2011•PubMedRequires access

[Mechanism of apoptosis in human leukemia NB4 cells induced by total astragalosides].

Xueying Hu, Ruixiang Xia, Chang-bin Cheng, Mingzhen Yang, Qingshu Zeng, Hailong Xia, Jiajia Li

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Abstract

OBJECTIVE: To investigate the effect of total astragalosides (TA) on proliferation and apoptosis in human leukemia NB4 cells in vitro. METHODS: The NB4 cells were treated with TA at different concentrations for 48 h in culture. Growth inhibition rates were measured by CCK-8 method. Flow cytometry was used to explore the cell apoptosis and the activity of NF-κB and Akt during apoptosis. RESULTS: TA at different concentrations (200, 400, 600, 800 mg/L) inhibited proliferation of NB4 cells in a dose-dependent manner (P < 0.05), and the inhibitory rates of TA on NB4 cells were (14.54 ± 3.20)%, (24.79 ± 3.98)%, (57.28 ± 4.71)% and (88.28 ± 4.65)%, respectively. In terms of the induction of apoptosis, there was a significant difference between the TA group and blank control [(1.80 ± 1.24)%, P < 0.05]. At TA doses of 200, 400 and 600 mg/L, the apoptotic rates of NB4 cells were (10.03 ± 3.31)%, (14.87 ± 3.65)%, (23.45 ± 1.90)%, respectively. Besides, TA induced apoptosis of NB4 cells in a dose-dependent manner in the groups of 200 mg/L, 400 mg/L, 600 mg/L (P < 0.05). But there was no significant difference in apoptotic rates between the groups of 800 mg/L and 600 mg/L [(23.45 ± 1.90)%, P > 0.05]. In the group of 800 mg/L, the necrotic cells increased highly and the necrotic rate reached (45.65 ± 3.16)%. After TA treatment of NB4 cells at different concentrations (200, 400, 600 mg/L), the expression of NF-κB protein was significantly decreased compared with that of the blank control (9.79 ± 0.95, P < 0.05), while Akt protein was not significantly decreased (P > 0.05). CONCLUSION: TA can inhibit the growth of NB4 cells and induce apoptosis in NB4 cells through an Akt-independent NF-κB signaling pathway.

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What this paper is about

OBJECTIVE: To investigate the effect of total astragalosides (TA) on proliferation and apoptosis in human leukemia NB4 cells in vitro. METHODS: The NB4 cells were treated with TA at different concentrations for 48 h in culture. Growth inhibition rates were measured by CCK-8 method. Flow cytometry was used to explore the cell apoptosis and the activity of NF-κB and Akt during apoptosis. RESULTS: TA at different concentrations (200, 400, 600, 800 mg/L) inhibited proliferation of NB4 cells in a dose-dependent manner (P < 0.05), and the inhibitory rates of TA on NB4 cells were (14.54 ± 3.20)%, (24.79 ± 3.98)%, (57.28 ± 4.71)% and (88.28 ± 4.65)%, respectively. In terms of the induction of apoptosis, there was a significant difference between the TA group and blank control [(1.80 ± 1.24)%, P < 0.05]. At TA doses of 200, 400 and 600 mg/L, the apoptotic rates of NB4 cells were (10.03 ± 3.31)%, (14.87 ± 3.65)%, (23.45 ± 1.90)%, respectively. Besides, TA induced apoptosis of NB4 cells in a dose-dependent manner in the groups of 200 mg/L, 400 mg/L, 600 mg/L (P < 0.05). But there was no significant difference in apoptotic rates between the groups of 800 mg/L and 600 mg/L [(23.45 ± 1.90)%, P > 0.05]. In the group of 800 mg/L, the necrotic cells increased highly and the necrotic rate reached (45.65 ± 3.16)%. After TA treatment of NB4 cells at different concentrations (200, 400, 600 mg/L), the expression of NF-κB protein was significantly decreased compared with that of the blank control (9.79 ± 0.95, P < 0.05), while Akt protein was not significantly decreased (P > 0.05). CONCLUSION: TA can inhibit the growth of NB4 cells and induce apoptosis in NB4 cells through an Akt-independent NF-κB signaling pathway.

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Available abstract

OBJECTIVE: To investigate the effect of total astragalosides (TA) on proliferation and apoptosis in human leukemia NB4 cells in vitro. METHODS: The NB4 cells were treated with TA at different concentrations for 48 h in culture. Growth inhibition rates were measured by CCK-8 method. Flow cytometry was used to explore the cell apoptosis and the activity of NF-κB and Akt during apoptosis. RESULTS: TA at different concentrations (200, 400, 600, 800 mg/L) inhibited proliferation of NB4 cells in a dose-dependent manner (P < 0.05), and the inhibitory rates of TA on NB4 cells were (14.54 ± 3.20)%, (24.79 ± 3.98)%, (57.28 ± 4.71)% and (88.28 ± 4.65)%, respectively. In terms of the induction of apoptosis, there was a significant difference between the TA group and blank control [(1.80 ± 1.24)%, P < 0.05]. At TA doses of 200, 400 and 600 mg/L, the apoptotic rates of NB4 cells were (10.03 ± 3.31)%, (14.87 ± 3.65)%, (23.45 ± 1.90)%, respectively. Besides, TA induced apoptosis of NB4 cells in a dose-dependent manner in the groups of 200 mg/L, 400 mg/L, 600 mg/L (P < 0.05). But there was no significant difference in apoptotic rates between the groups of 800 mg/L and 600 mg/L [(23.45 ± 1.90)%, P > 0.05]. In the group of 800 mg/L, the necrotic cells increased highly and the necrotic rate reached (45.65 ± 3.16)%. After TA treatment of NB4 cells at different concentrations (200, 400, 600 mg/L), the expression of NF-κB protein was significantly decreased compared with that of the blank control (9.79 ± 0.95, P < 0.05), while Akt protein was not significantly decreased (P > 0.05). CONCLUSION: TA can inhibit the growth of NB4 cells and induce apoptosis in NB4 cells through an Akt-independent NF-κB signaling pathway.

Key concepts: Apoptosis, Flow cytometry, Andrology, Significant difference, Molecular biology, Chemistry, Leukemia, In vitro

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