Effect of allicin on proliferation and apoptosis of KG-1 cells and its molecular mechanism.
10.19540/j.cnki.cjcmm.20180320.002
- Author:
Zheng LOU
1
;
Qing-Qing WEI
2
;
Da-Wei WANG
3
;
Huan-Peng GU
3
Author Information
1. The 2nd Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou 310053, China.
2. School of Stomatology, Zhejiang Chinese Medical University, Hangzhou 310053, China.
3. Basic Medical College, Zhejiang Chinese Medical University, Hangzhou 310053, China.
- Publication Type:Journal Article
- Keywords:
KG-1 cells;
allicin;
apoptosis;
cleaved caspase 3;
p-ERK
- From:
China Journal of Chinese Materia Medica
2018;43(12):2612-2617
- CountryChina
- Language:Chinese
-
Abstract:
Allicin is one of the main bioactive substances in garlic, with antibacterial, hypolipidemic and other pharmacological effects. In this study, apoptosis-related indicators were detected to explore the molecular mechanism of allicin on KG-1 cell proliferation inhibition. The apoptosis rate of KG-1 cells induced by allicin was detected by flow cytometry. The effect of allicin on the expressions of Bax, Bcl-2, survivin and ERK mRNA in KG-1 cells was detected by RT-qPCR. Western blot was used to detect the expressions of caspase 3, cleaved caspase 3, ERK1/2, p-ERK1/2 and survivin protein in KG-1 cells. According to the findings, compared with the control group, allicin could significantly inhibit the proliferation activity of KG-1 cells in a concentration-dependent and time-dependent manner. Flow cytometry showed that allicin could induce the apoptosis of KG-1 cells, which was mainly late apoptosis. The results of RT-qPCR showed that the expressions of Bax mRNA, Bcl-2, survivin and ERK mRNA in KG-1 cells increased after treatment with allicin. The results of Western-blot showed that after KG-1 cells were treated with allicin, the expressions of caspase 3 and its active form cleaved caspase 3 increased, the expressions of survivin, ERK1/2 and its active form p-ERK1/2 were decreased, of which p-ERK1/2 was down-regulated in a dose-dependent manner. The above results suggest that allicin inhibited the proliferation of KG-1 cells primarily by inducing late apoptosis; the execution of apoptosis involved cleaved caspase 3; the induction of apoptosis involved the protein expression, the decrease of ERK1/2andexpression of survivin and the dose-dependent decrease of p-ERK1/2; the mRNA expression involved the increase of Bax, and the down-regulation of survivin, Bcl-2 and ERK1/2.
