Combination of triptolide with sodium cantharidinate synergistically enhances apoptosis on
hepatoma cell line 7721.
10.11817/j.issn.1672-7347.2016.09.005
- Author:
Yuyan ZHOU
1
;
Mingyan WANG
2
;
Xuejuan PAN
1
;
Zaifeng DONG
1
;
Li HAN
1
;
Yong JU
1
;
Guodong WANG
1
Author Information
1. School of Pharmacy, Wannan Medical College, Wuhu Anhui 241000, China.
2. Pre-Clinical Medicine School, Nanjing University of Chinese Medicine, Nanjing 210046, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cantharidin;
pharmacology;
therapeutic use;
Carcinoma, Hepatocellular;
drug therapy;
Caspase 3;
drug effects;
Cell Line, Tumor;
Diterpenes;
pharmacology;
therapeutic use;
Down-Regulation;
Drug Therapy, Combination;
Epoxy Compounds;
pharmacology;
therapeutic use;
Humans;
Liver Neoplasms;
drug therapy;
NF-kappa B;
drug effects;
Phenanthrenes;
pharmacology;
therapeutic use;
Transcription Factor RelA
- From:
Journal of Central South University(Medical Sciences)
2016;41(9):911-917
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To determine the combined cytotoxic effect and the molecular basis of triptolide and sodium cantharidinate on hepatoma cell line 7721.
METHODS:After treating the hepatoma cell line 7721 with triptolide(9, 18, or 36 μg/mL) and/or sodium cantharidinate (2, 5, or 10 μg/mL), cell viability assay and apoptosis were examined by MTT and flocytometry, respectively. The protein levels of caspase 3 and nuclear factor κB were analyzed by Western blot.
RESULTS:Viability of hepatoma cell line 7721 was inhibited by either the therapy of triptolide and/or sodium cantharidinate (P<0.05) in a time- and dose-dependent manner. The combined effects of both drugs were better than those of the single drug (P<0.05). The combined therapy down-regulated the expression of NF-κB p65 (P<0.05) while up-regulated the expression of caspase-3 (P<0.05).
CONCLUSION:Triptolide and sodium cantharidinate exert a synergistic toxic effect on hepatoma cell line 7721, which is related to increasing capase-3 activity and suppression of NF- κB.
