Evaluation of Aloin and Aloe-Emodin as Anti-Inflammatory Agents in Aloe by Using Murine Macrophages

Park, Mi-Young; Kwon, Hoonjeong; Sung, Mi‐Kyung

doi:10.1271/bbb.80714

Cited by 211 publications

(122 citation statements)

References 33 publications

Supporting

Mentioning

116

Contrasting

Unclassified

Order By: Relevance

“…Our data indicate that aloe-emodin inhibits the transcription and protein expression of iNOS. This result is consistent with that of a previous report that aloe-emodin inhibits the expression of iNOS and cyclooxygenase-2 (Park et al, 2009). Our work also demonstrates that aloe-emodin markedly suppresses the LPS-stimulated transcription and production of IL-1β and IL-6.…”

Section: Discussionsupporting

confidence: 94%

“…Aloe-emodin has been found to have antibacterial, antiviral, hepatoprotective, and anticancer effects (Park et al, 2009); however, its effect on anti-inflammation is seldom reported. In the present study, we found that aloe-emodin potently inhibits the production of LPS-stimulated inflammatory mediators in RAW264.7 macrophages, including NO, IL-1β, and IL-6.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Aloe-emodin from rhubarb (Rheum rhabarbarum) inhibits lipopolysaccharide-induced inflammatory responses in RAW264.7 macrophages

Zhang

Meng

et al. 2014

Journal of Ethnopharmacology

166

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Aloe-emodin from rhubarb (Rheum rhabarbarum) inhibits lipopolysaccharide-induced inflammatory responses in RAW264.7 macrophages

Zhang

Meng

et al. 2014

Journal of Ethnopharmacology

166

View full text Add to dashboard Cite

“…Emodin has been previously reported to possess antiviral [16], antiinflammatory [17], antiulcerogenic [18], immunosuppressive [19], and chemopreventive activities [20]. Interestingly, antiproliferative effects of emodin have been observed in many tumor cell lines, including HER2/neuoverexpressing breast cancer [21], lung cancer [22], leukemia [23], HCC [24], and neuroblastoma [25] but not in normal cells, suggesting that emodin may have a significant therapeutic efficacy as an anticancer agent.…”

Section: Introductionmentioning

confidence: 99%

An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteins

et al. 2013

View full text Add to dashboard Cite

Recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is currently under clinical trials for cancer, however many tumor cells, including hepatocellular carcinoma (HCC) develop resistance to TRAIL-induced apoptosis. Hence, novel agents that can alleviate TRAIL-induced resistance are urgently needed. In the present report, we investigated the potential of emodin to enhance apoptosis induced by TRAIL in HCC cells. As observed by MTT cytotoxicity assay and the externalization of the membrane phospholipid phosphatidylserine, we found that emodin can significantly potentiate TRAIL-induced apoptosis in HCC cells. When investigated for the mechanism(s), we observed that emodin can downregulate the expression of various cell survival proteins, and induce the cell surface expression of both TRAIL receptors, death receptors (DR) 4 as well as 5. In addition, emodin increased the expression of C/EBP homologous protein (CHOP) in a time-dependent manner. Knockdown of CHOP by siRNA decreased the induction of emodin-induced DR5 expression and apoptosis. Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis. Also, the knockdown of X-linked inhibitor of apoptosis protein by siRNA significantly reduced the sensitization effect of emodin on TRAILinduced apoptosis. Overall, our experimental results clearly indicate that emodin can indeed potentiate TRAIL-induced Aruljothi Subramaniam and Ser Yue Loo contributed equally to this work.

show abstract

“…It functions through its anti-atherosclerosis, anti-bacterial, anti-cancer, and vasorelaxant properties (1)(2)(3)(4)(5)(6). The effects of emodin in protecting patients from both cerebral ischemia injury and myocardial ischemia/reperfusion injury have been associated with its role in inhibiting inflammation (7,8). Further study revealed that emodin may be involved in the modulation of rejection of liver transplantation (9,10).…”

Section: Introductionmentioning

confidence: 99%

Emodin inhibits the differentiation and maturation of dendritic cells and increases the production of regulatory T cells

Zhang

Li²,

Bu³

et al. 2011

Int J Mol Med

View full text Add to dashboard Cite

Abstract. The aim of this study was to characterize the effects of emodin on dendritic cells (DCs) and CD4 + CD25 + regulatory T cells (Tregs). Myeloid DCs were prepared from peripheral blood mononuclear cells of healthy human donors and treated with emodin at different concentrations. The phenotype and T cell stimulatory capacity of these DCs were analyzed. The expression ratios of CD80 and CD83 in DCs in the presence of emodin (100 µg/ml) were significantly decreased compared with that in DCs without emodin treatment (P<0.05). IL-12p70 production of DCs decreased significantly with emodin treatment (P<0.05). Furthermore, an approximately 2-fold decrease was observed in the ability of DCs pre-treated with emodin to induce T-lymphocyte proliferation. In addition, we found that emodin treatment increased the number of Tregs, which expressed lower levels of human leukocyte antigen (HLA-DR), glucocorticoid-induced tumor necrosis factor receptor (GITR), and cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) as compared to cells without emodin treatment. Our results suggest that emodin inhibits the differentiation and maturation of DCs and induces Tregs, which may be helpful for the modulation of the immune rejection after liver transplantation.

show abstract

Evaluation of Aloin and Aloe-Emodin as Anti-Inflammatory Agents in Aloe by Using Murine Macrophages

Cited by 211 publications

References 33 publications

Aloe-emodin from rhubarb (Rheum rhabarbarum) inhibits lipopolysaccharide-induced inflammatory responses in RAW264.7 macrophages

Aloe-emodin from rhubarb (Rheum rhabarbarum) inhibits lipopolysaccharide-induced inflammatory responses in RAW264.7 macrophages

An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteins

Emodin inhibits the differentiation and maturation of dendritic cells and increases the production of regulatory T cells

Contact Info

Product

Resources

About