- 期刊Rapid communications in mass spectrometry : RCM（Rapid Commun Mass Spectrom）
- 发表时间2026-12-30
- 作者Guo M, Liu Y, Hu Z, Du Y
- 卷期页码V40(24) : e70194
- DOI10.1002/rcm.70194
- PMID42864149
摘要机译
[目的]采用血清代谢组学和网络药理学相结合的方法，探讨复方阿胶姜（FFEJJ）防治化疗后骨髓抑制（MAC）的作用机制及药理活性成分。[方法]将SD大鼠随机分为空白组、模型组和FFEJJ组（10.8 g/kg）。
用环磷酰胺建立大鼠MAC模型，在造模的同时，连续15天，每日一次灌胃，测定血常规参数，观察脾脏和骨髓病理变化，采用非靶向血清代谢组学方法鉴定与MAC相关的差异代谢物及其相关途径。
采用液相色谱-质谱联用（LC-MS）分析FFEJJ的化学成分，并利用网络药理学进一步预测其机制和治疗MAC的药理活性化合物。[结果]FFEJJ明显改善MAC模型大鼠骨髓造血功能。
与空白组相比，模型组脾脏损伤明显，骨髓紊乱，骨髓腔内脂肪浸润明显。FFEJJ治疗后，MAC大鼠脾脏组织和骨髓状况明显改善。
内源性代谢产物的血清代谢组学分析鉴定了14种与MAC机制相关的正离子和负离子模式的差异代谢产物，主要涉及氨基酰基-tRNA生物合成、初级胆汁酸生物合成和不饱和脂肪酸生物合成等途径。使用LC-MS，在FFEJJ中鉴定了31个组分。
网络药理学预测提示FFEJJ治疗MAC的潜在药理活性化合物包括芹菜素、齐墩果酸、马斯林酸和壬二酸，其潜在机制可能部分与phosphatidylinositol3-激酶/丝氨酸-苏氨酸激酶（PI3K-Akt）信号通路有关。
[结论]FFEJJ可能通过调节内源性代谢紊乱促进MAC大鼠造血恢复，芹菜素、齐墩果酸、马斯林酸和壬二酸是多靶点活性化合物，PI3K-Akt信号通路是候选途径。
展开英文摘要原文
【OBJECTIVE】This study aimed to investigate the mechanism and pharmacologically active compounds of Fufang Ejiao Jiang (FFEJJ) in the prevention and treatment of myelosuppression after chemotherapy (MAC) through a combination of serum metabolomics and network pharmacology.
【METHODS】Sprague Dawley rats were randomly assigned to three groups: the blank group, the model group, and the FFEJJ group (10.8 g/kg). A MAC rat model was induced using cyclophosphamide. Simultaneously with model establishment, rats were intragastrically administered once daily for 15 consecutive days. The routine blood parameters of the rats were measured, and pathological changes in the spleen and bone marrow were observed. Nontargeted serum metabolomics was employed to identify differential metabolites associated with MAC and their related pathways. Liquid chromatography-mass spectrometry (LC-MS) was used to analyze the chemical composition of FFEJJ, and its mechanism and pharmacologically active compounds in the treatment of MAC were further predicted using network pharmacology.
【RESULTS】FFEJJ significantly improved the hematopoietic function of bone marrow in the MAC model rats. Compared to the blank group, the model group exhibited obvious spleen injury and bone marrow disorder, with noticeable fatty infiltration in the bone marrow cavity. Following FFEJJ treatment, the condition of spleen tissue and bone marrow in MAC rats was significantly improved. Serum metabolomics analysis of endogenous metabolites identified 14 differential metabolites associated with the MAC mechanism in both positive and negative ion modes, primarily involving pathways such as aminoacyl-tRNA biosynthesis, primary bile acid biosynthesis, and unsaturated fatty acid biosynthesis. Using LC-MS, 31 components were identified in FFEJJ. Network pharmacology predictions suggest that the potential pharmacologically active compounds of FFEJJ in the treatment of MAC include apigenin, oleanolic acid, maslinic acid, and azelaic acid. The underlying mechanism may be partly associated with the phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K-Akt) signaling pathway.
【CONCLUSION】FFEJJ promotes hematopoietic recovery in MAC rats, likely by regulating endogenous metabolic disorders. Apigenin, oleanolic acid, maslinic acid, and azelaic acid are predicted to be multitarget active compounds, with PI3K-Akt signaling as a candidate pathway.
相关物质
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