| 石海霞,吴海涛,祁睿,李艺群,马玥,赵永峰.基于miR-21-5p/PI3K/Akt信号通路探究辣木叶乙醇提取物对心肌梗死大鼠的保护作用.[J].中南医学科学杂志.,2025,(6):952-956. |
| 基于miR-21-5p/PI3K/Akt信号通路探究辣木叶乙醇提取物对心肌梗死大鼠的保护作用 |
| Protective effects of moringa oleifera leaf ethanol extract on myocardial infarction rats based on miR-21-5p/PI3K/Akt signaling pathway |
| 投稿时间：2025-02-03 修订日期：2025-09-30 |
| DOI：10.15972/j.cnki.43-1509/r.2025.06.003 |
| 中文关键词: 辣木叶乙醇提取物 急性心肌梗死 miR-21-5p/PI3K/Akt 炎症因子 |
| 英文关键词:moringa oleifera leaf ethanol extract acute myocardial infarction miR-21-5p/PI3K/Akt inflammatory factors |
| 基金项目:青海省卫生健康委一般指导性课题(2020-wjzd-54) |
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| 中文摘要: |
| 目的基于miR-21-5p/磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)信号通路探究辣木叶乙醇提取物(EE-MO)对急性心肌梗死(AMI)大鼠的保护作用及潜在机制。 方法建立SD大鼠AMI模型,实验分为假手术组、模型组、EE-MO低剂量组(5 mg/kg)、中剂量组(30 mg/kg)、高剂量组(60 mg/kg)。比较各组大鼠心功能、心肌损伤、心肌组织白细胞介素(IL)-6、IL-1β、肿瘤坏死因子-α(TNF-α)、miR-21-5p、PI3K、磷酸化(p)-PI3K、Akt、p-Akt水平。 结果与假手术组比较,模型组大鼠左心室收缩末期内径(LVIDs)升高,左室射血分数(LVEF)和短轴缩短率(FS)降低；与模型组比较,中、高剂量组LVIDs降低,LVEF和FS升高(P＜0.05)。与假手术组相比,模型组大鼠心肌纤维排列紊乱,伴大量炎症细胞浸润,且心肌间质纤维化程度升高；而各剂量组心肌纤维结构改善,炎症细胞浸润减轻,纤维化程度亦降低(P＜0.05)。与假手术组比较,模型组大鼠心肌组织匀浆液中IL-6、IL-1β、TNF-α升高,miR-21-5p、p-PI3K/PI3K和p-Akt/Akt降低；与模型组比较,中、高剂量组IL-6、IL-1β、TNF-α降低,miR-21-5p、p-PI3K/PI3K和p-Akt/Akt升高(P＜0.05)。 结论EE-MO可有效改善AMI大鼠心肌损伤,可能通过上调miR-21-5p,激活PI3K/Akt信号通路,以减轻心肌炎症。 |
| 英文摘要: |
| AimTo investigate the protective effects of moringa oleifera leaf ethanol extract (EE-MO) against acute myocardial infarction (AMI) in rats and explore the potential mechanism based on the miR-21-5p/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. MethodsAn AMI model was established in SD rats, and the animals were divided into sham, model, EE-MO low-dose (5 mg/kg), medium-dose (30 mg/kg), and high-dose (60 mg/kg) groups. Cardiac function, myocardial injury, and levels of interleukin (IL)-6, IL-1β, tumor necrosis factor-α (TNF-α), miR-21-5p, PI3K, phosphorylated (p)-PI3K, Akt, and p-Akt in myocardial tissue were compared among the groups. ResultsCompared with the sham group, the model group showed increased left ventricular internal systolic diameter (LVIDs) and decreased left ventricular ejection fraction (LVEF) and fractional shortening (FS). Compared with the model group, the medium- and high-dose groups exhibited decreased LVIDs and increased LVEF and FS (P＜0.05). Compared with the sham group, the model group displayed disordered myocardial fiber arrangement, significant inflammatory cell infiltration, and increased myocardial interstitial fibrosis. In contrast, all EE-MO dose groups showed improved myocardial fiber structure, reduced inflammatory infiltration, and decreased fibrosis (P＜0.05). Compared with the sham group, the model group exhibited elevated levels of IL-6, IL-1β, and TNF-α in myocardial tissue homogenate, along with decreased miR-21-5p, p-PI3K/PI3K, and p-Akt/Akt ratios. Compared with the model group, the medium- and high-dose groups demonstrated reduced IL-6, IL-1β, and TNF-α levels and increased miR-21-5p, p-PI3K/PI3K, and p-Akt/Akt ratios (P＜0.05). ConclusionEE-MO effectively alleviates myocardial injury in AMI rats, potentially by upregulating miR-21-5p and activating the PI3K/Akt signaling pathway to reduce myocardial inflammation. |
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