2010Zhejiang Journal of Traumatic SurgeryRequires access

The effects of emodin on pancreatic cance cells:an experimental study

Wei Zhang

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Abstract

Objective To explore the inhibition effect of emodin on human pancreatic carcinoma cell line PC-3 and its mechanism. Methods CCK-8 assay was used to observe the inhibitory actions of emodin on PC-3 cells at various concentrations. The apoptotic rate and growth cycle of the cells were detected by flow cytometry and fluorescence microscope. The changes of the cells ultrastructures were observed under electron microscope. The expression of apoptosis-related gene protein (Fas,Fas-L) was detected by immunohistochemical staining. Results emodin inhibited the proliferation of PC-3 cells in a concentration-dependent manner. Lots of early apoptotic cell were detected by fluorescence microscope. Marked apoptosis peak was observed and the cells were mainly blocked in G1 phase (55.19~85.80%). PC-3 cells showed obvious feature of apoptosis under electron microscope,such as intact cell membrane,concentration of plasma,pyknosis of chromatin and nuclear fragmentation. Fas and Fas-L protein were weakly (+) and negatively (-) expressed in controls respectively,but strongly expressed (+++) in emodin-treated cells. Conclusion Emodin can not only inhibit the proliferation but also induce the apoptosis of human pancreatic carcinoma cell PC-3.The mechanism is probably related to its effect on the regulation of Fas,Fas-L expression.

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Objective To explore the inhibition effect of emodin on human pancreatic carcinoma cell line PC-3 and its mechanism. Methods CCK-8 assay was used to observe the inhibitory actions of emodin on PC-3 cells at various concentrations. The apoptotic rate and growth cycle of the cells were detected by flow cytometry and fluorescence microscope. The changes of the cells ultrastructures were observed under electron microscope. The expression of apoptosis-related gene protein (Fas,Fas-L) was detected by immunohistochemical staining. Results emodin inhibited the proliferation of PC-3 cells in a concentration-dependent manner. Lots of early apoptotic cell were detected by fluorescence microscope. Marked apoptosis peak was observed and the cells were mainly blocked in G1 phase (55.19~85.80%). PC-3 cells showed obvious feature of apoptosis under electron microscope,such as intact cell membrane,concentration of plasma,pyknosis of chromatin and nuclear fragmentation. Fas and Fas-L protein were weakly (+) and negatively (-) expressed in controls respectively,but strongly expressed (+++) in emodin-treated cells. Conclusion Emodin can not only inhibit the proliferation but also induce the apoptosis of human pancreatic carcinoma cell PC-3.The mechanism is probably related to its effect on the regulation of Fas,Fas-L expression.

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Available abstract

Objective To explore the inhibition effect of emodin on human pancreatic carcinoma cell line PC-3 and its mechanism. Methods CCK-8 assay was used to observe the inhibitory actions of emodin on PC-3 cells at various concentrations. The apoptotic rate and growth cycle of the cells were detected by flow cytometry and fluorescence microscope. The changes of the cells ultrastructures were observed under electron microscope. The expression of apoptosis-related gene protein (Fas,Fas-L) was detected by immunohistochemical staining. Results emodin inhibited the proliferation of PC-3 cells in a concentration-dependent manner. Lots of early apoptotic cell were detected by fluorescence microscope. Marked apoptosis peak was observed and the cells were mainly blocked in G1 phase (55.19~85.80%). PC-3 cells showed obvious feature of apoptosis under electron microscope,such as intact cell membrane,concentration of plasma,pyknosis of chromatin and nuclear fragmentation. Fas and Fas-L protein were weakly (+) and negatively (-) expressed in controls respectively,but strongly expressed (+++) in emodin-treated cells. Conclusion Emodin can not only inhibit the proliferation but also induce the apoptosis of human pancreatic carcinoma cell PC-3.The mechanism is probably related to its effect on the regulation of Fas,Fas-L expression.

Key concepts: Apoptosis, Emodin, Flow cytometry, Molecular biology, Fragmentation (computing), Cell growth, Fluorescence microscope, Cell

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