|
| Anticancer drug | Biological system/model | Doses | Main results | Ref |
|
| EGCG: in vitro experiments |
| Oxaliplatin, cisplatin | A2780 and A2780R ovarian cancer cell lines parental and cisplatin resistant, respectively | ED50, ED75, ED90 (ED, effective dose) | Increased synergism at ED50 after the sequential administration of the phytochemical, at 4 h after oxaliplatin or cisplatin treatment (increased growth inhibitory effects) | [154, 155] |
| Oxaliplatin, cisplatin | DLD-1, HT-29 human colorectal adenocarcinoma cells | 100 μM EGCG
20 μM oxaliplatin or cisplatin | Decreased cell proliferation, induced autophagy | [156] |
|
| Curcumin: in vitro experiments |
| Carboplatin, etoposide, vincristine | Y 79 retinoblastoma cells | 5–10 μM curcumin
5–10 μg/mL carboplatin
0.1–5 μg/mL etoposide
0.1–5 nM vincristine | Increased apoptosis
Curcumin increased the sensitivity of retinoblastoma cells to carboplatin, etoposide, and vincristine | [183] |
| Oxaliplatin | A2780 and A2780R ovarian cancer cell lines parental and cisplatin resistant, respectively | ED50, ED75, ED90 (ED, effective dose) | Increased synergism at ED50 after the sequential administration of the phytochemical, at 4 h after oxaliplatin (increased growth inhibitory effects) | [154, 155] |
| Cisplatin | A2780R cisplatin resistant human ovarian cancer cell line | 1–10 μM curcumin analogs
10 μg/mL cisplatin | Cotreatment increased cytotoxicity (MTT assay), induced G2/M arrest, increased p21 and p53 levels, decreased Bcl-2 and Bcl-XL levels, increased caspase-9, caspase-3, and caspase-7 and PARP levels, increased apoptosis, and reduced STAT3 level | [157] |
|
| Curcumin: in vivo experiments |
| Cisplatin | Xenograft tumor in nude mice with A2780R cells Cisplatin resistant ovarian cancer cells | 100 ppm curcumin analogs in feed
4 mg/kg cisplatin i.p. | Cotreatment reduced the tumor volume, decreased constitutive activation of pSTAT3-Tyr705 and pSTAT3-Ser727, decreased Bcl-2 and Bcl-XL levels, and increased PARP levels | [157] |
|
