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  • Title: Improvement of icaritin on hematopoietic function in cyclophosphamide-induced myelosuppression mice.
    Author: Sun C, Yang J, Pan L, Guo N, Li B, Yao J, Wang M, Qi C, Zhang G, Liu Z.
    Journal: Immunopharmacol Immunotoxicol; 2018 Feb; 40(1):25-34. PubMed ID: 29077519.
    Abstract:
    CONTEXT: Icaritin (ICT), an intestinal metabolite of prenylflavonoids from Herba Epimedii, has been known to regulate many immune processes. But there are little studies of ICT on hematopoietic function. OBJECTIVE: We aimed to investigate the improvement of ICT on hematopoietic function in cyclophosphamide (CTX)-induced myelosuppression mice. METHODS: Mice were given CTX (50 mg/kg) by i.p. for five days to produce bone marrow depression model. 48 h after last treated with CTX, ICT was administrated at 10 mg/kg/d by p.o. for five days. Blood routine, body weight, thymus index and spleen index were tested. The bone marrow hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs), cell cycle and apoptosis of HSCs were quantified by flow cytometry. The bone marrow nucleated cells were counted by an automated cell counter. The histology of femoral bone was examined by Haemotoxylin and Eosin (H&E) staining. Serum erythropoietin (EPO), granulocyte colony-stimulating factor (G-CSF) and thyroperoxidase (TPO) were tested by ELISA kit. RESULTS: ICT (10 mg/kg) protected against CTX-induced myelosuppression, is evidenced by increased blood cell numbers, body weight, thymus index, spleen index and improved femoral bone morphology. ICT corrected the reduction of bone marrow HSCs and HPCs, promoted bone marrow HSCs entering the proliferative cycle phase and prevented cells proceeding to the apoptosis phase. Meanwhile, ICT increased the release of G-CSF and TPO in model mice serum. CONCLUSION: These results demonstrated that ICT improves myelosuppression by improving bone marrow hematopoietic microenvironment, promoting the proliferation and differentiation of HSCs, inhibiting the apoptosis of HSCs and stimulating the expression of G-CSF and TPO.
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