Experimental Study Of Wutou Chishizhi Tang Inhibiting Cell Apoptosis Of Acute Myocardial Infarction In Model Rats

Purpose:By studying the drug effect of WTCSZT to apoptosis of acute myocardial infarction in model rats,to investigate the internal mechanism of WTCSZT to inhibit apoptosis in acute myocardial infarction.Method:60 healthy male Wistar rats with a weight of 250~320g were selected.Except for the blank group,all the other groups were subjected to high ligation of the left anterior descend-ing coronary arteries to duplicate acute myocardial infarction in model rats.After making the model successfully,the rats were randomly divided into 6 groups: the blank group,the model group,the WTCSZT low dose group,the WTCSZT middle dose group,the WTCSZT high dose group and the urokinase group.The rats in the blank group and the model group were freely fed and drinking water.Each rat in the WTCSZT low,middle and high dose group was treated by means of intragastric administration.Each rat of the urokinase group was given at the dosage of 50 thousand until per milliliter in the way of the intraperitoneal injection every day.The treatment would continue one week.Until the 8th day,those rats were executed to draw materials.The mortality of rats in each group was calculated by recording the number of rats died after making model and before drawing materials.The contents of troponinT,creatine kinase isoenzyme,aspartate amino transferase and alanine amino transferase in blood serum were measured with 6A Semi automatic biochemical analyzer.The changes of cardiac muscle cell in each group were observed by hematoxylin-eosin staining.Detect the protein expression level of Bcl-2 and Bax gene by Western Blot.Result:1.Except for the normal group,the mortality of the rats in each group was about 20%~40% after making model and about 0%~10% before drawing materials.2.Compared with the blank group,the content of CTNT,CK-MK,AST and ALT in blood serum was remarkably increased in the model group(P<0.01),which had statistical sense.Compared with the model group,the content of CTNT(P<0.01),CK-MK(P<0.05),AST(P<0.01)and ALT(P<0.01)in blood serum was clearly decreased in the WTCSZT low dose group,the WTCSZT middle dose group,the WTCSZT high dose group and the urokinase group,whichhad statistical sense.Compared with the urokinase group,there are no significant difference in the content of CTNT,CK-MK,AST and ALT in the WTCSZT low dose group,the WTCSZT middle dose group and the WTCSZT high dose group.3.Compared with the blank group,the cell nuclei of rats were broken,a large number of inflammatory cells were infiltrated,many red cells were gathered and the myocardial fibers were seriously separated in the model group.Compared with the model group,the pathological changes of cardiac muscle cell improved markedly in the WTCSZT low dose group,the WTCSZT middle dose group,the WTCSZT high dose group and the urokinase group.The accumulation of red blood cells and the distribution of partial inflammatory cells existed evidently in the WTCSZT low dose group,but cardiac muscle fibers arranged orderly.the accumulation of red blood cells evidently declined,the inflammatory cells were obviously reduced.,cardiac muscle fibers arranged orderly in the WTCSZT middle dose group,the WTCSZT high dose group and the urokinase group.Compared with the urokinase group,there was no sharply difference in the WTCSZT low dose group,the WTCSZT middle dose group and the WTCSZT high dose group.4.Compared with the blank group,the expression of Bcl-2 obviously declined(P<0.01)and the expression of Bax significantly increased in the model group(P<0.01).Compared with the model group,the expression of Bcl-2 and Bax in the myocardial tissue was no statistically significant in the WTCSZT low dose group.The expression of Bcl-2 was notably up-regulated in the WTCSZT middle dose group,the WTCSZT high dose group and the urokinase group(P<0.01).The expression of Bax was clearly down-regulated in the WTCSZT middle dose group(P<0.05),the WTCSZT high dose group(P<0.01)and the urokinase group(P<0.01).Compared with the urokinase group,the expression of Bcl-2 was obviously different in the WTCSZT low dose group and the WTCSZT middle dose group(P<0.01),but no different in the WTCSZT high dose group.The expression of Bax was obviously different in the WTCSZT low dose group,but no significant difference in the WTCSZT middle dose group and the WTCSZT high dose group.Conclusion:1.The low,middle and high dose of WTCSZT can effectively reduce the degree of myocardial injury in model rats.There was no significant difference with urokinase in thetreatment.This suggests that WTCSZT has a therapeutic effect on acute myocardial infarction in model rats.2.The middle and high dose of WTCSZT can inhibit the myocardial apoptosis of acute myocardial infarction in model rats,especially in high dose.There was no difference between the high dose of WTCSZT and urokinase in the treatment.3.The internal mechanism of WTCSZT to inhibit the myocardial apoptosis of acute myocardial infarction is related to the up-regulation of the expression of Bcl-2 and the down-regulation of the expression of Bax.