Inhibition Effect of Eriodictyol to Growth of DG-75 Cells and the Related Action Mechanism.
10.19746/j.cnki.issn.1009-2137.2021.06.017
- Author:
Bin LIU
1
;
Dao WANG
2
;
Xia SUN
3
;
Xi-Xi ZHAO
1
;
Ming-Li XIANG
1
;
Li-Min JIN
4
;
Na LI
1
;
Shao-Qiong NIU
5
Author Information
1. Department of Pediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China.
2. Department of Pediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China,E-mail: deai315@163.com.
3. College of Nursing, Zhengzhou University, Zhengzhou 450052, Henan Province, China.
4. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China.
5. Department of Cardiology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang 471000, Henan Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Flavanones;
Phosphatidylinositol 3-Kinases/metabolism*;
Signal Transduction
- From:
Journal of Experimental Hematology
2021;29(6):1790-1796
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the effects of Eriodictyol to the growth, apoptosis and oxidative stress of Burkitt lymphoma (BL) cells and phosphorylation of protein kinase B (AKT) in children.
METHODS:The effects of Eriodictyol (0, 1.25, 2.5, 5, 10, 20, 40, 80, 160, 320 μmol/L) to viability of BL cell line DG-75 cells were detected by CCK-8. The effects of Eriodictyol (0, 10, 20, 40 μmol/L) to the proliferation activity of DG-75, apoptosis rate, levels of apoptosis-related proteins, oxidative stress indexes ［superoxide dismutase (SOD), malondialdehyde (MDA)］, mitochondrial membrane potential (MMP) and phosphorylation level of phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycinm (mTOR) were detected by clony formation assay and Wester blot.
RESULTS:When the treatment concentration of Eriodictyol was 20 μmol/L, the proliferation activity of the cells was decreased (P<0.05). The concentrations at 10, 20, 40 μmol/L were selected for subsequent experiments. Compared with 0 μmol/L Eriodictyol, the proliferation activity of DG-75, SOD activity, MMP, phosphorylation levels of PI3K, AKT and mTOR in 20 and 40 μmol/L Eriodictyol treatment groups were significantly decreased (P<0.05), while cells apoptosis rate, Cleaved-Caspase-3/Caspase-3, Bax/Bcl-2 and MDA level were significantly increased (P<0.05).
CONCLUSION:Eriodictyol may promote the mitochondrial apoptosis pathway by inhibiting the abnormal activation of PI3K/AKT/mTOR to reduce the proliferation activity of DG-75, and inhibit oxidative stress response to increase the apoptosis rate and play anti-tumor roles.
