ArticleChinese herbal medicines2026
Astragalus polysaccharides inhibit arsenic trioxide-induced BMSCs damage through inhibition of Jnk and p38 signaling pathways.
Article in Chinese herbal medicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Arsenic trioxide (ATO) is a clinically effective anticancer agent used in the treatment of leukemia. However, it exerts adverse effects on non-tumor cells, including bone marrow mesenchymal stem cells (BMSCs). This study aims to investigate the protective role and molecular mechanism of traditional Chinese medicine Astragalus polysaccharides (APS) in mitigating ATO-induced apoptosis in BMSCs. Methods: BMSCs exposed to ATO (0.5 μmol/L) were treated with APS (20, 40, 100, and 200 μg/mL). Cell viability, proliferation, and migration were assessed by using MTT, EdU staining, Transwell, and scratch wound healing assays. Apoptosis was evaluated via TUNEL assay, Hoechst 33258 staining, and flow cytometry. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were measured by using DCFH-DA and JC-1 staining. Apoptotic protein expression was analyzed by Western blotting. Results: ATO exposure significantly inhibited the proliferation and migration of BMSCs and induced apoptosis, while APS markedly attenuated the apoptosis of BMSCs induced by ATO, and significantly improved cell proliferation and migration ( Conclusion: Our study reveals that APS exert significant protective effects against ATO-induced apoptosis in BMSCs. The mechanisms involve suppressing ROS generation, maintaining mitochondrial membrane stability, enhancing cell viability, migration, and proliferation, as well as inhibiting Jnk and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways. The findings highlight potential molecular targets and novel strategies for the clinical prevention and treatment of ATO-related toxicity
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.