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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 weights of the leukemia mice which were treated with without or with emodin 2 weeks. BALB/c mice were intraperitoneally injected with WEHI-3 cells (1 × 105 cells/100 μL) in PBS for 2 weeks and/or treated with emodin once daily by oral administration for 14 days. Blood was collected and animals were sacrificed for examinations of weights of body (a) spleen (b) and liver (c) tissues, and then were individually weighed. Each point is the mean ± SD and similar results were observed in at least three independent experiments (n = 10) followed by one-way ANOVA followed by Dunnett's test.
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fig7: Emodin affected the weights of the leukemia mice which were treated with without or with emodin 2 weeks. BALB/c mice were intraperitoneally injected with WEHI-3 cells (1 × 105 cells/100 μL) in PBS for 2 weeks and/or treated with emodin once daily by oral administration for 14 days. Blood was collected and animals were sacrificed for examinations of weights of body (a) spleen (b) and liver (c) tissues, and then were individually weighed. Each point is the mean ± SD and similar results were observed in at least three independent experiments (n = 10) followed by one-way ANOVA followed by Dunnett's test.

Mentions: The BALB/c mice after injection with WEHI-3 cells were treated with or without emodin (5 and 10 mg/kg). Results indicate that emodin increased the body weight of mice (Figure 7(a)) but decreased the weights of spleen (Figure 7(b)) and liver (Figure 7(c)) when compared with the leukemia mice group.


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 weights of the leukemia mice which were treated with without or with emodin 2 weeks. BALB/c mice were intraperitoneally injected with WEHI-3 cells (1 × 105 cells/100 μL) in PBS for 2 weeks and/or treated with emodin once daily by oral administration for 14 days. Blood was collected and animals were sacrificed for examinations of weights of body (a) spleen (b) and liver (c) tissues, and then were individually weighed. Each point is the mean ± SD and similar results were observed in at least three independent experiments (n = 10) followed by one-way ANOVA followed by Dunnett's test.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig7: Emodin affected the weights of the leukemia mice which were treated with without or with emodin 2 weeks. BALB/c mice were intraperitoneally injected with WEHI-3 cells (1 × 105 cells/100 μL) in PBS for 2 weeks and/or treated with emodin once daily by oral administration for 14 days. Blood was collected and animals were sacrificed for examinations of weights of body (a) spleen (b) and liver (c) tissues, and then were individually weighed. Each point is the mean ± SD and similar results were observed in at least three independent experiments (n = 10) followed by one-way ANOVA followed by Dunnett's test.
Mentions: The BALB/c mice after injection with WEHI-3 cells were treated with or without emodin (5 and 10 mg/kg). Results indicate that emodin increased the body weight of mice (Figure 7(a)) but decreased the weights of spleen (Figure 7(b)) and liver (Figure 7(c)) when compared with the leukemia mice group.

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