Effects of Benzoyl Aconitine on Autophagy and Apoptosis of Human Lung Cancer Cell Line A 549
- VernacularTitle:苯甲酰乌头原碱对人肺癌A549细胞自噬和凋亡的影响
- Author:
Xin SHAO
1
,
2
;
Bin HAN
2
;
Xianhong JIANG
3
;
Feng LI
1
,
2
;
Mei HE
2
;
Fu LIU
1
Author Information
1. School of Pharmacy，North Sichuan Medical College，Sichuan Nanchong 637000，China
2. Dept. of Pharmacy，the Affiliated Hospital of North Sichuan Medical College，Sichuan Nanchong 637000，China
3. Dept. of Clinical Medicine，North Sichuan Medical College，Sichuan Nanch ong 637000，China
- Publication Type:Journal Article
- Keywords:
Benzoyl aconitine;
Non-small cell lung cancer;
A549 cells;
Proliferation;
Autophagy;
Apoptosis
- From:
China Pharmacy
2019;30(20):2782-2788
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE： To study the effects of benzoyl aconitine （BAC） on autophagy and apoptosis of human lung cancer A549 cells， and to investigate its mechanism in anti-non-small cell lung cancer. METHODS： A549 cells were treated with different doses of BAC （10， 50， 100， 200， 400 μmol/L）， and then cell morphology was obtained； the proliferation inhibition rate of the cell was determined by CCK-8 assay. The cells were divided into control group （without drug）， BAC low-dose and high-dose groups （200， 400 μmol/L）. After treated with relevant drugs， the apoptosis rate of cells was determined by flow cytometry. The gene and protein expression of apoptosis-related factors Bcl-2， Bax， Caspase-3 as well as autophagy-related factors Beclin1， LC3， P62 were determined by RT-PCR and Western blotting assay. RESULTS： After treated with different doses of BAC， the cells were shrunken and sparsely arranged； inhibitory rate of cell proliferation was increased significantly in BAC 100， 200， 400 μmol/L groups （P＜0.05 or P＜0.01）. Results of flow cytometry showed that the apoptotic rates of cells were increased to different extents in BAC low-dose and high-dose groups after treated for 24 and 48 h， in a concentration and time-dependent manner. Compared with control group， mRNA and protein expression of Bcl-2 and P62 were decreased to different extents in BAC groups； mRNA expression of Bax， Caspase-3， Beclin1 and LC3 as well as protein expression of Bax， Active caspase-3， P62， Beclin1， LC3Ⅱ/Ⅰ were increased to different extent； there was statistical significance in mRNA expression of Caspase-3， and protein expression of Bcl-2， Active Caspase-3， Beclin1， LC3Ⅱ/Ⅰ and P62 in BAC low-dose group as well as all target mRNA and protein expression in BAC high-dose group （P＜0.05 or P＜0.01）， in dose-dependent manner. CONCLUSIONS： BAC can inhibit the proliferation and promote the apoptosis of A549 cells， promote Beclin1， LC3（LC3Ⅱ/Ⅰ），Bax and Caspase-3 （Active Caspase-3） gene and their protein expression， but inhibit P62 and Bcl-2 gene and their protein expression. The mechanism may be related to BAC inducing apoptosis by promoting excessive autophagy of cells.
