Research Paper Volume 13, Issue 12 pp 16804—16815
Therapeutic targets and molecular mechanism of calycosin for the treatment of cerebral ischemia/reperfusion injury
- 1 Department of Neurosurgery, Guigang City People’s Hospital, The Eighth Affiliated Hospital of Guangxi Medical University, Guigang, Guangxi, PR China
- 2 Department of Pharmacy, The Second People’s Hospital of Nanning City, The Third Affiliated Hospital of Guangxi Medical University, Nanning, PR China
- 3 College of Pharmacy, Guangxi Medical University, Nanning, PR China
- 4 Department of Neurosurgery Area 1, Guigang City People’s Hospital, The Eighth Affiliated Hospital of Guangxi Medical University, Guigang, Guangxi, PR China
- 5 Department of Pharmacy, Guigang City People’s Hospital, The Eighth Affiliated Hospital of Guangxi Medical University, Guigang, Guangxi, PR China
Received: November 17, 2020 Accepted: March 14, 2021 Published: June 27, 2021https://doi.org/10.18632/aging.203219
How to Cite
Copyright: © 2021 Yu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This study was designed to understand the pivotal anti-cerebral ischemia/reperfusion injury (CIRI) targets and pathways of calycosin through network pharmacology and molecular docking analyses. In this study, bioinformatics tools were employed to characterize and identify the pharmacological functions and mechanisms of calycosin for CIRI management. The network pharmacology data identified potential, merged CIRI-associated targets of calycosin including tumor protein p53 (TP53), protein kinase B (AKT1), vascular endothelial growth factor A (VEGFA), interleukin 6, tumor necrosis factor (TNF), and mitogen-activated protein kinase 1 (MAPK1). Molecular docking analysis indicated the binding efficacy of calycosin with three of the targets, namely TP53, AKT1, and VEGFA. The biological processes of calycosin for the treatment of CIRI are mainly involved in the improvement of endothelial cell proliferation and growth, inflammatory development, and cellular metabolism. In addition, the anti-CIRI actions of calycosin were primarily through suppression of the toll-like receptor, PI3K-AKT, TNF, MAPK, and VEGF signaling pathways. Taken together, the current bioinformatic findings revealed pivotal targets, biological functions, and pharmacological mechanisms of calycosin for the treatment of CIRI. In conclusion, calycosin, a functional phytoestrogen, can be potentially used for the treatment of CIRI in future clinical trials.