| 摘要: |
| [目的] 探讨愈梗通瘀汤（YGTY）通过调节磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（AKT）信号通路对急性心肌梗死（AMI）大鼠心肌损伤的影响及作用机制。[方法] 采用左冠状动脉前降支结扎法建立AMI大鼠模型，将造模成功大鼠随机分为模型（AMI）组、YGTY低、中、高剂量（YGTY-L、M、H）组、卡托普利（CPT）组、YGTY-H+PI3K激活剂（740 Y-P）组，每组15只；另设15只假手术（Sham）组作为对照。干预4周后，通过超声心动图评估心功能；2，3，5-三苯基四氮唑（TTC）染色测定心肌梗死面积；HE与Masson染色分析组织病理变化与纤维化程度；ELISA法检测血清心肌损伤标志物及组织炎症因子水平；TUNEL染色观察心肌细胞凋亡；免疫组化检测心肌髓过氧化物酶（MPO）与分化簇68（CD68）以评估炎性细胞浸润；生化法及荧光染色测定心肌超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量、活性氧（ROS）水平；Western blot法检测心肌B细胞淋巴瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）及通路相关蛋白表达。[结果] 与AMI组比较，YGTY-L组、YGTY-M组、YGTY-H组及CPT组左心室舒张末期内径、左心室收缩末期内径、心肌梗死面积、炎症评分及胶原容积分数、肌钙蛋白Ⅰ、肌钙蛋白T、肌酸激酶同工酶MB水平、凋亡率和Bax蛋白表达、中性粒细胞（MPO标记）和巨噬细胞（CD68标记）浸润数量、细胞间黏附分子1、补体片断5a、基质金属蛋白酶9、白细胞介素-1β、白细胞介素-6、肿瘤坏死因子α水平、MDA和ROS水平、p-PI3K/PI3K、p-AKT/AKT水平降低，左心室射血分数、左心室短轴缩短率、Bcl-2蛋白表达、SOD水平升高（P<0.05）；与YGTY-H组比较，YGTY-H+740 Y-P组上述指标均呈相反趋势（P<0.05）。[结论] YGTY可能通过抑制PI3K/AKT信号通路，减轻心肌炎症、氧化应激与细胞凋亡，从而改善AMI大鼠的心肌损伤。 |
| 关键词: 愈梗通瘀汤 急性心肌梗死 PI3K/AKT信号通路 心肌损伤 |
| DOI：10.11656/j.issn.1672-1519.2026.09.13 |
| 分类号:R542.2 |
| 基金项目:郑州市医疗卫生领域科技创新指导计划项目（2024YLZDJH222）。 |
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| Effects of Yugeng Tongyu Decoction on myocardial injury rats with acute myocardial infarction via regulating the PI3K/AKT signaling pathway |
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ZHANG Xiwei1, LI Xige1, WANG Yan2
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1.Department of Traditional Chinese Medicine, The 7th People's Hospital of Zhengzhou, Zhengzhou 450000, China;2.Department of Cardiology, The 7th People's Hospital of Zhengzhou, Zhengzhou 450000, China
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| Abstract: |
| [Objective] To investigate the effect and mechanism of Yugeng Tongyu Decoction（YGTY）on myocardial injury rats with acute myocardial infarction（AMI）through regulating the phosphatidylinositol 3-kinase/protein kinase B（PI3K/AKT）signaling pathway. [Methods] An AMI rat model was established by ligating the left anterior descending coronary artery. Successfully modeled rats were randomly divided into the following groups（n=15 per group）：model（AMI），YGTY low-，medium-，and high-dose（YGTY-L， M，H），captopril（CPT），and YGTY-H+PI3K activator（740 Y-P）group. An additional 15 rats underwent sham surgery as controls. After 4 weeks of intervention，cardiac function was evaluated by echocardiography. Myocardial infarct size was measured using 2，3，5- triphenyltetrazolium（TTC）staining. Histopathological changes and fibrosis were analyzed via hematoxylin-eosin（HE）and Masson staining. Serum markers of myocardial injury and tissue inflammatory factors were detected by enzyme-linked immunosorbent assay （ELISA）. Cardiomyocyte apoptosis was assessed using deoxyribonucleotide terminal transferase-mediated nick terminal labeling （TUNEL）staining. Myeloperoxidase（MPO）and differentiation cluster 68（CD68）levels were examined by immunohistochemistry to evaluate inflammatory cell infiltration. Superoxide dismutase（SOD）activity，malondialdehyde（MDA）content，and reactive oxygen species（ROS）levels were measured using biochemical assays and fluorescent staining. Protein expression of B-cell lymphoma-2（Bcl- 2），Bcl-2-associated X protein（Bax），and pathway-related proteins was determined by Western blot. [Results] Compared with the AMI group，the YGTY-L，YGTY-M，YGTY-H，and CPT groups showed decreased left ventricular end-diastolic diameter，left ventricular end- systolic diameter，myocardial infarct size，inflammation score，collagen volume fraction，levels of cardiac troponin I，cardiac troponin T， creatine kinase-MB，apoptosis rate，Bax expression，neutrophil（MPO-positive） and macrophage（CD68-positive） infiltration， intercellular adhesion molecule-1，complement component 5a，matrix metalloproteinase-9，interleukin-1β，interleukin-6，tumor necrosis factor-α，MDA，ROS，and p-PI3K/PI3K and p-AKT/AKT ratios，while left ventricular ejection fraction，left ventricular fractional shortening，Bcl-2 expression，and SOD activity were significantly increased（P<0.05）. In contrast，the YGTY-H + 740 Y-P group exhibited opposite trends in all these indicators compared to the YGTY-H group（P<0.05）. [Conclusion] YGTY may alleviate myocardial inflammation，oxidative stress and cell apoptosis by inhibiting the PI3K/AKT signaling pathway，thereby improving myocardial damage in AMI rats. |
| Key words: Yugeng Tongyu Decoction acute myocardial infarction PI3K/AKT signaling pathway myocardial injury |
