Objective To investigate the role of apelin-13, a vasoactive peptide, in rat myocardial ischemia-reperfusion injury in vivo and explore its signal transduction pathway. Methods Rats were randomly divided into control group (n=10) and Apelin-13 group (n=15), and in vivo models of rat myocardial ischemia-reperfusion injury were established. Normal saline (control group) or Apelin-13 (Apelin-13 group) was administered intravenously 5 min before reperfusion. TTC and Evan's blue staining were used to determine the infarction size (IS) and area at risk (AAR), apoptotic cells were quantified by TUNEL method, and the expression of ERK1/2 was determined by Western blotting. Results IS/AAR and apoptosis index of Apelin-13 group were significantly lower than those in control group [(38.33±12.95) % vs (52.61±11.00)% and (0.21±0.02) vs (0.31±0.05)](P <0.05). The expression of p-ERK1/2 in Apelin-13 group was significantly increased than that in control group [(1.15±0.16) vs (0.63±0.07)](P < 0.05). Conclusion Apelin-13 may protect rat hearts from in vivo ischemia-reperfusion injury, reduce infarction size and attenuate myocardial apoptosis, which may be mediated by the activation of ERK1/2 MAPK signal transduction pathway.

Objective To study the relationship between Noble grade and distribution of myocardial bridge and atherosclerosis. Methods The clinical data of 192 patients with myocardial bridge diagnosed by coronary artery angiography were retrospectively analysed.The clinical symptoms,electrocardiographic and echocardiographic findings were analysed to explore the relationship between Noble grade and distribution of myocardial bridge and atherosclerosis,and the outcomes of medical treatment were also investigated. Results The positive rate of myocardial bridge detected by coronary artery angiography was 10.2%,which was usually observed in the middle part of left anterior descending coronary artery.All the patients with grade 3 of Noble grade experienced chest pain or palpitation,43.8% had ischemic ST-T changes on electrocardiogram,and 37.5% had abnormal segmental ventricular wall on echocardiography.However,patients with Noble grade 1 and 2 did not have ischemic ST-T changes on electrocardiogram or abnormal segmental ventricular wall on echocardiography.The prevalence of atherosclerosis in proximal coronary artery of myocardial bridge was significantly higher than those of mural coronary artery and distal coronary artery(P

0.05).Compared with non-myocardial infarction group,the prevalence of normal segmental ventricular wall motion and ejection fraction in myocardial infarction group was significantly lower,while those of akinesia and paradoxical motion were significantly higher(P

Objective: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose. Methods: CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis. Results: High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (. P<0.05). Conclusions: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.