Effect of Ginsenoside Rg1 in Treating Aplastic Anemia in Mice via MAPK Pathway

目的：本研究旨在评价人参皂苷Rg1对AA的保护作用，并进一步探讨其机制。方法：本研究通过注射环磷酰胺(CTX)建立骨髓抑制小鼠模型。CTX + Rg1组小鼠Rg1灌胃13 d。HE检测骨髓、胸腺和脾脏的病理变化。取小鼠眼眶血进行血常规检查。然后用流式细胞仪检测骨髓细胞的比例。通过WB检测MAPK通路中p-p38、p38、p-JNK、JNK、p-ERK、ERK的表达。结果：病理检查显示，CTX严重破坏小鼠骨髓、胸腺和脾脏的结构特征，降低骨髓造血细胞的比例。Rg1可通过抑制MAPK信号通路显著减轻小鼠骨髓抑制。结论：本研究提示人参皂苷Rg1通过MAPK信号通路缓解骨髓抑制作用，对AA有一定的治疗作用。Objective: This study was designed to evaluate the protective effects of ginsenoside Rg1 on AA and further investigate the underlying mechanism. Methods: In this study, Cyclophosphamide (CTX) was injected to establish the myelosuppression mouse model. The mice in the CTX + Rg1 group were treated with Rg1 for 13 days. The pathological changes of bone marrow, thymus, and spleen were detected through HE (Hematoxylin-Eosin St). Orbital blood of mice was collected for blood routine examination. Afterwards, the proportions of bone marrow cells were evaluated by flow cytometry assay. MAPK pathway was detected via WB for the expressions of p-p38, p38, p-JNK, JNK, p-ERK, and ERK. Results: Pathological examination revealed that CTX severely damaged the structural features of the bone marrow, thymus, and spleens, and decreased the proportion of hematopoietic cells in the bone marrow of mice. Treatment of Rg1 significantly alleviated myelosuppression in mice by inhibiting MAPK signaling pathway. Conclusion: This study suggested that ginsenoside Rg1 treated AA by alleviating myelosuppression through MAPK signaling pathway.