Research Paper Volume 16, Issue 15 pp 11535—11552
Exploring the mechanism by which Angelica sinensis improves haematopoietic function in aplastic anaemia
- 1 Department of Gerontology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China
- 2 Department of Acupuncture, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China
- 3 Department of Science and Education, Shandong Mental Health Center, Jinan 250014, China
- 4 Department of Hematology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China
Received: December 8, 2023 Accepted: May 29, 2024 Published: June 26, 2024
https://doi.org/10.18632/aging.205971How to Cite
Copyright: © 2024 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Angelica sinensis (AS) can improve the haematopoietic function, but the treatment mechanism is unknown. Transfusion dependency was estimated by Kaplan–Meier survival analyses and Cox proportional-hazard model in AS treated apalstic anemia (AA) patients. After that, the AA GEO database was analysed, the up differentially expressed genes (DEGs) of AA were combined with AS targets for the intersection of targets. After the AA mouse model was established, the effect of AS was confirmed by haematopoietic function tests. The same experiment plus mitochondrial apoptotic pathway tests in vivo were performed in Angelica sinensis polysaccharide (ASP)-treated mice, the key ingredient in AS. For in vitro experiment, bone marrow nucleated cells (BMNCs) were tested. Clinical data confirmed that the level of transfusion dependency and IL17A were lower in AS-users compared to non-AS users (p < 0.001). The intersection of targets between AA and AS most concentrated on inflammation and apoptosis. Then, the same effect was found in AS treated AA mice model. In both in vivo and in vitro tests, ASP demonstrated the ability to mitigate P38/MAPK-induced Bax-associated mitochondrial apoptosis, while also reducing the levels of activated Th17 cells and alleviating abnormal cytokine levels. So, the protective effect of AS and ASP on hematopoietic function lies in their ability to prevent apoptosis.