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Emodin Induces Apoptotic Death in Murine Myelomonocytic Leukemia WEHI-3 Cells In Vitro and Enhances Phagocytosis in Leukemia Mice In Vivo.

Chang YC, Lai TY, Yu CS, Chen HY, Yang JS, Chueh FS, Lu CC, Chiang JH, Huang WW, Ma CY, Chung JG - Evid Based Complement Alternat Med (2011)

Bottom Line: Emodin stimulated the productions of ROS and Ca(2+) and reduced the level of ΔΨ(m) by flow cytometry.Our results from Western blotting suggest that emodin triggered apoptosis of WEHI-3 cells through the endoplasmic reticulum (ER) stress, caspase cascade-dependent and -independent mitochondrial pathways.In in vivo study, emodin enhanced the levels of B cells and monocytes, and it also reduced the weights of liver and spleen compared with leukemia mice.

View Article: PubMed Central - PubMed

Affiliation: School of Chinese Medicine, China Medical University, Taichung 404, Taiwan.

ABSTRACT
Emodin is one of major compounds in rhubarb (Rheum palmatum L.), a plant used as herbal medicine in Chinese population. Although many reports have shown that emodin exhibits anticancer activity in many tumor cell types, there is no available information addressing emodin-affected apoptotic responses in the murine leukemia cell line (WEHI-3) and modulation of the immune response in leukemia mice. We investigated that emodin induced cytotoxic effects in vitro and affected WEHI-3 cells in vivo. This study showed that emodin decreased viability and induced DNA fragmentation in WEHI-3 cells. Cells after exposure to emodin for 24 h have shown chromatin condensation and DNA damage. Emodin stimulated the productions of ROS and Ca(2+) and reduced the level of ΔΨ(m) by flow cytometry. Our results from Western blotting suggest that emodin triggered apoptosis of WEHI-3 cells through the endoplasmic reticulum (ER) stress, caspase cascade-dependent and -independent mitochondrial pathways. In in vivo study, emodin enhanced the levels of B cells and monocytes, and it also reduced the weights of liver and spleen compared with leukemia mice. Emodin promoted phagocytic activity by monocytes and macrophages in comparison to the leukemia mice group. In conclusions, emodin induced apoptotic death in murine leukemia WEHI-3 cells and enhanced phagocytosis in the leukemia animal model.

No MeSH data available.


Related in: MedlinePlus

Effects of emodin on apoptosis and DNA damage in WEHI-3 cells by using DAPI staining and Comet assay. Cells (2 × 105 cells/well) in 12-well plate were incubated with 0, 25, 50, and 100 μM emodin for 24 h and apoptosis was determined using DAPI staining (a). Data represent mean ± SD of at least three experiments. Cells were treated with 0, 50, and 100 μM emodin for 24 h and then were harvested for the examination of DNA damage using the Comet assay (b) as described in Section 2. Comet tail length was calculated, quantified and expressed in mean ± S.D for at least three replicates. *Significantly different compared with DMSO-treated control, P < .05, and ***significantly different from the control sample at P < .001.
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fig2: Effects of emodin on apoptosis and DNA damage in WEHI-3 cells by using DAPI staining and Comet assay. Cells (2 × 105 cells/well) in 12-well plate were incubated with 0, 25, 50, and 100 μM emodin for 24 h and apoptosis was determined using DAPI staining (a). Data represent mean ± SD of at least three experiments. Cells were treated with 0, 50, and 100 μM emodin for 24 h and then were harvested for the examination of DNA damage using the Comet assay (b) as described in Section 2. Comet tail length was calculated, quantified and expressed in mean ± S.D for at least three replicates. *Significantly different compared with DMSO-treated control, P < .05, and ***significantly different from the control sample at P < .001.

Mentions: To investigate the mechanism of emodin-induced leukemic cell death, the effect of emodin on DNA damage was evaluated. The effects of emodin on DNA integrity were further analyzed using the DAPI staining and Comet assay. Emodin-induced chromatin condensation (an apoptotic characteristic) in a dose-dependent response (Figure 2(a)). Also, emodin triggered DNA damage after 24-h treatment and quantification of the number of leukemic WEHI-3 cells displaying a Comet tail strongly increased after emodin treatment (Figure 2(b)).


Emodin Induces Apoptotic Death in Murine Myelomonocytic Leukemia WEHI-3 Cells In Vitro and Enhances Phagocytosis in Leukemia Mice In Vivo.

Chang YC, Lai TY, Yu CS, Chen HY, Yang JS, Chueh FS, Lu CC, Chiang JH, Huang WW, Ma CY, Chung JG - Evid Based Complement Alternat Med (2011)

Effects of emodin on apoptosis and DNA damage in WEHI-3 cells by using DAPI staining and Comet assay. Cells (2 × 105 cells/well) in 12-well plate were incubated with 0, 25, 50, and 100 μM emodin for 24 h and apoptosis was determined using DAPI staining (a). Data represent mean ± SD of at least three experiments. Cells were treated with 0, 50, and 100 μM emodin for 24 h and then were harvested for the examination of DNA damage using the Comet assay (b) as described in Section 2. Comet tail length was calculated, quantified and expressed in mean ± S.D for at least three replicates. *Significantly different compared with DMSO-treated control, P < .05, and ***significantly different from the control sample at P < .001.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108103&req=5

fig2: Effects of emodin on apoptosis and DNA damage in WEHI-3 cells by using DAPI staining and Comet assay. Cells (2 × 105 cells/well) in 12-well plate were incubated with 0, 25, 50, and 100 μM emodin for 24 h and apoptosis was determined using DAPI staining (a). Data represent mean ± SD of at least three experiments. Cells were treated with 0, 50, and 100 μM emodin for 24 h and then were harvested for the examination of DNA damage using the Comet assay (b) as described in Section 2. Comet tail length was calculated, quantified and expressed in mean ± S.D for at least three replicates. *Significantly different compared with DMSO-treated control, P < .05, and ***significantly different from the control sample at P < .001.
Mentions: To investigate the mechanism of emodin-induced leukemic cell death, the effect of emodin on DNA damage was evaluated. The effects of emodin on DNA integrity were further analyzed using the DAPI staining and Comet assay. Emodin-induced chromatin condensation (an apoptotic characteristic) in a dose-dependent response (Figure 2(a)). Also, emodin triggered DNA damage after 24-h treatment and quantification of the number of leukemic WEHI-3 cells displaying a Comet tail strongly increased after emodin treatment (Figure 2(b)).

Bottom Line: Emodin stimulated the productions of ROS and Ca(2+) and reduced the level of ΔΨ(m) by flow cytometry.Our results from Western blotting suggest that emodin triggered apoptosis of WEHI-3 cells through the endoplasmic reticulum (ER) stress, caspase cascade-dependent and -independent mitochondrial pathways.In in vivo study, emodin enhanced the levels of B cells and monocytes, and it also reduced the weights of liver and spleen compared with leukemia mice.

View Article: PubMed Central - PubMed

Affiliation: School of Chinese Medicine, China Medical University, Taichung 404, Taiwan.

ABSTRACT
Emodin is one of major compounds in rhubarb (Rheum palmatum L.), a plant used as herbal medicine in Chinese population. Although many reports have shown that emodin exhibits anticancer activity in many tumor cell types, there is no available information addressing emodin-affected apoptotic responses in the murine leukemia cell line (WEHI-3) and modulation of the immune response in leukemia mice. We investigated that emodin induced cytotoxic effects in vitro and affected WEHI-3 cells in vivo. This study showed that emodin decreased viability and induced DNA fragmentation in WEHI-3 cells. Cells after exposure to emodin for 24 h have shown chromatin condensation and DNA damage. Emodin stimulated the productions of ROS and Ca(2+) and reduced the level of ΔΨ(m) by flow cytometry. Our results from Western blotting suggest that emodin triggered apoptosis of WEHI-3 cells through the endoplasmic reticulum (ER) stress, caspase cascade-dependent and -independent mitochondrial pathways. In in vivo study, emodin enhanced the levels of B cells and monocytes, and it also reduced the weights of liver and spleen compared with leukemia mice. Emodin promoted phagocytic activity by monocytes and macrophages in comparison to the leukemia mice group. In conclusions, emodin induced apoptotic death in murine leukemia WEHI-3 cells and enhanced phagocytosis in the leukemia animal model.

No MeSH data available.


Related in: MedlinePlus