ArticleFrontiers in immunology2026
Ziyuglycoside II ameliorates chemotherapy-induced neutropenia by promoting neutrophil differentiation and functional recovery via SPI1 and C/EBPϵ transcriptional regulation.
Article in Frontiers in immunology, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chemotherapy-induced neutropenia (CIN) remains a major dose-limiting toxicity associated with myelosuppressive chemotherapy regimens. The development of therapeutic strategies capable of effectively restoring neutrophil production and function could address a critical unmet clinical issue. ZGSII, a bioactive compound derived from Methods: A murine model of cyclophosphamide-induced neutropenia and the human promyelocytic leukemia cell line NB4 were employed to evaluate the effects of ZGSII alleviating chemotherapy-induced neutropenia and promoting neutrophil differentiation, through blood cell count, flow cytometry analysis, and Wright-Giemsa staining. The underlying molecular mechanisms of ZGSII in treatment CIN were systematically investigated through integrated approaches including transcriptomics profiling, computational simulations, and Results: This study demonstrated that ZGSII effectively alleviates cyclophosphamide-induced neutropenia and bone marrow suppression in murine models, promoting neutrophil reconstitution without inducing excessive bone marrow mobilization. Transcriptomic analysis revealed that ZGSII restores neutrophil-related transcriptional programs, enriched pathways associated with leukocyte migration, myeloid cell activation, and inflammatory regulation. Integration of publicly granulopoiesis datasets enabled the identification of 37 key genes associated with neutrophil differentiation and maturation. Mechanistically, computational modeling suggests potential interaction of ZGSII with SPI1 and C/EBPϵ, restoring their protein expression and driving granulocytic differentiation. Functional assays further confirmed that ZGSII enhances neutrophil phagocytosis activity, reactive oxygen species (ROS) production, and cytokine homeostasis. Notably, administration of ZGSII conferred significant survival advantages in neutropenic mice following challenge with Conclusions: ZGSII alleviates CIN by regulating SPI1 and C/EBPϵ transcriptional activity to promote neutrophil differentiation and functional recovery. These findings provides a preclinical proof for ZGSII as a therapeutic adjuvant or alternative treatment option for CIN.
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.