Efficacy and Mechanism of Shenbai Jiedu Prescription Against Proliferation of HCT116 Cells
10.13422/j.cnki.syfjx.20220423
- VernacularTitle:参白解毒方抑制HCT116细胞增殖的药效及机制
- Author:
Dong JIANG
1
;
Haibo CHENG
1
;
Weixing SHEN
1
;
Changliang XU
1
;
Jiani TAN
1
;
Yueyang LAI
1
;
Dongdong SUN
1
;
Liu LI
1
;
Minmin FAN
1
;
Chengtao YU
1
;
Jun XIAO
2
Author Information
1. The First Clinical College of Nanjing University of Chinese Medicine， Nanjing 210023， China
2. Jiangsu Province Hospital of Chinese Medicine， Affiliated Hospital of Nanjing University of Chinese Medicine， Nanjing 210004， China
- Publication Type:Journal Article
- Keywords:
cancer poison;
colorectal cancer （CRC）;
apoptosis;
cell cycle;
nuclear factor kappa-B （NF-κB） signaling pathway
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(13):34-41
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanism by which Shenbai Jiedu prescription （SBJDF） inhibits the proliferation of colorectal cancer （CRC） HCT116 cells. MethodAfter 48 h treatment of HCT116 cells with SBJDF （0， 0.25， 0.5， 1， 2， 4 g·L-1）， the viability of HCT116 cells were determined by methyl thiazolyl tetrazolium （MTT） colorimetry. Following the classification of cells into blank control group and SBJDF （1， 2， 4 g·L-1） groups， the effect of SBJDF on HCT116 cell morphology was observed under an inverted microscope. The effects of SBJDF on the proliferation of HCT116 cells and mitochondrial membrane potential （Δψm） were detected by colony formation assay and JC-1 probe， respectively. The flow cytometry was then performed for determining cell cycle distribution and apoptosis. The effects of SBJDF on cell cycle-， apoptosis-， and nuclear factor kappa-B （NF-κB） signaling pathway-related proteins were determined by Western blot. ResultSBJDF effectively inhibited the vitality of HCT116 cells and changed their morphology in a concentration-dependent manner. Compared with the blank control group， SBJDF at 1， 2， 4 g·L-1 significantly reduced cell colony formation （P<0.05， P<0.01），and SBJDF at 2 and 4 g·L-1 arrested the HCT116 cell cycle at G0/G1 phase （P<0.05， P<0.01）. Compared with the blank control group， SBJDF at 1， 2， 4 g·L-1 remarkably down-regulated the protein expression of CyclinD1 （P<0.05， P<0.01）. SBJDF at 2 and 4 g·L-1 lowered the CyclinA2 and cyclin-dependent kinase 4 （CDK4） （P<0.05， P<0.01）. SBJDF at 4 g·L-1 reduced the cyclin-dependent kinase 1 （CDK1） （P<0.01）. Compared with the blank control group， SBJDF at 2 and 4 g·L-1 induced HCT116 cell apoptosis， down-regulated the protein expression of anti-apoptosis-related proteins Bcl-2 and Bcl-xl as well as the NF-κB signaling pathway-related proteins IκB kinase α （IKKα），inhibitor α of NF-κB （IκBα），and phospho-NF-κB p65 （p-p65） （P<0.05， P<0.01）， and diminished the mitochondrial membrane potential of HCT116 cells. ConclusionSBJDF inhibits the proliferation of HCT116 cells， which may be related to its inhibition of the activation of NF-κB signaling pathway and the induction of cell cycle arrest and apoptosis.
