Total saponins of Panax ginseng (TSPG) promote erythroid differentiation of human CD34⁺ cells via EpoR-mediated JAK₂/STAT₅ signaling pathway
2009
Chen, D. | Zuo, G. | Li, C. | Hu, X. | Guan, T. | Jiang, R. | Li, J. | Lin, X. | Li, F. | Luo, C. | Wang, H. | Lei, C. | Long, X. | Wang, Y. | Wang, J.
Ethnopharmacological relevance: Total saponins of Panax ginseng (TSPG), main constituents extracted from Panax ginseng, a highly valued traditional Chinese medicine, have been shown to be an effective agent on hematopoiesis. Objective: To investigate the effect and mechanism underlying in which TSPG promote human CD34⁺ hematopoietic stem and progenitor cells to differentiate into erythroid-lineage cells. Materials and methods: The effect of TSPG on erythroid differentiation of purified CD34⁺ cells derived from umbilical cord blood (UCB) was determined by methylcellulose assay system and colorimetry for hemoglobin content. The changes of EpoR expression in umbilical cord blood mononuclear cells (UCB-MNCs) and purified CD34⁺ cells were detected with Western blotting and flow cytometry, respectively, and observed under laser scanning confocal microscope (LSCM). RT-PCR was performed to examine EpoR mRNA expression in CD34⁺ cells. The effects of TSPG-pretreatment on Epo-induced JAK₂ and STAT₅ tyrosine phosphorylation were analyzed by immunoprecipitation. Results: The addition of TSPG (20-70mg/L) increased the colony formation rate of BFU-E. TSPG (50mg/L) alone used significantly increased the hemoglobin content, the addition of AG490 evidently reduced TSPG-induced elevation of hemoglobin content. TSPG increased the expression of EpoR on the surface membrane of CD34⁺ cells but did not change the expression of EpoR in total UCB-MNCs. TSPG also increased the expression of EpoR mRNA in CD34⁺ cells. TSPG markedly enhanced Epo-induced tyrosine phosphorylation of JAK₂ and STAT₅ in UCB-MNCs. Conclusion: These findings suggest that TSPG may enhance the erythroid differentiation of hematopoietic stem and progenitor cells via Epo/EpoR-mediated JAK₂/STAT₅ signaling pathway.
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