The mechanism of alteronol inhibiting the proliferation of human promyelocytic leukemia HL-60 cells.
- Author:
Liang-Liang LIU
1
;
Na CHEN
;
Xuan YUAN
;
Ying YAO
;
Bo ZHANG
;
Qiu-Sheng ZHENG
Author Information
1. Key Laboratory of Xinjiang Endemic Phytomedicine Resources, School ofPharmacy, Shihezi University, Shihezi 832002, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
administration & dosage;
pharmacology;
Apoptosis;
drug effects;
Cell Cycle;
drug effects;
Cell Proliferation;
drug effects;
Cyclin D1;
metabolism;
Dose-Response Relationship, Drug;
HL-60 Cells;
Humans;
Naphthoquinones;
administration & dosage;
pharmacology;
Phosphorylation;
Retinoblastoma Protein;
metabolism
- From:
Acta Pharmaceutica Sinica
2012;47(11):1477-1482
- CountryChina
- Language:Chinese
-
Abstract:
This study is to investigate the mechanism of human promyelocytic leukemia HL-60 cells proliferation induced by alteronol in vitro. Human promyelocytic leukemia HL-60 cells cultured in vitro were treated with different concentrations of alteronol. Inhibition rate was detected by SRB assay. Cellular morphological changes were observed by Hoechst and AO/EB (acridine orange/ethidium bromide dye) staining. The apoptosis rate was determined by Annexin V-FITC/PI assay. Cell cycle distribution was determined by flow cytometry. Western blotting analysis was carried out to determine the cell cycle related proteins. The proliferation of HL-60 cells treated with alteronol was inhibited in a concentration-dependent manner. Based on cell viability assay, observation on cell morphology and apoptosis rate, it confirmed that alteronol played an obvious role in proliferation inhibition of human promyelocytic leukemia HL-60 cells, but it did not induce apoptosis in human promyelocytic leukemia HL-60 cells in different concentrations groups. Alteronol could effectively inhibit the proliferation of human promyelocytic leukemia HL-60 cells inducing cell cycle arrest at G1 phase, as well as, alteration expression of cell cycle proteins level of CyclinD1 and pRb.
