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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

Emodin affected the percentage of viable cells and DNA fragmentation in WEHI-3 cells. Cells (1 × 104 cells/well; 96-well plates) were plated in RPMI 1640 medium + 10% fetal bovine serum (FBS) with 0, 25, 50, 100, and 150 μM of emodin for 24 and 48 h. The cells were collected by centrifugation and the viable cells were determined by using the MTT assay (a). Cells were treated with 0, 50, and 100 μM of emodin for 24 h, and then DNA was isolated for DNA gel electrophoresis (b) as described in Section 2. Columns, mean of three determinations; bars, SD. a, P < .05 shows significantly different when compared with DMSO-treated control; b, c, and d, P < .05 indicates significantly different compared with 25, 50, and 100 μM emodin-treated groups, respectively (one-way ANOVA followed by Bonferroni's test for multiple comparisons).
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fig1: Emodin affected the percentage of viable cells and DNA fragmentation in WEHI-3 cells. Cells (1 × 104 cells/well; 96-well plates) were plated in RPMI 1640 medium + 10% fetal bovine serum (FBS) with 0, 25, 50, 100, and 150 μM of emodin for 24 and 48 h. The cells were collected by centrifugation and the viable cells were determined by using the MTT assay (a). Cells were treated with 0, 50, and 100 μM of emodin for 24 h, and then DNA was isolated for DNA gel electrophoresis (b) as described in Section 2. Columns, mean of three determinations; bars, SD. a, P < .05 shows significantly different when compared with DMSO-treated control; b, c, and d, P < .05 indicates significantly different compared with 25, 50, and 100 μM emodin-treated groups, respectively (one-way ANOVA followed by Bonferroni's test for multiple comparisons).

Mentions: The doses of emodin (50 to 150 μM) are required to induce cell death in WEHI-3 cells for 24-h treatment and the percentage of viable cells decrease was 41–63% (Figure 1(a)). However, emodin (25–150 μM) for 48-h treatment decrease viable cells and the results show 19–82% (Figure 1(a)). Herein, emodin in the concentration as low as 25 μM initiated cell death of WEHI-3 cells and the IC50 is 100 μM (Figure 1(a)). DNA gel electrophoresis assay indicated that 100–150 μM of emodin-induced DNA fragmentation in WEHI-3 cells after exposure for 24 h (Figure 1(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)

Emodin affected the percentage of viable cells and DNA fragmentation in WEHI-3 cells. Cells (1 × 104 cells/well; 96-well plates) were plated in RPMI 1640 medium + 10% fetal bovine serum (FBS) with 0, 25, 50, 100, and 150 μM of emodin for 24 and 48 h. The cells were collected by centrifugation and the viable cells were determined by using the MTT assay (a). Cells were treated with 0, 50, and 100 μM of emodin for 24 h, and then DNA was isolated for DNA gel electrophoresis (b) as described in Section 2. Columns, mean of three determinations; bars, SD. a, P < .05 shows significantly different when compared with DMSO-treated control; b, c, and d, P < .05 indicates significantly different compared with 25, 50, and 100 μM emodin-treated groups, respectively (one-way ANOVA followed by Bonferroni's test for multiple comparisons).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Emodin affected the percentage of viable cells and DNA fragmentation in WEHI-3 cells. Cells (1 × 104 cells/well; 96-well plates) were plated in RPMI 1640 medium + 10% fetal bovine serum (FBS) with 0, 25, 50, 100, and 150 μM of emodin for 24 and 48 h. The cells were collected by centrifugation and the viable cells were determined by using the MTT assay (a). Cells were treated with 0, 50, and 100 μM of emodin for 24 h, and then DNA was isolated for DNA gel electrophoresis (b) as described in Section 2. Columns, mean of three determinations; bars, SD. a, P < .05 shows significantly different when compared with DMSO-treated control; b, c, and d, P < .05 indicates significantly different compared with 25, 50, and 100 μM emodin-treated groups, respectively (one-way ANOVA followed by Bonferroni's test for multiple comparisons).
Mentions: The doses of emodin (50 to 150 μM) are required to induce cell death in WEHI-3 cells for 24-h treatment and the percentage of viable cells decrease was 41–63% (Figure 1(a)). However, emodin (25–150 μM) for 48-h treatment decrease viable cells and the results show 19–82% (Figure 1(a)). Herein, emodin in the concentration as low as 25 μM initiated cell death of WEHI-3 cells and the IC50 is 100 μM (Figure 1(a)). DNA gel electrophoresis assay indicated that 100–150 μM of emodin-induced DNA fragmentation in WEHI-3 cells after exposure for 24 h (Figure 1(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