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目的:探讨杨梅素对小鼠梗死后心肌重塑和心力衰竭的影响及调控机制。方法:结扎左冠状动脉前降支建立心肌梗死的模型,将雄性C57/BL6J小鼠随机分为3组(每组20只):假手术组、心肌梗死组、心肌梗死+杨梅素组。心肌梗死+杨梅素组给予杨梅素250 mg/kg/d灌胃,假手术组和心肌梗死组给予同体积5%羧甲基纤维素钠灌胃。药物治疗1月后,小鼠心脏超声检测心功能;Masson染色评估胶原容积分数(collagen volume fraction,CVF);电镜检测心肌线粒体损伤;Western blot检测p-Mst1、LC3和p62的表达。结果:与假手术组相比,心肌梗死组心功能显著降低(P<0.05),心肌ANP和BNP mRNA水平显著增高(P<0.05),CVF显著增高(P<0.05),线粒体明显肿胀,p-Mst1表达和LC3Ⅱ/LC3Ⅰ比率显著增高(P<0.05),p62表达显著降低(P<0.05);与心肌梗死组相比,心功能显著增加(P<0.05),心肌ANP和BNP mRNA水平显著降低(P<0.05),CVF显著降低(P<0.05),线粒体超微结构有显著改善,p-Mst1、p62表达显著降低(P<0.05),LC3Ⅱ/LC3Ⅰ比率显著增高(P<0.05)。结论:杨梅素可能通过抑制Mst1减轻小鼠梗死后心肌重塑和心力衰竭。
Objective: To investigate the effect and mechanism of myricetin on myocardial remodeling and heart failure after infarction in mice. Methods: The model of myocardial infarction was established by ligation of left anterior descending coronary artery. Male C57 / BL6J mice were randomly divided into 3 groups (20 in each group): sham operation group, myocardial infarction group, myocardial infarction + myricetin group. Myocardial infarction + myricetin group was given myricetin 250 mg / kg / d gavage, sham operation group and myocardial infarction group were given the same volume of 5% sodium carboxymethyl cellulose. After 1 month of drug treatment, heart function was detected by echocardiography in mice; collagen volume fraction (CVF) was assessed by Masson staining; myocardial mitochondrial damage was detected by electron microscopy; and p-Mst1, LC3 and p62 were detected by Western blot. Results: Compared with the sham-operation group, the cardiac function of myocardial infarction group was significantly lower (P <0.05), the levels of ANP and BNP mRNA were significantly increased (P <0.05), the CVF was significantly higher (P <0.05) Compared with myocardial infarction group, the cardiac function increased significantly (P <0.05), and the level of ANP and BNP mRNA in myocardium significantly increased (P <0.05) (P <0.05). The CVF was significantly decreased (P <0.05), the ultrastructure of mitochondria was significantly improved, the expression of p-Mst1, p62 was significantly decreased (P <0.05), and the ratio of LC3Ⅱ / LC3Ⅰ was significantly increased (P <0.05). Conclusions: Myricetin may reduce myocardial remodeling and heart failure after infarction in mice by inhibiting Mst1.