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Effects of Pinocembrin Pretreatment on Connexin 43 (Cx43) Protein Expression After Rat Myocardial Ischemia-Reperfusion and Cardiac Arrhythmia
背景与目的
心肌梗死常诱发心律失常，缺血再灌注可加重心肌损伤。有研究表明乔松素可缓解脑缺血和降低心肌梗死面积。因此，本研究通过建立大鼠心肌I/R模型并评估乔松素对室性心律失常和缝隙连接蛋白Cx43表达的影响。
方法
将雄性SD大鼠随机分为假手术组、模型组和乔松素(30 mg/kg)预处理组（n=15）。结扎左冠状动脉前降支30 min建立I/R模型。乔松素预处理组于术前10min经静脉注入乔松素。观察并记录缺血前10min、缺血后10min、再灌注30、60、120min的 HR、MAP、RPP和心率失常情况。利用ELISA法测定血浆CK-MB和cTnI水平，随后进行HE染色，用光谱测定法检测Na+-K+ ATP酶和Ca2+-Mg2+ ATP酶的水平，IHC法测定Cx43的表达，Western blot检测Kir2.1蛋白的表达情况。
结 果
模型组大鼠HR、MAP和 RPP明显低于假手术组，乔松素预处理组血浆指数较高。在模型组和乔松素预处理组中，心率失常指数、CK-MB和 cTnI含量较高,而 Na+-K+ATP酶、 Ca2+-Mg2+ATP酶、 Cx43和 Kir2.1 蛋白表达明显降低 (P<0.05)。
结 论
乔松素通过增强Na+-K+ATP酶和 Ca2+-Mg2+ATP酶的活性，上调Cx43 和 Kir2.1蛋白的表达从而缓解I/R大鼠的室性心律失常。
原始文献摘要
Zhang P, Xu J, Hu W, et al. Effects of Pinocembrin Pretreatment on Connexin 43 (Cx43) Protein Expression After Rat Myocardial Ischemia-Reperfusion and Cardiac Arrhythmia [J] . Med. Sci. Monit. 2018 Jul 19 ;24DOI：10.12659/MSM.909162
Abstract
Background: Cardiac infarction frequently leads to arrhythmia and ischemia/reperfusion (I/R) aggravates cardiac injury.
Pinocembrin can resist cerebral ischemia and decrease cardiac infarction area. This study thus generated a rat myocardial I/R model to assess the effect on ventricular rhythm and expression of gap junction connexin (Cx43).
Material/Methods: Male SD rats were randomly assigned into sham, model, and pinocembrin (30 mg/kg) pretreatment groups
(N=15 each). The I/R model was generated by ligation of the left anterior descending coronary artery for 30 min. The pinocembrin group received intravenous injection 10 min before surgery. Heart rate (HR), mean artery pressure (MAP), rate pressure product (RPP), and arrhythmia were observed at 10 min before ischemia, 30 min after ischemia, and at 30, 60, and 120 min after reperfusion. ELISA was used to assess serum CK-MB and cTnI levels.Na+-K+ATPase and Ca+-Mg2+ATPase levels were quantified by spectrometry, followed by HE staining, IHC approach for Cx43 expression, and Western blot for Kir2.1 protein expression.
Results: Model rats had significantly lower HR, MAP, and RPP than in the sham group, and the pinocembrin pretreatment group had higher serum indexes. Arrhythmia index, CK-MB, and cTnI were higher in the model and pinocembrin groups, while Na+-K+ATPase, Ca+-Mg2+ATPase, Cx43, and Kir2.1 proteins were lower (p<0.05).
Conclusions: Pinocembrin alleviated ventricular arrhythmia in I/R rats via enhancing Na+-K+ATPase and Ca+-Mg2+ATPase activity and upregulating Cx43 and Kir2.1 protein expression.
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