Astragalus polysaccharide induces apoptosis of human KG-1a cells through inhibiting PTEN-PI3K-Akt signaling pathway
10.3760/cma.j.issn.1009-9921.2014.04.008
- VernacularTitle:黄芪多糖通过阻断PTEN-PI3K-Akt信号通路诱导人类KG-1a细胞凋亡的研究
- Author:
Minhui HE
;
Fang CHEN
;
Yanping HU
;
Nan ZHANG
;
Shuang FU
;
Xuan LIU
;
Jihong ZHANG
- Publication Type:Journal Article
- Keywords:
Leukemia,myelocytic,acute;
Astragalus polysaccharide;
PTEN;
Akt
- From:
Journal of Leukemia & Lymphoma
2014;23(4):219-222
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of astragalus polysaccharide (AP) on proliferation and apoptosis of human acute myelocytic leukemia cell line KG-1a and the underlying mechanisms.Methods Human acute myelocytic leukemia cell line KG-la was cultured under 37 ℃ and 5 ％ C02,when appropriate cell passage and cryopreservation were performed.After treatment for 48 h with different concentrations of AP,the proliferative activity and apoptosis rate of KG-1a cells were examined by CCK-8 assay and flow cytometry,respectively.The expressions of p-Akt and bcl-2 protein in AP-treated KG-1a cells were evaluated by Western blot.The expression of PTEN mRNA by quantified real-time PCR.Results The proliferative activity of KG-la cell was obviously suppressed by AP treatment,and the inhibition rate increased in a dosedependent manner.The flow cytometry showed that,compared with the control group,the apoptosis rates of KG-1a cells were significantly increased after treatment with AP for 48 h.The early apoptosis rates were (1.98±0.16) ％,(12.60±0.48) ％,(16.31±0.73) ％,the late apoptotic rates were (3.11±0.19) ％,(17.17±1.40) ％,(21.17 ± 0.81)％,the differences were statistically significant (P ＜ 0.05).Western blot showed that the expressions of p-Akt and bcl-2 protein in KG-1a cells decreased significantly after treatment with AP (P ＜ 0.05).In contrast,the mRNA level of PTEN increased (P ＜0.05),which was shown by real-time PCR.Conclusion AP could repress cellular proliferation activity of KG-1a cells,which could be attributed to inhibition of PTEN-PI3K-Akt signaling pathway.
