Experimental study of K562 leukemia cells apoptosis induced by emodin
Jin Dan-ting
Abstract
Jin Dan-ting
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.
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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