ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Ethnopharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1578237
Total Ginsenoside Induces Fetal Hemoglobin in β-Thalassemia: Evidence from In Vitro and In Vivo of Mice Model
Provisionally accepted
- 1The First People’s Hospital of Yunnan Province, Kunming, China
- 2School of Medicine, Kunming University of Science and Technology, Kunming, Yunnan Province, China
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The search for effective treatments for β-thalassemia has identified total ginsenoside (TG) as a promising fetal hemoglobin (HbF) inducer. This study investigates TG's potential to enhance HbF expression using both in vitro and in vivo models. K562 cells, erythroid progenitor cells (ErPCs), and Townes model mice were used to evaluate TG's effects on hemoglobin, HbF, and γ-globin gene expression. High-performance liquid chromatography analyzed TG composition, while flow cytometry and immunofluorescence quantified HbF levels, and reverse transcription-quantitative polymerase chain reaction assessed γ-globin gene transcription. The results showed that TG significantly upregulated hemoglobin, HbF, and γ-globin gene expression in K562 cells at concentrations of 100-200 μg/ml without adverse effects on cell proliferation or morphology. In ErPCs, TG treatment also significantly increased HbF and γ-globin gene expression. Furthermore, in Townes model mice, 14 days of intraperitoneal TG administration at 200 mg/kg and 400 mg/kg increased the proportion of HbF-positive cells to 31.75 ± 0.92% and 34.90 ± 1.70%, respectively, compared to 11.33 ± 4.91% in the negative control group. These findings suggest that TG is a potent inducer of HbF, showing significant therapeutic potential for β-thalassemia, and effectively enhances HbF production in both in vitro and in vivo models, providing a strong foundation for future studies aimed at developing TG as a safer, more effective treatment for βthalassemia.
Keywords: β-thalassemia, Fetal Hemoglobin, Reactivation, γ-globin gene, Total ginsenoside
Received: 17 Feb 2025; Accepted: 24 Jul 2025.
Copyright: © 2025 Cai, Chan, He, Kong, Cai, Guo and Zhu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Baosheng Zhu, The First People’s Hospital of Yunnan Province, Kunming, China
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