科研之友
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摘要
Objective: To investigate the protective effect and mechanism of swimming on cardiac microvasculature in rats with myocardial infarction (MI). Method: Eighty Wistar rats (160- 180g) were randomly divided into 4 groups: sham operation group, model group, swimming group, and Diaoxinxuekang group, with 20 in each group. The MI model was prepared by ligating the main coronary artery of the left coronary artery. The operation in the sham operation group was identical to that in the model group except that the coronary artery was not ligated. Fourteen days after the completion of MI model preparation, the swimming training time of rats in the swimming group was 8 weeks. Cardiac function and electrocardiogram were detected by echocardiography system and BL-420F biological function experiment system. Cardiac microvascular density was measured by gel ink assay. The protein expressions of Caspase-3, PECAM-1, PI3K, p-PI3K, AKT, p-AKT, eNOS and p-eNOS were detected by Western blot. The content of NO in the heart tissue was measured by the kit. Result: ST segment in the swimming group or Diaoxinxuekang group was significantly lower than that in the model group (P=0.002, P=0.000). Small animal ultrasound results showed that LVEF value in the swimming group or Diaoxinxuekang group was significantly higher than that in the model group (P=0.038, P=0.003, LVFS value in the swimming group or Diaoxinxuekang group was significantly higher than that in the model group (P=0.028, P=0.000). HE results showed that swimming and Diaoxinxuekang significantly reduced the infarct area of the model rats. Western Blot results showed that the expression of Caspase-3 protein in the swimming group or Diaoxinxuekang group was significantly lower than that in the model group (P=0.035, P= 0.000). In addition, the cardiac microvascular density in the swimming group or Diaoxinxuekang group was significantly higher than that in the model group (P=0.015, P=0.000). Meanwhile, Western Blot results showed that the protein expression level of PECAM-1 in the swimming group was significantly up-regulated compared with that in the model group (P=0.025). The expression level of p-PI3K in the swimming group was significantly up-regulated compared with that in the model group (P=0.013). The protein expression of p-AKT in the swimming group was significantly higher than that of the model group (P=0.02). The protein expression of peNOS in the swimming group was significantly increased compared with that in the model group (P=0.02).In addition, NO content in the swimming group was significantly higher than that in the model group (P=0.011). Conclusion: Swimming can increase cardiac microvascular shear stress, activate PECAM- 1/PI3K/AKT/eNOS signaling pathway, promote NO release, increase cardiac microvascular perfusion in infarcted area, inhibit cardiac myocyte apoptosis, and thus improve the prognosis of MI rats.
