Park SH. Potential of ginsenoside Rg1 to treat aplastic anemia via mitogen activated protein kinase pathway in cyclophosphamide-induced myelosuppression mouse model. World J Stem Cells 2024; 16(11): 900-905 [DOI: 10.4252/wjsc.v16.i11.900]
Corresponding Author of This Article
See-Hyoung Park, Associate Professor, PhD, Biological and Chemical Engineering, Hongik University, Sejongro 2639, Sejong 30016, South Korea. shpark74@hongik.ac.kr
Research Domain of This Article
Hematology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Stem Cells. Nov 26, 2024; 16(11): 900-905 Published online Nov 26, 2024. doi: 10.4252/wjsc.v16.i11.900
Potential of ginsenoside Rg1 to treat aplastic anemia via mitogen activated protein kinase pathway in cyclophosphamide-induced myelosuppression mouse model
See-Hyoung Park
See-Hyoung Park, Biological and Chemical Engineering, Hongik University, Sejong 30016, South Korea
Author contributions: Park SH designed the overall concept and outline of the manuscript; Park SH contributed to the discussion and design of the manuscript, the writing, editing, and reviewing the manuscript.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: See-Hyoung Park, Associate Professor, PhD, Biological and Chemical Engineering, Hongik University, Sejongro 2639, Sejong 30016, South Korea. shpark74@hongik.ac.kr
Received: August 21, 2024 Revised: October 12, 2024 Accepted: November 20, 2024 Published online: November 26, 2024 Processing time: 97 Days and 6 Hours
Abstract
Aplastic anemia (AA) is a rare but serious condition in which the bone marrow fails to produce sufficient new blood cells, leading to fatigue, increased susceptibility to infection, and uncontrolled bleeding. In this editorial, we review and comment on an article by Wang et al published in 2024. This study aimed to evaluate the potential therapeutic benefits of ginsenoside Rg1 in AA, focusing on its protective effects and uncovering the underlying mechanisms. Cyclophosphamide (CTX) administration caused substantial damage to the structural integrity of the bone marrow and decreased the number of hematopoietic stem cells, thereby establishing an AA model. Compared with the AA group, ginsenoside Rg1 alleviated the effects of CTX by reducing apoptosis and inflammatory factors. Mechanistically, treatment with ginsenoside Rg1 significantly mitigated myelosuppression in mice by inhibiting the mitogen activated protein kinase signaling pathway. Thus, this study indicates that ginsenoside Rg1 could be effective in treating AA by reducing myelosuppression, primarily through its influence on the mitogen activated protein kinase signaling pathway. We expect that our review and comments will provide valuable insights for the scientific community related to this research and enhance the overall clarity of this article.
Core Tip: An animal model of aplastic anemia was established in mice using cyclophosphamide, and pathological changes in the bone marrow were analyzed using hematoxylin-eosin staining of the tissues. Blood samples were collected from the mice to analyze blood cell composition. This study also examined the changes in cellular components and protein expression in the mitogen activated protein kinase signaling pathway within the bone marrow to determine whether ginsenoside Rg1 can mitigate myelosuppression through the mitogen activated protein kinase pathway.