Therapeutic effects of Di'ao Xinxuekang on myocardial ischemia-reperfusion injury in rats
10.11958/j.issn.0253-9896.2015.05.012
- VernacularTitle:地奥心血康对大鼠心肌缺血再灌注损伤的治疗作用
- Author:
Haijuan ZHENG
;
Weiting WANG
;
Chunhua HAO
;
Zhuanyou ZHAO
;
Lida TANG
- Publication Type:Journal Article
- Keywords:
myocardial reperfusion injury;
heart function tests;
cell adhesion molecules;
apoptosis;
inflammatory cytokines;
Di'ao Xinxuekang(DAXXK)
- From:
Tianjin Medical Journal
2015;43(5):491-495
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the therapeutic effect of Di'ao Xinxuekang (DAXXK) on myocardial ischemia-reperfusion injury in rats, and to explore its mechanisms. Methods The myocardial ischemia-reperfusion injury model was established by the ligation of descending coronary artery in rats. Then animals after the modeling were randomized into model group, DAXXK-d (31.5 mg/kg) group, DAXXK-g (63.0 mg/kg) group and Diltiazem (24.8 mg/kg) group. A separate sham group was used as control. The treatment group was given DAXXK once a day for 7 days. Cardiac function and cardiac configuration were measured by color Doppler ultrasound diagnostic method. Hemodynamics was measured by Millar catheter method. The arterial oxygen saturation and blood oxygen pressure were measured by i-STAT 300 blood gas analyzer. Inflammatory cytokines interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, adhesion molecules VCAM-1, ICAM-1, and apoptosis-related protein Bcl-2, Bax were detected by ELISA. Myocardial apoptosis was measured using TUNEL method. Results Compared with model group, the left ventricular fractional shortening (FS), the systolic and diastolic function were improved, and the left ventricular pressure maximum rise/ fall rates (± LVdp/dtmax) were increased, in DAXXK group. DAXXK improved lung function, increased arterial oxygen pressure and oxygen content. The inflammatory cytokines IL-1β, IL-6, TNF-α and adhesion molecules ICAM-1 and VCAM-1 were decreased in DAXXK group. The myocardial swelling and inflammatory infiltration were relieved, myocardial apoptosis was reduced, the expression of Bcl-2 protein was increased and the expression of Bax protein was decreased in DAXXK group. Conclusion DAXXK can protect myocardial ischemia-reperfusion injury, which involved in the inhibition of apoptosis and reduction of inflammatory cytokines.
