| Objective:The purpose of the present study was to investigate the protective effect of Acanthopanax prescription on myocardial ischemia reperfusion injury and its mechanism, and to provide scientific basis for the development of new drugs.Methods:Twenty-four Japanese big-eared rabbits were randomly divided into control group( A group), model group( B group) and acanthopanax group ( c group ). The rabbits in each group were respectively perfused with the equivalent amount of saline and medicine(10ml/kg, a day) for seven weeks. The operation was done one hour after the last perfusion. The rabbits in each group were given a venous injection in the ear of 25% of ethyl carbamate(4ml/kg)for anesthesia and were fixed in the back, with endotracheal intubation through the central cut of the neck and the exposed heart through the cut in the center of the chest. With the pericardia cut open and the left atrial auricle (LAA) pliered and turned outside slightly, the rabbits in B and C group underwent 30 minutes of left anterior descending coronary arterial ligation with thread at the point of 2-3mm under LAA(The rabbits in A group were threaded only, not ligated), and then had 3 hours of coronary arterial perfusion. Blood samples were extracted from the artery 3 hours after perfusion to measure its index of hemorheology. The rabbits were instantly killed after blood extraction and 100mg of myocardial tissues was extracted to make plasma for measuring SOD, GSH-Px activity and MDA in rabbits with automatic biochemical analyzer and analyzing Bc1-2 and Bax expression in myocardial tissues of rabbits with SABC method. ECG(II) was given 5minutes, 20minutes and 40minutes before and after ligation and 1hour and 3 hours of perfusion to determine and compare the changes of ST at each stage prior or posterior to ischemia.Results:1 Model group had a higher level of MDA and lower level of SOD and GSH-Px activity, with remarkable difference, as compared to control group. Acanpathopanax prescription group had lower level of MDA while SOD and GSH-Px activity were obviously increased compared with model group.2 Model group significantly had a lower level of NO and NOS activity than that of control group and acanpathopanax prescription group, which indicated that acanpathopanax prescription could greatly increase the growth of NO and NOS activity of myocardial tissues.3 There was significant difference between model group and control group in blood-determination of low cut, high viscosity and plasma viscosity, which proved the preparation of the models successful. But acanpathopanax prescription could remarkably decrease blood-determination of low cut, high viscosity and plasma viscosity in rabbits with acute IRI.4 Acanpathopanax prescription group had a higher level of Bc1-2 and lower level of Bax than that of model group, with statistical meaning while there was no difference about the level of Bc1-2 and Bax in control group.Conclusions:1 Acanpathopanax prescription can remarkably reduce the index of blood viscosity and improve the slow blood flow and microcirculation of myocardial tissues and level of ST, thus protecting ischemia-reperfusion heart.2 Acanpathopanax prescription can significantly reduce MDA level of ischemia reperfusion myocardial tissues and increase NO, SOD,GSH-Px and NOS activity. It plays a remarkable role in clearing Oxygen free radicals and protecting myocardial tissues.3 Acanpathopanax prescription can prompt the expression of Bc1-2 and inhibit Bax expression and the apoptosis of myocardial cells, which shows that the protective effect of acanpathopanax prescription is related to the regulation of Bc1-2 and Bax expression. |
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