Research Paper
Mechanism of baixiangdan capsules on anti-neuroinflammation: combining dry and wet experiments
- 1 College of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250000, China
- 2 College of Foreign Languages, Shandong University of Traditional Chinese Medicine, Jinan 250000, China
- 3 Preventive Treatment Center, Shenzhen Integrated Traditional Chinese and Western Medicine Hospital, Shenzhen 518000, China
- 4 Department of Psychiatry, Boai Hospitai of Zhongshan, Zhongshan 528400, China
- 5 Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan 250000, China
- 6 College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250000, China
- 7 Innovation Research Institute of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250000, China
- 8 Department of Neurosurgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, China
- 9 Department of Traditional Chinese Medicine, Shandong Mental Health Center, Shandong University, Jinan 250000, China
Received: April 3, 2023 Accepted: July 17, 2023
https://doi.org/10.18632/aging.How to Cite
Copyright: © 2023 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.
Abstract
Neuroinflammation plays an important role in the pathogenesis of neurological disorders, and despite intensive research, treatment of neuroinflammation remains limited. BaiXiangDan capsule (BXD) is widely used in clinical practice. However, systematic studies on the direct role and mechanisms of BXD in neuroinflammation are still lacking. We systematically evaluated the potential pharmacological mechanisms of BXD on neuroinflammation using network pharmacological analysis combined with experimental validation. Multiple databases are used to mine potential targets for bioactive ingredients, drug targets and neuroinflammation. GO and KEGG pathway analysis was also performed. Interactions between active ingredients and pivotal targets were confirmed by molecular docking. An experimental model of neuroinflammation was used to evaluate possible therapeutic mechanisms for BXD. Network pharmacological analysis revealed that Chrysoeriol, Kaempferol and Luteolin in BXD exerted their anti-neuroinflammatory effects mainly by acting on targets such as NCOA2, PIK3CA and PTGS2. Molecular docking results showed that their average affinity was less than −5 kcal/mol, with an average affinity of −8.286 kcal/mol. Pathways in cancer was found to be a potentially important pathway, with involvement of PI3K/AKT signaling pathways. In addition, in vivo experiments showed that BXD treatment ameliorated neural damage and reduced neuronal cell death. Western blotting, RT-qPCR and ELISA analysis showed that BXD inhibited not only the expression of IL-1β, TNF-α and NO, but also NF-κB, MMP9 and PI3K/AKT signaling pathways. This study applied network pharmacology and in vivo experiments to explore the possible mechanisms of BXD against neuroinflammation, providing insight into the treatment of neuroinflammation.