Objective Astrgaloside Ⅳ derivative (ASId) is one of Astragaloside Ⅳ (ASI) derivatives with higher water-solubility and may have more druggability than ASI. The present study aims at observing the effects of ASId on cardiovascular parameters in chronic heart failure in rats. Methods Using echocardiographic and haemodynamic measurements, the effects of ASId on congestive heart failure (CHF) induced by ligation of the left coronary artery in rats were investigated.ventricle (LV) pressure (dp/dt) in ASId treated groups were significantly increased. Both LV volumes in diastole and in systole were decreased significantly after ASId treatment, accompanied with a trend towards normalization of relative stress. ASId treatment also inhibited compensatory hypertrophy of depressed heart. Conclusion ASId could improve cardiac functions and inhibite compensatory hypertrophy and LV remodelling, which suggests the possibility of ASId as a new therapeutic drug for the treatment of CHF.

Objective The astragaloside Ⅳ(ASI)has been proved to play an important role in protecting against cell death on cardiovascular diseases.This study aims to investigate the effect of the astragaloside derivate.(ASId)on confronting oxidative stress and hypertrophy in myocardial cells.Methods Following exposure embryonic rat cardiac H9c2 cells to hydrogen peroxide(H2O2)and angiotensin Ⅱ for developing oxidative stress and hypertrophy,ASId at final concentrations(0.1,1,and 10 μmol/L)was added to study its role in protecting cardiomyocytes by biochemical detection and cell size measurement In addition,the mitochondrial permeability transition pore(mPTP)opener atractyloside(20 μmol/L)and inhibitor cyclosporin A(CSA)(1 μmol/L)were employed to investigate the possible mechanisms for anti-oxidation.Results ASId at 1 and 10 μmol/L in cultures suppressed oxidative stress at different degrees,which induced the decrease in LDH activity and MDA content,and also the increase in SOD activity in comparable with the model group; The mPTP opener atractyloside and inhibitor CSA weakened and strengthened the role of ASId,respectively.ASId at 10 μmol/L inhibited cell hypertrophy,and the cell diameter,surface area,and protein content were all decreased in comparable of those cells in model group.Conclusion ASId is involved in the cytoprotective effects on oxidative stress through a pathway mediated by mPTP,and also has a protective effect against hypertrophy.

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.

Objective To study the application of 99Tcm in rabbit cerebral thromboembolic stroke and thrombolysis effect of recombinant tissue plasminogen activator (rt-PA).Methods The 0.5 mL radioactive pertechnetate sodium (specification:5 mCi/2mL and radiation intensity 92.5 MBq/mL) was combined with 30 μL stannous chloride (5 mg/mL),and the 20 μL mixture was joined to whole blood,red blood cells,and plasma for labelling.Then 50 μL CaCl2 (0.5 mol/L) and bovine thrombin (50 IU/mL) were doped in mixture,and rapidly sucked into a polyethylene plastic pipe (PE80).Thrombus was formed for 2 h at 37 ℃ and cut into small pieces of 10 mm.Autologous blood clots combined with 99Tcm from external carotid artery were injected to internal carotid artery of rabbit,the radioactivity (counts per minute,CPM) was measured by gamma counting instrument,and the improvement of rt-PA 4.5 mg/kg (clinical equivalent dose) on this model was observed.Results After thromboembolism,CPM increased approximately by (5.1 ± 1.3) times,which suggested that the model was reliable.The rt-PA 4.5 mg/kg had significant progressive thrombolysis effect.Conclusion 99Tcm tracer technology could be applied to rabbit cerebral stroke model,which is stable and reliable