General Hospital of Northern Theater Command, Department of Cardiovascular Surgery, China.
Dis Markers. 2022 Mar 9;2022:8707061. doi: 10.1155/2022/8707061. eCollection 2022.
To investigate the role of leptin in regulating cell inflammation and protecting myocardium after myocardial ischemia-reperfusion injury in rats through signaling pathway at tissue and molecular protein levels.
Healthy female SD rats were randomly divided into 4 groups, which were sham, I/R group, leptin low-dose intervention group, and high-dose intervention group (40 g/kg and 80 g/kg, respectively). Cardiac hemodynamics, myocardial enzymology, inflammatory indices, and pathological changes were observed. Western blot was used to observe the expression of PI3K, AKT, and NFB protein by leptin.
Leptin can improve the hemodynamics of cardiac ischemia-reperfusion rats, improve the expression of myocardial enzymology, reduce the release of cardiac and serum inflammatory factors, increased PI3k, AKT, and NFB expression, and reduce the occurrence of inflammation from the perspective of gross pathology, thus protecting the body.
Leptin pretreatment can reduce MIRI injury, and the protective mechanism may be that leptin upregulates PI3K-AKT-NFB expression in myocardial tissue to reduce inflammation and promote repair of I/R injury.
通过组织和分子蛋白水平的信号通路,研究瘦素在调节大鼠心肌缺血再灌注损伤后细胞炎症和保护心肌中的作用。
将健康雌性 SD 大鼠随机分为 4 组,分别为假手术组、I/R 组、瘦素低剂量干预组和高剂量干预组(40μg/kg 和 80μg/kg)。观察心脏血流动力学、心肌酶学、炎症指标和病理变化。Western blot 观察瘦素对 PI3K、AKT 和 NFB 蛋白表达的影响。
瘦素预处理可减轻 MIRI 损伤,其保护机制可能是通过上调心肌组织中 PI3K-AKT-NFB 的表达,减少炎症反应,促进 I/R 损伤的修复。
瘦素可改善心肌缺血再灌注大鼠的血液动力学,改善心肌酶学的表达,减少心脏和血清炎症因子的释放,增加 PI3k、AKT 和 NFB 的表达,从大体病理上减轻炎症的发生,从而起到保护作用。