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    Article

    Mechanism of Cistanche deserticola Ma in the Treatment of Myocardial Ischemia-Reperfusion (I/R) Injury Based on Network Pharmacology and in vitro Experiments

    Yuan-Jia Yue1,2, Yu Li3, Huimin Wang1, Zhao Ji1, Xing Rong1, Lin Jiang1,2★★ Corresponding author

    1. 1Department of Pharmacy, The Fourth College of Clinical Medicine, Xinjiang Medical University, Urumqi, CHINA.
    2. 2Department of Pharmacy, Xinjiang Uygur Autonomous Region Hospital of Traditional Chinese Medicine, Urumqi, CHINA.
    3. 3Department of Neurosurgery ICU, Xinjiang Uygur Autonomous Region People’s Hospital, Urumqi, China.

    CORRESPONDENCE

    Lin Jiang

    Department of Pharmacy, The Fourth College of Clinical Medicine, Xinjiang Medical University, Urumqi, CHINA.

    597900175@qq.com

    Volume 20, Issue 2 · pp. 423–429 · PUBLISHED 2024 · DOI: 10.1177/09731296231214855

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Objectives: To investigate the mechanism of Cistanche deserticola Ma (CDA) in the treatment of myocardial ischemiareperfusion (I/R) injury by network pharmacology and cell experiments. Materials and Methods: The main active components of CDA were collected from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). I/R-related targets were identified from DisGeNET, OMIMD, and TTD; the I/R protein–protein interaction (PPI) network was constructed using the STRING input. The targets of CDA that inhibit I/R injury in Matescape and Microshengxin were subjected to Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Cell viability, levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA), and protein expression of phosphatidylinositol 3-kinase (PI3K) and serine/threonine kinase 1 (Akt1) were determined. Results: A total of 236 targets were identified, with PI3K, Akt, epithelial growth factor receptor (EGFR), and another kinase being the major targets, and according to GO and KEGG analysis, CDA was most likely to inhibit I/R through the PI3K-Akt pathway. The optimal concentration of 10% medicated serum of CDA was determined to be the most effective concentration. The levels of LDH and MDA were significantly decreased in the CDA and BEZ23 groups, but the levels of SOD were significantly increased, thereby alleviating cell damage. In addition, the expression of PI3K, Akt, and p-AKT proteins was significantly reduced in the CDA group. Conclusion: CDA alleviates I/R injury through antioxidation and inhibition of the PI3K/Akt signaling pathway.

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      Yue, Y., Li, Y., Wang, H., Ji, Z., Rong, X., & Jiang, L. (2024). Mechanism of Cistanche deserticola Ma in the Treatment of Myocardial Ischemia-Reperfusion (I/R) Injury Based on Network Pharmacology and in vitro Experiments. Pharmacognosy Magazine, 20(2), 423–429. https://doi.org/10.1177/09731296231214855