Effect of ginsenoside Rh2(S) on apoptosis of human leukemia cell by inhibiting HDAC6
10.7501/j.issn.0253-2670.2018.24.021
- Author:
Ze-Hong LIU
1
Author Information
1. Department of Physiology, Chongqing Medical and Pharmaceutical College
- Publication Type:Journal Article
- Keywords:
Acetylation modification;
Akt;
Apoptosis;
Ginsenoside Rh2(S);
GSK-3β;
HDAC6;
HSP90;
LLeukemia;
β-catenin
- From:
Chinese Traditional and Herbal Drugs
2018;49(24):5876-5881
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the specific mechanism of ginsenoside Rh2(S) inducing the apoptosis of leukemia cells. Methods The effect of Rh2(S) on proliferation of leukemia cells K562 and KG1a was measured by cell counting kit-8 assay (CCK-8 assay). The growth states of cells were observed under the inverted phase microscope, and cell cycle distribution, and apoptosis were determined by flow cytometry (FCM). The expression levels of HDAC6, HSP90, Akt, GSK-3β, β-catenin, and cell cycle apoptosis related proteins were ascertained by Western blotting. Results The results of CCK-8 showed that Rh2(S) had the most obvious inhibitory effect on the proliferation of leukemia cells. Rh2(S) significantly induced apoptosis and led to cell cycle arrest at G0/G1 phase of leukemia cells by FCM. While the microscope observation showed that the number of cells was decreased and normal cell morphology changed. Rh2(S) decreased the expression of Bcl-2, Cyclin D1, HDAC6, HSP90, p-Akt, and β-catenin and increased the expression of Bax, Ac-α-tubulin, and GSK-3β by Western blotting. Conclusion Rh2(S) can effectively inhibit the proliferation and promote the apoptosis of K562 and KG1a cells, its specific mechanism may relate to inhibitting the expression of HDAC6, resulting in a decline in the expression of HSP90, so as to further inhibit the activity of Akt activation of GSK-3, and finally inhibit Wnt/β-catenin pathway.
