Moxa Cone Moxibustion at Zusanli(ST36) acupoint alleviate myelosuppression mouse induce by CTX and promote hematopoietic cell proliferation via HPA axis

Abstract

Abstract Objective. Clinical studies have reported that moxibustion alleviates the side effects of chemotherapy, such as myelosuppression; however, its therapeutic mechanisms remain unclear. We investigated whether moxa cone moxibustion (MCM) promotes recovery from chemotherapy-induced myelosuppression via the hypothalamus-pituitary adrenal (HPA) axis. Methods. A myelosuppression model was established in mice using cyclophosphamide (CTX), and they were grouped into control, model, and moxibustion groups. In the moxibustion group, the mice received MCM at ST36 for 7 days. The peripheral blood cells were detected using an automatic blood cell analyzer; serum levels of corticotropin-releasing hormone (CRH), corticotropin (ACTH), corticosterone (CORT) and glucocorticoid receptor (GRF) a/β were detected using enzyme-linked immunosorbent assay (ELISA); the expression and cell cycle of bone marrow hematopoietic cells were detected using flow cytometry (FC); and BGISEQ Instrument model-DNBseqTM Platform was used for RNA sequencing. The differentially expressed genes (DEGs) were subjected to gene ontology (GO) function enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Results. Compared with the control group, the contents of the peripheral blood and LSK and HSC in the moxibustion group were significantly higher (P<0.05). Following moxibustion therapy, the S and G2 phases of bone marrow hematopoietic stem cells decreased significantly, while the G1 phase increased. The CRH, ACTRH, and CORT levels decreased (P<0.05), while GRF-a and GRFβ levels increased (P<0.05). Additionally, 193 DEGs were down-regulated in the control group and up-regulated in the moxibustion group, while 481 DEGs were up-regulated in the control group and down-regulated in the moxibustion group. GO analysis revealed that cross-DEGs were enriched in cell-cell junction, membrane raft, membrane microdomain, and T-cell receptor complex involved in T-cell activation, T-cell differentiation, and lymphocyte differentiation, which exerted the MF of cytokine binding, receptor activity, and activity. KEGG analysis revealed that hematopoietic cell lineage, primary immunodeficiency, cytokine-cytokine receptor interactions, and other pathways were significantly enriched in the moxibustion group. Conclusion. MCM could alleviate myelosuppression induced by CTX and promote hematopoietic cell proliferation via the HPA axis and promote the proliferation and differentiation of bone marrow hematopoietic cells by regulating gene expression.