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    Article

    Mechanism Investigation of Tianxiangdan Against Myocardial Ischemia Based on Network Pharmacology, Molecular Docking, and in vitro Experimental

    Lin Jiang1★, Yuan-Jia Yue2, Mei Tang3, Yu-Che Wu4, Xiao Liu4, Yu Li5★ Corresponding author

    1. 1State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi, CHINA.
    2. 2Pharmacy Department, The Fourth College of Clinical Medicine, Xinjiang Medical University, Urumqi, CHINA.
    3. 3Pharmacy Department, Urumqi First People’s Hospital, Urumqi, CHINA.
    4. 4Department of Pharmacy, The Xinjiang Technical Institute of Physics & Chemistry, Urumqi, CHINA.
    5. 5Neurosurgery ICU, Xinjiang Uygur Autonomous Region People’s Hospital, Urumqi, China.

    CORRESPONDENCE

    Lin Jiang

    State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi, CHINA.

    597900175@qq.com

    Received: 21-10-2023; Accepted: 28-11-2023.

    Volume 20, Issue 3 · pp. 784–793 · PUBLISHED 2024 · DOI: 10.1177/09731296231220992

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Objectives: Tianxiangdan capsule (TXD) has been clinically used in the treatment of coronary heart disease angina pectoris. This study aimed to evaluate the mechanisms of TXD against myocardial ischemia and provide evidence for its subsequent clinical application. Materials and Methods: Active components and mechanisms of action of TXD against myocardial ischemia were predicted and analyzed by network pharmacology and molecular docking. The chemical constituents in TXD were determined by HPLC- MS. The oxidative damage model was established using H2O2, which caused myocardial ischemia damage. The MTT assay and Hoechst 33342 staining were used to evaluate cell viability, while cleaved caspase-3 immunofluorescence staining was used to determine cell apoptosis. The fluorescent probe method detected ROS and intracellular Ca2+, while spectrophotometry was used to measure SOD, MDA, and NO levels in myocardial cells. Western blotting was used to detect the expression levels of ERɑ, PI3K, p-PI3K, AKT, p-AKT, and eNOS in cells. Results: It was found that TXD plays a protective role in myocardial ischemia through the estrogen pathway. The TXD drugcontaining plasma exhibited increased cell survival rates and suppressed MDA levels, elevated SOD and NO levels, and significantly suppressed ROS levels as well as intracellular Ca2+ levels. Moreover, the TXD drug-containing plasma pretreated cells had significantly suppressed PI3K, p-PI3K, AKT, and p-AKT expression levels, as well as elevated ERɑ and eNOS expression levels. Conclusion: TXD activates estrogen receptor ERɑ, enhances NO release of cardiomyocytes through the estrogen signaling pathway, improves intracellular Ca2+ overload, oxidative stress injury, and apoptosis, and plays a protective role in myocardial ischemia injury.

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      Jiang, L., Yue, Y., Tang, M., Wu, Y., Liu, X., & Li, Y. (2024). Mechanism Investigation of Tianxiangdan Against Myocardial Ischemia Based on Network Pharmacology, Molecular Docking, and in vitro Experimental. Pharmacognosy Magazine, 20(3), 784–793. https://doi.org/10.1177/09731296231220992