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| Cell line | Cell type | Specific results | Mode of action | References |
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| U87 | Glioblastoma | The cells were treated with evodiamine (10 µM) and TRAIL (50 ng/ml) either separately or in combination for 24 h. TRAIL alone did not induce apoptosis, whereas evodiamine significantly induced apoptosis in U87 glioblastoma cells after 24 h (apoptosis rate: 35%–70%). | Sensitizing cells to TRAIL via the death receptor pathway | [56] |
| A549 and H1299 | Lung epithelial cancer | Evodiamine (20–40 µM) treatment of A549 cells for 24 h significantly increased the number of apoptotic cells by sixfold. | Activating both the intrinsic and the extrinsic apoptosis pathways | [57] |
| U937 | Leukemia | The cells were treated with evodiamine (0.2–0.8 µmol/L) for 18 h. Evodiamine induced apoptosis in a dose-dependent manner (sub-G1 population: 5%–45%). | Activating caspase-dependent and caspase-independent pathways | [58] |
| MC3 and HSC4 | Oral cancer | The cells were treated with various concentrations of evodiamine (0.25, 0.5, and 1 μM for MC3 cells; and 0.2, 2, and 20 μM for HSC4 cells) for 24 h. The apoptotic effect of evodiamine was confirmed by 4′-6-diamidino-2-phenylindole (DAPI) staining. Evodiamine-treated cells displayed nuclear condensation and fragmentation—hallmarks of apoptosis. | Inhibiting the AKT pathway | [59] |
| H446 and H1688 | Small cell lung cancer | The induction of apoptosis was detected in H446 or H1688 cells after 24 h of treatment with 10 μM evodiamine. The apoptosis rate of evodiamine-treated H446 (∼15%) or H1688 (∼11%) cells was much higher than that of the untreated cells (blank control, ∼5% or ∼4%). | Activating mitochondria-dependent and endoplasmic reticulum stress-induced pathways | [60] |
| U87-MG | Glioblastomas | The percentage of autophagy induced by evodiamine (0, 0.1, 6, 10 μM) increased to a maximum at 24 h, but not at 48 h, indicating that evodiamine-induced autophagy in a dual-regulated manner. | Activating calcium/c-Jun N-terminal kinase and calcium/mitochondria-mediated pathways | [61, 62] |
| Panc-1 and SW1990 | Pancreatic cancer | PANC-1 and SW1990 cells were treated with evodiamine (1.0, 5.0, and 10 µM) for 48 h. The exposure of cells to evodiamine led to a dose-dependent increase in apoptosis. Apoptosis rate: 2.5%–17.5% (Panc-1); 4%–18% (SW1990). | Inhibiting the PI3K-Akt and the MAPK/ERK signaling pathways | [63] |
| Murine Lewis lung carcinoma | Lung carcinoma | The cells exhibited an increase in MDC fluorescence within 1.5–6 h after evodiamine treatment, while the peak of autophagy activity was observed in 1.5 h treatment. In addition, evodiamine-treated cells displayed a greater number of distinct spots within the cytoplasm or perinuclear regions compared with controls. | Activating caspase-independent pathways | [64] |
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