Table 2.
Inhibition effect on Nrf-2/ARE pathway in cancer models.
| Compound | Concentration | Cell Line | Cell Type | Effect | Ref |
|---|---|---|---|---|---|
| Chrysin | 10–20 µM | BEL-7402/ADM cells | Hepatocellular carcinoma | ↓ mRNA and protein expression of Nrf2, HO-1, MRP5, and aldo-keto reductase family 1 member B10 (AKR1B10) | [137] |
| Chrysin [nanostructural lipid carriers] |
5–50 µM | MCF-7 | Breast cancer | ↓mRNA and protein expression of Nrf2; NQO1, HO1 i MRP1 | [141] |
| Chrysin | 10–60 µM | T98, U251, U87 | human glioblastomas | ↓ Nrf2, NQO-1, HO-1 (Keap1-independent); ↓ ERK signaling | [142] |
| Apigenin | 10 μM | BEL-7402/ADM | Hepatocellular carcinoma | inhibiting miR-101/Nrf2 pathway |
[143] |
| Kaempferol | 25 μM | A549, NCIH460 | NSCLC | ↓ mRNA and protein expression of Nrf2; ↓ AKR1C1, NQO1, HO1 i GS; ↑ ROS |
[144] |
| 25–50 μM | PANC-1, PaCa-2 | pancreatic cancer | ROS-dependent suppression Akt/mTOR signaling; ↓ Keap; Nrf2 (ambiguous impact) |
[145] | |
| Quercetin | 50 μM | human xenograft acute myeloid leukemia (AML) models, and in vitro using leukemia cell lines | ↓ Nnf2 nuclear localization; ↓ pNrf2 ↓ HDAC4; |
[146] |
The arrow ↑ or ↓ indicates an increase or decrease in concentration/expression or content in the cells, respectively.