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| Effects of Yugeng Tongyu Decoction on myocardial injury rats with acute myocardial infarction via regulating the PI3K/AKT signaling pathway |
| Hits 4 Download times 0 Received:June 07, 2026 |
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| DOI
10.11656/j.issn.1672-1519.2026.09.13 |
| Key Words
Yugeng Tongyu Decoction;acute myocardial infarction;PI3K/AKT signaling pathway;myocardial injury |
| Author Name | Affiliation | | ZHANG Xiwei | Department of Traditional Chinese Medicine, The 7th People's Hospital of Zhengzhou, Zhengzhou 450000, China | | LI Xige | Department of Traditional Chinese Medicine, The 7th People's Hospital of Zhengzhou, Zhengzhou 450000, China | | WANG Yan | Department of Cardiology, The 7th People's Hospital of Zhengzhou, Zhengzhou 450000, China |
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| Abstract
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| [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. |
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