ArticleDrug design, development and therapy2022
Dioscin Regulating Bone Marrow Apoptosis in Aplastic Anemia.
Article in Drug design, development and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Chinese herbal medicine and its active compounds in attenuating renal injuryFrontiers in endocrinology · 2023Pooled it
- Bone Marrow Failure Model Mimics Aplastic Anemia Patients: Single-Cell Landscape of Immune Response Reveals Novel Mechanisms of Immune Imbalance in AA.Cancer medicine · 2026Article
- Mechanism of Babao Dan on fluorouracil-induced bone marrow suppression and T cell immune disorder through MAPK pathway.Scientific reports · 2026Article
- Shisiwei Jianzhong decoction inhibits the adipogenic differentiation of bone marrow mesenchymal stem cells by downregulating nuclear factor of activated T cells, cytoplasmic 4 in non-severe aplastic anemia.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Immune suppressive drugs negatively regulate the CD8Heliyon · 2024Article
- Traditional Chinese medicine for treating aplastic anemia.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2023Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Aplastic anemia (AA), a disease of bone marrow failure, is caused by CD8 Purpose: Our study is aimed to investigate the effect and mechanism of dioscin (DNS) for treating AA. Methods: Briefly, we established and evaluated the AA mouse model, DNS and positive control drugs were used for intervention treatment. After 14 days of intervention, femoral bone marrow pathology, bone marrow mononuclear cells (BMMCs) apoptosis rate, bone marrow CD34+ cell surface Fas (CD95) expression and Fas signaling pathway key proteins were detected. Results: After the establishment of the AA mouse model, the number of peripheral blood cells including granulocytes, erythrocytes, hemoglobin, platelets and reticulocytes in the AA group model was significantly decreased compared with the group control (P < 0.01). The degree of bone marrow hyperplasia in the sternum and femur is extremely low. After different drug interventions, compared with the group model, the number of peripheral blood cells in the AA mice rebounded significantly in group DNS (P < 0.01). Not only that the apoptosis rate of BM-MCs decreased (P < 0.01), meanwhile, the CD95 molecule expressed on the CD34+ bone marrow cells had a significant decline (P < 0.01), and the expression level of the key proteins of Fas signaling pathway was also significantly decreased (P < 0.01). Conclusion: DNS recovered the peripheral pancytopenia and bone marrow failure in AA mice. DNS reduced the key protein of Fas signaling pathway level to inhibit apoptosis of bone marrow cells to treat AA.
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