Effects of cultivated Cordyceps sinensis on proliferation and apoptosis of human leukemia K562 cells.
10.19540/j.cnki.cjcmm.20180125.008
- Author:
Xue-Lian BAI
1
;
Shu-Xian YANG
1
;
Yu SHAN
1
;
Wen-Jia LI
2
;
Jing LI
2
;
Ying XIAO
2
;
Xue-Feng HU
2
;
Li CAO
1
Author Information
1. Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China.
2. Key Laboratory of State Administration of Traditional Chinese Medicine, Sunshine Lake Pharma Co., Ltd., Dongguan 523850, China.
- Publication Type:Journal Article
- Keywords:
Cordyceps sinensis;
apoptosis;
leukemia;
proliferation
- From:
China Journal of Chinese Materia Medica
2018;43(10):2134-2139
- CountryChina
- Language:Chinese
-
Abstract:
The present study was designed to investigate the effect of cultivated Cordyceps sinensis (CCS) on leukemia-derived K562 cells, and further explore the underlying mechanisms. After routine culture of K562 cells, MTT assay was used to detect the effect of CCS on survivel of human leukemia cell lines K562;DAPI staining was used to observe the morphological changes of the nucleus and AO/EB staining was used to observe cell apoptosis. JC-1 staining was employed to detect the changes in mitochondrial membrane potential. Flow cytometry (FCM) was used to detect cell cycle distribution, and Western blot analysis was used to detect the expression levels of Bax, Bcl-2, caspase 3, caspase 8, cyclin D1, CDK2, and CDK4 in K562 cells. The results showed that CCS (0.345-5.524 g·L⁻¹) substantially suppressed proliferation of K562 cells and induced G₁/S phase arrest in a dose-dependent manner. DAPI and AO/EB staining indicated that cell apoptosis was significantly induced by CCS treatment, accompanied by decreased mitochondrial membrane potential demonstrated by JC-1 staining. Western blot results showed that CCS significantly increased the expression of Bax and, meanwhile, decreased the expression levels of Bcl-2, cyclin D1, CDK2, CDK4, caspase 3 and caspase 8. Collectively, our data demonstrated that CCS dose-dependently suppressed cell proliferation and induced cell apoptosis in K562 cells, and the mechanism might be associated with inducing cell cycle arrest, regulating Bcl-2/Bax ratio and activating the mitochondrial apoptosis pathway.
