[The dynamic expression changes of myocardium p-p38MAPK, NF-κB and COX-2 in rats after an exhausted exercise].

OBJECTIVE: To observe the dynamic expression changes of p38 mitogen-activated protein kinase (p38MAPK), nucler facter kappa B (NF-κB) and cyclooxygenase-2 (COX-2) in myocardial tissue after an exhausted exercise and study the impact of p38MAPK, NF-κB and COX-2 on its myocardial damage. METHODS: Sixty Wister male rats were randomly divided into the control group (n = 10) and the exhausted exercise group (n = 50). Then the exhausted exercise group was further divided into 5 subgroups, namely 0 h, 3 h, 6 h, 12 h, 24 h after an exhausted exercise (n = 10). The myocardial injury animal model was set up by using an exhausted swimming exercise and the expression of p-p38MAPK, NF-κB and COX-2 were examined by Western blot. RESULTS: Compared with the control group, the expression of p-p38MAPK were increased significantly (P < 0.01) in all the groups and the 3 h group was the highest( P < 0.01); The expression of NF-κB were increased significantly (P < 0.05) in all the groups but 0 h P > 0.05) and the 6h group was increased significantly compared with the other groups( P < 0.05); The expression of COX-2 were increased significantly( P < 0.05) in all the groups but 0 h and the 24 h groups was increased significantly compared with the other groups(P < 0.05). CONCLUSION: p38MAPK was activated in an acute exhausted exercise, p-p38MAPK may play an important role in modulating NF-κB and COX-2 expression and mediating the exhausted exercise induced myocardial damage.

Methylamine irisolidone, a novel compound, increases total ATPase activity and inhibits apoptosis in vivo and in vitro.

We propose to further research the protective effect of MMI on myocardium ischemic rat model and H9c2 cells that underwent cell apoptosis induced by hypoxia. We established the myocardium ischemic rat model via the cardiac surgical procedures in vivo and treated the model rats with different concentration of MMI. In vitro, with the pretreatment of MMI for 12 h in the model of Na2S2O4-induced hypoxia injury, the H9c2 cells viability was determined by MTT assay. We found that MMI had significantly improved cardiac function of the myocardial ischemia, and significantly decreased the reactive oxygen species level. The expression of P53, Bcl-2, Bax, and caspase-9 was also induced by MMI. In vitro study revealed a concentration-dependent increase in cell viability associated with MMI pretreatment. Annexin V-FITC and PI staining results showed that MMI had a preventive effect on hypoxia-induced apoptosis in H9c2 cells. MMI also inhibited the mitochondrial membrane potential decrease and increased total ATPase activity during hypoxia in H9c2 cells. In conclusion, MMI can enhance the cardiac function in myocardial ischemic rat and increase cell viability and attenuate the apoptosis in H9c2 cells induced by hypoxia, which was associated with inhibiting MMP decreasion and increasing total ATPase activity.