Protective Effects of Danhong Injection on Myocardial Injury Induced by Doxorubicin in Lewis Lung Canc-er Mice
- VernacularTitle:丹红注射液对多柔吡星所致Lewis肺癌小鼠心肌损伤保护作用的研究
- Author:
Yufei YAO
;
Lefeng WANG
;
Xiang LIU
;
Yuxin YAN
;
Ming CHEN
;
Wenjuan LI
;
Xuanying CHEN
- Keywords:
Lewis lung cancer mice;
Danhong injection;
Doxorubicin;
Myocardial injury;
Myocardial protection
- From:
China Pharmacist
2017;20(3):429-433
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the protective effects of Danhong injection ( DH) on myocardial damage induced by doxorubicin ( DOX) in Lewis tumor bearing mice. Methods:The model of Lewis lung cancer in mice was established by underarm injecting tumor cells, and then randomly divided into four groups:the model control group, DOX group, DH group and DH+DOX group. After the experiment, myocardial and tumor tissue were separated from Lewis tumor bearing mice, and the excised tumors were weighted. The activities of lactate dehydrogenase ( LDH) , creatine kinase ( CK) , manganese superoxide dismutase ( SOD) , catalase ( CAT) and glu-tathione peroxidase ( GPx) , and the content of malondialdehyde ( MDA) were determined by a colorimetric method. Flow cytometry was used to determine the levels of apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential (△Ψm). Re-sults:Compared with that in the model control group, a significant decrease of tumor weight was shown in both DOX group and DH+DOX group (P<0. 01). DH had no significant influence on the anticancer function of DOX. The activity of LDH and CK, and the ap-optosis in myocardium cells significantly increased (P<0. 01). Compared with DOX group, the activities of LDH and CK, and the ap-optosis significantly decreased in DH+DOX group (P<0. 01). The activities of △Ψm, SOD, CAT and GPx significantly increased (P<0.05orP<0.01). ThecontentofMDAandROSgenerationbothdecreased(P<0.01).Conclusion:DHhasnosignificantin-fluence on the antitumor effect of DOX. The combination of DH and DOX shows cadioprotective effect on the myocardial damage through improving mitochondrial antioxidant defense capacity, ameliorating oxidative stress and maintaining △Ψm homeostasis.
