| Objective: Target and mechanism of the protective effect of MAPKs signaling pathway on the protective effect of myocardial ischemia in rats.Methods:The(SBPG Taigao Thailand to change to record 100 healthy clean grade male SD rats, to ligate the coronary artery to the left anterior descending branch(sham operation control group only wear line ligation) formation of myocardial ischemia injury animal model before and after ligation of lead II ECG ST segment changes and left ventricular anterior wall expands outward cyanosis modeling success with ischemic injury model of rat into 64, then randomly divided into 6 groups: model group(I / R), sham operation group(sham), heartache Thai low dose group(LDG), heartache dose group(MDG), heartache dose group(HDG) and musk Baoxin Pill group. Began after the establishment of the model, every morning to rats by intragastric administration, drug group according to body surface area), reduced dosage of epigenetic:heartache Thai LDG, MDG, HDG respectively in accordance with the 0.432g/ml, 0.864g/ml,1.728g/m gavage, SBPG according to 1.414g/ml(dissolved in distilled water) intragastric administration and other groups to give such as volume of distilled water. 1 times /d, 2 weeks of common medicine. Observation of plasma CK, LDH, SOD, MDA concentration after the experiment; the pathological changes of ischemic myocardial structure; at the same time, starting from the MAPKs signal pathway, detect the expression of phosphorylated ERK1, P38 protein,JNK.Results: Compared with I / R, decreased compared with I / R(1) treatment for 2 weeks, and sham,I / R plasma CK, LDH and MDA concentration increased significantly(P < 0. 01), plasma concentrations of SOD decreased(P < 0.05); and SBPG obviously rat plasma CK and LDH and MDA concentration significantly increased SOD concentration(P < 0.01); and I / R group,heartache Thai HDG obviously decreased in rat plasma CK, LDH and MDA concentration significantly increased the concentrations of SOD(P < 0.01); and, heartache Thai MDG can significantly decrease the plasma CK, LDH and MDA concentration(P < 0.01), and significantly increased the concentrations of SOD(P < 0. 01), heartache Thai LDG can reduce LDH, MDA concentration(P < 0. 05), elevated plasma SOD concentration(P < 0. 05).(2) after 2 weeks of treatment, compared with I/R, the low, middle and high heart Thailand and musk heart pill group p38, expression of P-JNK protein significantly decreased(P < 0.01), while the expression of P-ERK increased(P < 0.01);(3) after 2 weeks of treatment, compared with I/R, LDG, MDG,HDG, SBPG, SHAM expression of myocardial P-p38 and HDG, and MDG are respectively two two LDG, P-p38 expression decreased, SHAMP-p38 expression less(P < 0.01);(4) after 2 weeks of medication, in various drug groups, namely LDG, MDG, HDG and SBPG were compared, we can see that the induction effect of Thailand, heartache, in each group the expression of P-ERK was increased(P < 0.05 or P < 0.01);(5) after 2 weeks of treatment, the treatment group to reduce myocardial injury than I/R in varying degrees, reduce the infiltration of inflammatory cells, edema;(6) 2 weeks after treatment, SHAM group had no infarction Region, and the I / R group compared to the group, the myocardial infarction area has shrunk, the difference is statistically significant(P< 0.01), compared with the LDG group, MDG, HDG, SBPG group is infarct size is reduced, and the difference is statistically significant(P < 0.01), and MDG, HDG, SBPG group difference between the three had no statistical significance(P > 0.05).Conclusion:HDG can effectively inhibit the injury of myocardial cells in rats with acute myocardial ischemia. One of the mechanisms may be related to the activation of MAPKs signal transduction pathway. Therefore, MAPKs signaling pathway is involved in the molecular mechanism of myocardial injury in rats induced by Thailand heart function of acute myocardial ischemia. And the effect of MDG and HDG was significantly better than that of LDG. |
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