Elemene's effect on apoptosis of human lung cancer cells of A549 and its related molecular mechanisms
- VernacularTitle:榄香烯对肺癌A549细胞凋亡影响及分子机制研究
- Author:
Bin-Liang WANG
1
;
Yuan-Yuan CAI
;
Rong-Ying ZHANG
Author Information
1. 浙江省台州市第一人民医院呼吸内科
- Keywords:
Elemene;
Lung cancer cells of A549;
Cell apoptosis;
Molecular mechanisms
- From:
Shanghai Journal of Preventive Medicine
2015;27(11):690-693
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the inhibitory effect and molecular mechanism of elemene on A549 lung cancer cells. Methods Lung adenocarcinoma cancer cells A549 were treated with elemene of 10 mu g/mL, 20 mu g/mL, 40 mu g/mL, 80 mu g/mL, 160 mu g/mL, marked as observation group 1~5, with a blank control group 6 set up.The cell cycle and cell apoptosis rate were detected with flow cytometry at 24 h, 48 h, 72 h after elemene treatment, and eIF4E protein levels by Wsetern Bolt method. Results (1) At 24 h after treatment, there was no obvious change in each cell cycle, and the difference in cell percentage in G2/M phase, the sub-G1 phase was of no statistical significance ( P>0.05);and at 48 h, 72 h after treatment, the cell ratio in observation group during G2/M phase was significantly decreased compared with control group, and the difference between the two was statistically significant (P<0.05), but compared within the observation point, there was no statistical difference (P>0.05); The higher the concentration of elemene was, the more obvious was its inhibitory effect.( 2 ) With the growth of drug concentration, the cell apoptosis rate was markedly elevated .(3) In comparison with control group, 24 h after treatment, eIF4E expression in observation group was on the decline.And the higher the concentration was, the lower was the expression. Conclusion The inhibitory effect of elemene on A549 lung cancer cell is strong, and its influence on cell cycle is of dependency on dose and time; Cell apoptosis rate increased with the increase of drug concentration, but higher doses can cause side effects, reduce the apoptosisrate;physiological mechanism of A549 cell proliferation inhibition may be related to expression of inhibiting eIF4E.
