To investigate whether miR-124-3p influences cell apoptosis, inflammatory response, and oxidative stress in rats with acute myocardial infarction (AMI) by mediating the SIRT1/FGF21/CREB/PGC1α pathway. A dual-luciferase reporter gene assay was performed to verify the relationship between miR-124-3p and SIRT1. AMI rats were established via coronary artery ligation after injection with agomiR-124-3p, antagomiR-124-3p, and/or SIRT1 siRNA, and triphenyltetrazolium chloride (TTC), HE, and TUNEL stainings were performed. Bio-Plex rat cytokine assays were performed to determine proinflammatory factor levels. qRT-PCR and Western blotting were used to examine the mRNA and protein expression, respectively. The activity levels of antioxidant enzymes in myocardial tissues were also measured. miR-124-3p was confirmed to target SIRT1 in the H9C2 cells. AMI rats exhibited increased miR-124-3p expression and decreased SIRT1 expression in myocardial tissues. HE staining showed a disorganized cell arrangement and inflammatory cell infiltration in the myocardial tissues of the AMI rats, which was more severe in the rats injected with SIRT1 and agomiR-124-3p but was ameliorated in those treated with antagomiR-124-3p. Moreover, the AMI rats in the antagomiR-124-3p group presented with a reduction in infarct area with an increase in antioxidant enzyme activity, Bcl-2 expression, and activation of the FGF21/CREB/PGC1α pathway, as well as a decrease in cell apoptosis rate, Bax and Caspase-3 expression, and levels of proinflammatory factors, effects that were reversed by si-SIRT1. Inhibiting miR-124-3p expression may activate the FGF21/CREB/PGC1α pathway to reduce cell apoptosis, alleviate the inflammatory response, and attenuate oxidative stress in AMI rats by targeting SIRT1.

研究 miR-124-3p 是否通过介导 SIRT1/FGF21/CREB/PGC1α 通路影响急性心肌梗死 (AMI) 大鼠的细胞凋亡、炎症反应和氧化应激。进行双荧光素酶报告基因测定以验证 miR-124-3p 和 SIRT1 之间的关系。AMI大鼠在注射agomiR-124-3p、antagomiR-124-3p和/或SIRT1 siRNA后通过冠状动脉结扎建立，并进行三苯基四唑氯化物（TTC）、HE和TUNEL染色。进行 Bio-Plex 大鼠细胞因子测定以确定促炎因子水平。qRT-PCR和Western印迹分别用于检查mRNA和蛋白质表达。还测量了心肌组织中抗氧化酶的活性水平。证实 miR-124-3p 靶向 H9C2 细胞中的 SIRT1。AMI大鼠表现出增加的miR-124-3p表达和降低心肌组织中SIRT1的表达。HE染色显示AMI大鼠心肌组织细胞排列紊乱和炎性细胞浸润，在注射SIRT1和agomiR-124-3p的大鼠中更为严重，而在给予antagomiR-124-3p的大鼠中则有所改善。此外，antagomiR-124-3p 组的 AMI 大鼠梗塞面积减少，抗氧化酶活性增加，这在注射 SIRT1 和 agomiR-124-3p 的大鼠中更为严重，但在用 antagomiR-124-3p 治疗的大鼠中得到改善。此外，antagomiR-124-3p 组的 AMI 大鼠梗塞面积减少，抗氧化酶活性增加，这在注射 SIRT1 和 agomiR-124-3p 的大鼠中更为严重，但在用 antagomiR-124-3p 治疗的大鼠中得到改善。此外，antagomiR-124-3p 组的 AMI 大鼠梗塞面积减少，抗氧化酶活性增加，Bcl-2表达和 FGF21/CREB/PGC1α 通路的激活，以及细胞凋亡率、Bax和Caspase-3表达以及促炎因子水平的降低，这些作用被 si-SIRT1 逆转。抑制 miR-124-3p 表达可能通过靶向 SIRT1 激活 FGF21/CREB/PGC1α 通路，从而减少细胞凋亡，减轻炎症反应，减轻 AMI 大鼠的氧化应激。