The Pxpression Of P38Mitogen Activated Protein Kinases In Post-infarcted Patients’ Peripheral Blood Mononuclear Cells.

Objective We all know that the myocardial inflammatory reaction、increasing the work loadof residual myocardial cells and a cariety of humoral factors changing after acute myocardialinfarction(AMI) can result in cardiac output in patients with a sharp decline and causeseriousconsequences. We collected acute myocardial infarction in patients with peripheralvenous blood samples,and explore the relationship between p38and inflammation..Methods1. Case collection: We collected the40AMI patients form the Ningxia medicalUniversity General Hospital or First People’s Hospital of Yinchuan city as the experimentalgroup. The experimental group were subdivided into3hours group、6hours group、12hourgroup and24hour group; We also collected20healthy adults as a healthy control group.Regardless of the experimental group members or members of the control group, we extracttheir peripheral venous blood9ml-10ml afer its members agreed and sent to the laboratory forchecking.2.The cleavage of mononuclear cells and total protein extraction: We put the EPcontaining monocytes intu centrifuge. After3000rmp/min for5minutes,we can see the whitemonocyte at the bottom of EP. Then we removed supermatant and filled the PBS into the EPto blowing the monocytes. After this process,3000rmp/min for5minutes again and repeated2-3times we can collect the pure monocytes in two EP tube. After three EP number1、2and3,The Trizol reagent was added on the1stEP tube for lysising mononuclear cells and added2、3EP tube protein extracts200μl. Then we put the tubes on the shaker after15minutes. After weshaking, we put them in centrifuge, the supermatant was collected after14000rmp/min for15minutes. So the p38α or p38in blood mononuclear can be detected by fluorescencequantitative PCR and western blot. The TNF-α content in serum measured by ELISA. Thecombination of these data can study the expression of p38protein in acute myocardial infarction in patients with peripheral blood mononuclear cells and its expression relationshipwith TNF-α.Result:1. Fluorescence quantitative PCR: The p38α gene expression in MI group wasdifferent from healty control group. There was a significant beteen two groups (F=54.70, P=0.000<0.05); On this basis, we thought that the healthy controls patients p38α gene expressionwas1, and after the occurrence of acute myocardial infarction of3、6、12and24hours, thep38α gene expression in peripheral blood mononuclear cells increased1.196、1.429、1.673and1.165times than that of healthy control group.2. Western blot: The total p38proteinbetween four subgroups and healthy controls were not statistically significant (F=1.763, P=0.149>0.05); But the phosphorylation of p38protein between the healthy control group andfour subgroups were statistically significant (F=1857.56, P=0.000<0.05); This charging afteracute myocardial infarction shows that total p38protein in monocytes was not significantchanges but the phosphorylation of the p38protein were more obvious changes. This meansthat the p38protein’s expression was gradually increased and reached a peak after12hours inacute myocardial infarction, followed by phosphorylation of p38protein levels graduallydeclined;3.ELISA checking serum TNF-α concentration: The difference of serumconcentration of TNF-α between the MI group and health control group was statisticallysignificant (F=360.25, P=0.000<0.05); the difference in the four subgroups were stillstatistically significant (P=0.000<0.05). These can prompt that after occurrence of acutemyocardial infarction (24hours), the serum TNF-α concentration were gradually increased ifwe did not give patients treatment. Conclusion:1. Patients with acute myocardial infarctionwithin12hours after their blood mononuclear cells p38α gene sustained activation, theexpression continued to increase, its function may not increase the level of p38proteintranslation, but the implementation of a potential signal transduction guide function.2.Patients with acute myocardial infarction within24hours, the expression of total p38proteinin monocytes in their blood was no significant changing but the phosphorylated p38protein’s expression levels continued to increase in myocardial infarction12hours, its function is toactivate its downstream signaling molecules and play a vital role in the process ofdeterioration of cardiac function after myocardial infarction;3.Patients with acute myocardialinfarction within24hours, if we do not give any treatment, the serum concentrations ofTNF-α in will continue to rise, this change may be caused by phosphorylated p38protein anda number of cell stress injury.