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, Hongxu Guan Department of Neurology, Second Affiliated Hospital, Shandong First Medical University , Tai’an 271000 , China Search for other works by this author on: Oxford Academic Xiaoting Yang Taishan Nursing Vocational College , Tai’an 271000 , China Search for other works by this author on: Oxford Academic Mingfeng Yang Key Laboratory of Cerebral Microcirculation in Shandong First Medical University , Tai’an, Shandong 271000 , China Search for other works by this author on: Oxford Academic Haitao Wang Department of Neurology, Second Affiliated Hospital, Shandong First Medical University , Tai’an 271000 , China Correspondence: Department of Neurology, Second Affiliated Hospital, Shandong First Medical University, Taian, No. 366 Taishan Street, Tai’an City 271000, Shandong Province, China. E-mail: tru6540@163.com Search for other works by this author on: Oxford Academic
https://orcid.org/0009-0001-6326-4914 Journal of Pharmacy and Pharmacology, rgae067, https://doi.org/10.1093/jpp/rgae067
Published:
21 June 2024
Article history
Received:
11 November 2023
Accepted:
20 May 2024
Published:
21 June 2024
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Hongxu Guan, Xiaoting Yang, Mingfeng Yang, Haitao Wang, Targeting MAPK14 in microglial cells: neuroimmune implications of Panax ginseng in post-stroke inflammation, Journal of Pharmacy and Pharmacology, 2024;, rgae067, https://doi.org/10.1093/jpp/rgae067
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Abstract
Aim
This study investigates the molecular mechanisms through which Panax ginseng and Panax notoginseng saponin (PNS) mitigate neuroinflammatory damage and promote neural repair postischemic stroke, utilizing bioinformatics, and experimental approaches.
Background
Cerebral infarction significantly contributes to disability worldwide, with chronic neuroinflammation worsening cognitive impairments and leading to neurodegenerative diseases. Addressing neuroimmune interactions is crucial for slowing disease progression and enhancing patient recovery, highlighting the need for advanced research in neuroimmune regulatory mechanisms and therapeutic strategies.
Objective
To elucidate the effects of the traditional Chinese medicine components Panax ginseng and PNS on neuroinflammatory damage following ischemic stroke, focusing on the molecular pathways involved in mitigating inflammation and facilitating neural repair.
Methods
The study employs single-cell sequencing and transcriptomic analysis to investigate gene expression changes associated with cerebral infarction. Gene set enrichment analysis and weighted gene co-expression network analysis are used to identify key molecular markers and core genes. Furthermore, pharmacological profiling, including functional assays, assesses the impact of Ginsenoside-Rc, a PNS derivative, on microglial cell viability, cytokine production, and reactive oxygen species (ROS) levels.
Results
Our analysis revealed that MAPK14 is a critical mediator in the neuroinflammatory response to ischemic stroke. Ginsenoside-Rc potentially targets and modulates MAPK14 activity to suppress inflammation. Experimental validation showed that Ginsenoside-Rc treatment, combined with MAPK14 silencing, significantly alters MAPK14 expression and mitigates neuroinflammatory damage, evidenced by reduced microglial cell death, inflammatory factor secretion, and ROS production.
Conclusion
Ginsenoside-Rc’s modulation of MAPK14 offers a promising therapeutic strategy for reducing neuroinflammation and potentially improving cognitive recovery post-ischemic stroke. This supports the therapeutic application of the traditional Chinese medicine Sanqi in ischemic stroke care, providing a theoretical and experimental foundation for its use.
Others
Future work will focus on extending these findings through clinical trials to evaluate the efficacy and safety of Ginsenoside-Rc in human subjects, aiming to translate these promising preclinical results into practical therapeutic interventions for ischemic stroke recovery.
cerebral infarction, Panax ginseng, neuroinflammation, MAPK14, single-cell sequencing, transcriptomic analysis
© The Author(s) 2024. Published by Oxford University Press on behalf of the Royal Pharmaceutical Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.
This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/pages/standard-publication-reuse-rights)
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