Honokiol-induced apoptosis of human non-Hodgkin lymphoma Raji cells and its possible mechanism.
- Author:
Wei CHEN
1
;
Guan-wen LIN
;
Qing ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents, Phytogenic; pharmacology; Apoptosis; drug effects; Biphenyl Compounds; pharmacology; Burkitt Lymphoma; pathology; Caspase 8; metabolism; Cell Line, Tumor; Cell Proliferation; drug effects; Humans; Lignans; pharmacology; Lymphoma, Non-Hodgkin; pathology; bcl-Associated Death Protein; genetics; metabolism
- From: Journal of Southern Medical University 2011;31(11):1918-1921
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the apoptosis-inducing effect of honokiol on human non-Hodgkin lymphoma Raji cells and the possible mechanism.
METHODSRaji cells were treated with different concentrations of honokiol, and the proliferation of the cells was detected using MTT assay. Flow cytometry was employed to analyze the cell cycle changes and apoptosis of honokiol-treated cells. Caspase 8 activity in the cells was measured by caspase 8 kit, and RT-PCR was used to detect the expression of apoptosis-related genes Bcl-2, Bad, and Bax.
RESULTSHonokiol significantly inhibited the growth of Raji cells in a time- and dose-dependent manner, with IC(50) concentration of 17.53, 12.61, and 7.4 µg/ml at 12, 24, 48 h, respectively. Flow cytometry revealed cell cycle arrest at G0/G1 phase following honokiol treatment. The apoptosis rates of Raji cells treated with 7.5 and 15 µg/ml honokiol were significantly higher than that of the control cells [(18.24∓2.53)%, (28.44∓2.48)% vs (4.84∓1.15)%, P<0.01]. Caspase 8 activity in Raji cells was significantly enhanced by honokiol (P<0.05). The mRNA expression of the apoptosis-promoting gene Bad was significantly increased following honokiol treatment (P<0.01), while the expressions of Bcl-2 and Bax remained unchanged.
CONCLUSIONHonokiol can induce apoptosis in Raji cells possibly in relation to enhancement of caspase 8 activity and Bad gene expression.