the DNR group at the end of the third and fourth weeks. The number of SERCA2a positive cells in the DNR group at the end of the third and fourth weeks was significantly less than that in the control group at the same time points[(42. 2 ± 1. 2)vs(65. 30 ± 1. 6),(35. 2 ± 6. 0)vs(66. 7 ± 1. 5),all P﹤0. 05]. Conclusion DNR may inhibit the expression of SERCA2a in myocardial tissue and it may be one of the mechanisms of DNR′s myocardial toxicity.
