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Emodin induces apoptosis through caspase 3-dependent pathway in HK-2 cells
Cuifen Wang1, Xudong Wu, Min Chen
1Jiangsu Center for Drug Screening, China Pharmaceutical University, Nanjing, China.
Abstract:
Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a major constituent of rhubarb. Although it has been claimed to have a wild spectrum of therapeutic value, its side effects, especially in human kidney cells have not been well characterized. In the present study, we treated human proximal tubular epithelial cell line HK-2 cells with emodin in vitro and evaluated its toxic effects with cell viability, cell cycle phases and induction of apoptosis/necrosis and activity of caspase 3. The proliferation of HK-2 cells was inhibited by emodin in a dose- and time-dependent manner. Cell cycle analysis revealed that HK-2 cells were locked in G1 phase by emodin as for 12h. Apoptosis was supported by the Annexin V/propidium iodide (PI) assay and the occurrence of a sub-G1 peak. Emodin caused an increase in caspase 3-like activities and a caspase 3 inhibitor, Ac-DEVD-CHO, attenuated the apoptosis. These results suggested that HK-2 cells are sensitive to emodin-induced cytotoxic effects, which are mediated through the induction of apoptosis in caspase 3-dependent pathway.
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Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
