| Objective:(1)Acute myocardial infarction was induced by ligation of the left anterior descending branch of the rat coronary artery,and evaluates the effectiveness of the model.(2)By preparing a model of myocardial infarction,we explored the effects of type A kinase anchor protein 5(AKAP5)-mediated β-adrenergic receptors(β-ARs)on cardiac function in rats after myocardial infarction and its possible mechanism.(3)By preparing a model of myocardial infarction,we explored the effect of type A kinase anchor protein 5(AKAP5)on β-adrenergic receptor(β-AR)on myocardial hypertrophy in rats after myocardial infarction and its possible mechanism.Methods:(1)The healthy adult SD rats were anesthetized with 10% chloral hydrate.After routine intubation,they were connected to the ventilator and the parameters of the ventilator were adjusted to maintain the stability of vital signs.Open the thorax to expose the heart,cut the pericardium to find the coronary arteries,and ligate the left anterior descending branch.The electrocardiogram changes before and after the operation were recorded by a multi-channel physiological instrument.(2)Adult rats of similar weight were randomly divided into sham operation control group(sham group),myocardial infarction model group(model group),metoprolol group(Metoprolol group).The model group and the metoprolol group were modeled by conventional myocardial infarction.The control group only opened the chest cavity and pericardium without ligating the coronary arteries.Normal feeding was performed for 4 weeks,and drug intervention was performed for 8 weeks.M-mode echocardiography was used to evaluate the cardiac function of rats in each group,and Western Blot method was used to detect changes in the expression levels of AKAP5,PLN,and p-PLN.interaction.(3)The cardiac hypertrophy of each group was evaluated by the ratio of heart to weight(HW / BW),and Western Blot was used to detect the changes in the expression levels of COL1,COL3,NFATc3/p-NFATc3,and GATA-4.The precipitation method was used to detect the interaction between AKAP5 and PP2 B.Results:(1)After the anterior descending coronary artery is ligated,the ischemia of the left ventricle and the apex can be seen to be white.At the same time,the ECG showed that the ST-T segment of lead Ⅱ was significantly elevated after the ligation.(2)Echocardiography: Compared with the control group,the cardiac ejection fraction(EF value)of the model group and the metoprolol group were significantly reduced(P <0.05);compared with the metoprolol intervention group,the cardiac ejection rate The score was significantly higher than the model group(P <0.05).When myocardial insufficiency decreased after myocardial infarction,the content of AKAP5 and the relative expression of p-PLN/PLN were lower than those in the control group(P <0.05).After metoprolol intervention,the AKAP5 content and the relative expression of p-PLN/PLN were higher than those of the model group(P <0.05).In the co-immunoprecipitation system using AKAP5 as the target protein,the expression of PKA and PLN proteins was detected.(3)When myocardial hypertrophy occurred after myocardial infarction,the heart-to-body weight ratio(HW / BW)and the expression of COL1 and COL3 were increased compared with the control group(P <0.05);after the metoprolol intervention,the heart / weight ratio The expression levels of COL1 and COL3 were decreased compared with the model group(P <0.05).The expression levels of NFATc3/p-NFATc3 and GATA-4 in the model group and metoprolol group were significantly increased compared with the control group(P <0.05),and NFATc3/p-NFATc3,GATA-4 in the metoprolol group were significantly increased compared with the model group The expression level was decreased(P <0.05).In the co-immunoprecipitation system with AKAP5 as the target protein,the expression of PP2 B protein was detected.Conclusion:(1)Ligation of the left anterior descending coronary artery can effectively prepare a rat model of acute myocardial infarction.(2)AKAP5 may mediate β-AR to regulate cardiac function after myocardial infarction in rats.(3)AKAP5 may mediate β-AR to regulate myocardial hypertrophy in rats after myocardial infarction. |
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