Emodin is extracted from Rheum palmatum L. that had been used as folk medicine in Chinese population. Emodin have been shown to induce cell death and apoptosis in many human cancer cell lines, such as lung, cervical, melanoma, esophagus and liver cancers. However, there is no available information to address Emodin induced apoptosis in WEHI-3 cells. We examined the effects of Emodin on murine leukemia WEHI-3 cells and enhance macrophage phagocytosis in vivo. Therefore, the results from flow cytomertic analysis indicated that Emodin arrest cell cycle in G0/G1 and induced apoptosis in examined cell line.
We also used DAPI stain and DNA gel electrophoresis to confirm Emodin induced apoptosis in WEHI-3 cell line. Flow cytometric also used for analysis the levels of reactive oxygen species, Ca2+ and mitochondrial membrane potential (MMP) in WEHI-3 cell lines. The results showed Emodin promoted ROS and Ca2+ production and decreased the MMP level. Western blotting show that Emodin treatment gradually decreased the levels of anti-apoptotic protein (Bcl-2), but increased the levels of the pro-apoptotic protein (Bax). Emodin promoted the release of cytochrome c from mitochondria based on the changes of MMP and the activation of caspase-3 before leading to apoptosis.
In this study, we examined the in vivo effects of Emodin on leukemia WEHI-3 cells and on macrophage phagocytosis. The weights of the livers and spleens were decreased in the Emodin-treated groups compared to the control groups. The Emodin treatment increased the percentage of CD11b and CD19 marker cells in WEHI-3-injected mice and decreased the percentage of Mac-3 indicating that the differentiation of the precursor of macrophage and B cells was inhibited. The Emodin treatment promoted the activity of macrophage phagocytosis in the peripheral blood mononuclear cells (PBMC) and peritoneal cells. In conclusion, Emodin can inhibit WEHI-3 cells in vitro and promote macrophage phagocytosis in vivo.
