Abstract Context: ShengMaBieJia decoction (SMBJD) is used to treat solid and hematological tumours; however, its anti-angiogenesis activity remains unclear. Objective: This study verified the anti-angiogenic effects of SMBJD in vitro and in tumour-bearing acute myeloid leukaemia (AML) mouse models. Materials and methods: In vivo, the chicken chorioallantoic membrane (CAM) and BALB/c null mouse xenograft models were treated with SMBJD (0, 2, 4, and 8 mg/mL) for 48 h and for 2 weeks, respectively. Anti-angiogenic activity was assessed according to microvessel density (MVD) and immunohistochemistry (IHC) targeting CD31 and VEGFR2. In vitro, proliferation viability, migratory activity and tube formation were measured. Western blots and polymerase chain reaction (PCR) assays were used to examine the levels of PI3K, Akt, and VEGF. Results: HPLC analyses revealed the active constituents of SMBJD such as liquiritin, cimifugin, ferulic, isoferulic, and glycyrrhizic acids. In vitro, SMBJD treatment decreased cellular migration, chemotaxis, and tube formation at non-cytotoxic concentrations (2, 4, and 8 mg/mL) in a time- and dose-dependent manner. The dosage of less than IC20 is considered safe. In vivo, CAM models exhibited a decrease in MVD, and the tissues of xenografted mice possessed reduced CD31 and VEGFR2 expression. Conditioned media (CM) from AML cells (HL60 and NB4 cells) treated with non-cytotoxic doses of SMBJD inhibited chemotactic migration and tube formation in vitro. Both CM (HL60) and CM (NB4) exhibited downregulated expression of PI3K, Akt, and VEGF. Discussion and conclusions: SMBJD inhibited angiogenesis in AML through the PI3K/AKT pathway, which might be combined with targeted therapy to provide more effective treatment.

中文翻译：

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生麻痹加汤体外及在急性髓系白血病荷瘤小鼠模型中的抗血管生成活性

摘要 背景：生麻痹加汤（SMBJD）用于治疗实体瘤和血液瘤；然而，其抗血管生成活性仍不清楚。目的：本研究验证了 SMBJD 在体外和荷瘤急性髓系白血病 (AML) 小鼠模型中的抗血管生成作用。材料和方法：在体内，鸡绒毛尿囊膜 (CAM) 和 BALB/c 无效小鼠异种移植模型分别用 SMBJD（0、2、4 和 8 毫克/毫升）处理 48 小时和 2 周。根据靶向 CD31 和 VEGFR2 的微血管密度 (MVD) 和免疫组织化学 (IHC) 评估抗血管生成活性。在体外，测量了增殖活力、迁移活性和管形成。蛋白质印迹和聚合酶链反应 (PCR) 测定用于检查 PI3K、Akt 和 VEGF 的水平。结果：HPLC 分析揭示了 SMBJD 的活性成分，如甘草苷、升麻素、阿魏酸、异阿魏酸和甘草酸。在体外，SMBJD 治疗在非细胞毒性浓度（2、4 和 8 毫克/毫升）下以时间和剂量依赖性方式减少细胞迁移、趋化性和管形成。低于IC20的剂量被认为是安全的。在体内，CAM 模型表现出 MVD 降低，异种移植小鼠的组织具有降低的 CD31 和 VEGFR2 表达。来自用非细胞毒性剂量的 SMBJD 处理的 AML 细胞（HL60 和 NB4 细胞）的条件培养基 (CM) 在体外抑制了趋化迁移和管形成。CM (HL60) 和 CM (NB4) 均表现出 PI3K、Akt 和 VEGF 的下调表达。讨论和结论：SMBJD 通过 PI3K/AKT 通路抑制 AML 中的血管生成，