2009Chongqing Yike Daxue xuebaoRequires access

Experimental study of K562 leukemia cells apoptosis induced by emodin

Jin Dan-ting

Open publisher page 0 citations

Abstract

Objective: To study the mechanism of K562 leukemia cells proliferation and apoptosis induced by emodin. Methods: Inhibitory effect of emodin on proliferation of K562 leukemia cells was assayed by MTT method. The morphologic changes of K562 cells were observed under microscop after Wight-Giemsa staining. Apoptosis was checked by Annexin V/PI. The changes of cell cycle and apoptosis were detected by flow cytometry. The activities of Caspase-3,8,9 were checked by chromatometry to analyze the apoptosis of K562 cells. Results: The proliferation of K562 leukemia cells was significantly inhibited by emodin. The IC50 of K562 cells inhibited with emodin for 24 h,48 h and 72 h were 80,50 and 40 μmol/L respectively. Typical morphological changes of K562 cells were observed by microscopy. The proliferation of K562 cells was obviously inhibited in dose-dependent manner. In Annexin V/PI,emodin induced K562 cells toward apoptosis in dose-dependent manner(P0.01). The result of flow cytometry indicated that the cell cycle was blocked in G0/G1 phase (P0.01). After treated with emodin,the activities of Caspase-3,8,9 were significantly higher than those in the normal control (P0.01). Conclusion:Emodin inhibits proliferation and induces apoptosis ofK562 leukemia cells,and up-regulatingthe experession of Caspase may be one of its mechanisms.

About this research paper

What this paper is about

Objective: To study the mechanism of K562 leukemia cells proliferation and apoptosis induced by emodin. Methods: Inhibitory effect of emodin on proliferation of K562 leukemia cells was assayed by MTT method. The morphologic changes of K562 cells were observed under microscop after Wight-Giemsa staining. Apoptosis was checked by Annexin V/PI. The changes of cell cycle and apoptosis were detected by flow cytometry. The activities of Caspase-3,8,9 were checked by chromatometry to analyze the apoptosis of K562 cells. Results: The proliferation of K562 leukemia cells was significantly inhibited by emodin. The IC50 of K562 cells inhibited with emodin for 24 h,48 h and 72 h were 80,50 and 40 μmol/L respectively. Typical morphological changes of K562 cells were observed by microscopy. The proliferation of K562 cells was obviously inhibited in dose-dependent manner. In Annexin V/PI,emodin induced K562 cells toward apoptosis in dose-dependent manner(P0.01). The result of flow cytometry indicated that the cell cycle was blocked in G0/G1 phase (P0.01). After treated with emodin,the activities of Caspase-3,8,9 were significantly higher than those in the normal control (P0.01). Conclusion:Emodin inhibits proliferation and induces apoptosis ofK562 leukemia cells,and up-regulatingthe experession of Caspase may be one of its mechanisms.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective: To study the mechanism of K562 leukemia cells proliferation and apoptosis induced by emodin. Methods: Inhibitory effect of emodin on proliferation of K562 leukemia cells was assayed by MTT method. The morphologic changes of K562 cells were observed under microscop after Wight-Giemsa staining. Apoptosis was checked by Annexin V/PI. The changes of cell cycle and apoptosis were detected by flow cytometry. The activities of Caspase-3,8,9 were checked by chromatometry to analyze the apoptosis of K562 cells. Results: The proliferation of K562 leukemia cells was significantly inhibited by emodin. The IC50 of K562 cells inhibited with emodin for 24 h,48 h and 72 h were 80,50 and 40 μmol/L respectively. Typical morphological changes of K562 cells were observed by microscopy. The proliferation of K562 cells was obviously inhibited in dose-dependent manner. In Annexin V/PI,emodin induced K562 cells toward apoptosis in dose-dependent manner(P0.01). The result of flow cytometry indicated that the cell cycle was blocked in G0/G1 phase (P0.01). After treated with emodin,the activities of Caspase-3,8,9 were significantly higher than those in the normal control (P0.01). Conclusion:Emodin inhibits proliferation and induces apoptosis ofK562 leukemia cells,and up-regulatingthe experession of Caspase may be one of its mechanisms.

Key concepts: K562 cells, Apoptosis, Emodin, Annexin, Flow cytometry, Leukemia, Molecular biology, Cell growth

Related papers

Back to paper searchBrowse research topicsOriginal source
Experimental study of K562 leukemia cells apoptosis induced by emodin — Research Paper | ScholarLens