Effects of dihydromyricetin on proliferation and apoptosis of human lung adenocarcinoma cells and its mechanism
10.3781/j.issn.1000-7431.2015.11.455
- Author:
Pingfang LU
1
Author Information
1. Department of Cardiothoracic Surgery, Affiliated Hospital of Guangdong Medical University
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Bcl-2;
Cell proliferation;
Dihydromyricetin;
Gene;
Lung neoplasms
- From:
Tumor
2015;35(10):1098-1105
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of dihydromyricetin on proliferation and apoptosis of human lung adenocarcinoma cell line NCI-H1975 in vitro, and to explore its molecular mechanism. Methods: After treatment with different concentrations of dihydromyricetin (10, 25, 50, 75 and 100 μmol/L) for different time (12, 24 and 48 h), the proliferation of human lung adenocarcinoma NCI-H1975 cells was detected by CCK-8 assay. The cell cycle and apoptosis rate of NCI-H1975 cells treated with different concentrations of dihydromyricetin (25, 50 and 100 μmol/L) for 24 h were determined by flow cytometry, and the change of cell morphology was observed by inverted phase contrast microscopy. Real-time fluorescent quantitative-PCR and Western blotting were used to analyze the expression levels of Bcl-2, Bax and Bad genes in NCI-H1975 cells treated with 25, 50 or 100 μmol/L dihydromyricetin for 24 h. Results: Dihydromyricetin significantly inhibited the proliferation of human lung adenocarcinoma NCI-H1975 cells in a dose- and time-dependent manner (P < 0.05). Dihydromyricetin significantly induced apoptosis of NCI-H1975 cells (P < 0.01), but it did not induce cell cycle arrest (P > 0.05). Furthermore, dihydromyricetin significantly decreased the expression levels of Bcl-2 mRNA and protein in NCI-H1975 cells (both P < 0.05), and up-regulated the expression levels of Bax mRNA and protein as well as the expression level of phospho-Bad protein (all P < 0.05), but did not change the expression levels of Bad mRNA and protein (both P > 0.05). Conclusion: Dihydromyricetin can suppress the growth of human lung adenocarcinoma cells through regulating the expression of Bcl-2 protein family in mitochondrial apoptotic pathway. Dihydromyricetin may be a potential drug for the treatment of lung carcinoma.
