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Jing Gung Chung – One of the best experts on this subject based on the ideXlab platform.

  • Aloe Emodin induces cell death through s phase arrest and caspase dependent pathways in human tongue squamous cancer scc 4 cells
    Anticancer Research, 2009
    Co-Authors: Tsan Hung Chiu, Te Chun Hsia, Jai Sing Yang, Ping Ping Wu, Chia Yu, Chin Chin Ho, Hsu Feng Lu, Gibson W Wood, Jing Gung Chung

    Abstract:

    AloeEmodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of AloeEmodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that AloeEmodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 μM of AloeEmodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. AloeEmodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (ΔΨ m ) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N- acetylcysteine (NAC) and caspase inhibitors markedly blocked AloeEmodin-induced apoptosis. AloeEmodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. AloeEmodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.

  • AloeEmodin affects the levels of cytokines and functions of leukocytes from Sprague-Dawley rats.
    In vivo (Athens Greece), 2006
    Co-Authors: Jack Kai Sheng Chan, Te Chun Hsia, Song Shei Lin, Ssu-ching Chen, Yung Hsien Chang, Jing Gung Chung

    Abstract:

    AloeEmodin has shown anti-neoplastic activity against some human cancer cell lines. This study aimed to explore the effects of AloeEmodin on the phagocytosis of macrophages, the activity of natural killer (NK) cells and the expression of cytokines in leukocytes from Sprague-Dawley rats. Leukocytes were collected, placed into culture plates and the functions of macrophages and NK cells and the percentage of viable cells were determined by flow cytometric analysis. Incubation of leukocytes with various concentrations of AloeEmodin caused a dose-dependent decrease of viable cells, a decrease of phagocytosis by macrophages, and a decrease of the activity of NK cells. Evaluation of cytokines in leukocytes by ELISA indicated that AloeEmodin increased the levels of interleukin (IL)-1‚ and tumor necrosis factor (TNF)-·. The results were also confirmed by PCR assay for the mRNA expression of the examined cytokines. There is much evidence that inflammatory responses are associated with cytokines which are released from leukocytes. Cytokines are soluble hormone-like protein mediators, produced by diverse cell types in response to various stimuli including other cytokines. The most important cytokine activities are associated with the immune response, inflammation, tissue injury or repair, and organ dysfunction (1-4). AloeEmodin (1,8-dihydroxy-3-(hydroxymethyl)-anthra- quinone) (AE) is an active component from the roots and rhizomes of Rheum palmatum and is also naturally present

  • Aloe Emodin induced in vitro g2 m arrest of cell cycle in human promyelocytic leukemia hl 60 cells
    Food and Chemical Toxicology, 2004
    Co-Authors: Hsin-chun Chen, Wen Tsong Hsieh, W. C. Chang, Jing Gung Chung

    Abstract:

    Abstract In this study, we have evaluated the chemopreventive role of AloeEmodin in human promyelocytic leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. AloeEmodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with AloeEmodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with AloeEmodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of AloeEmodin. The increase of the levels of p27 may be the major factor for AloeEmodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed AloeEmodin induced apoptosis in HL-60 cells. The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 μM AloeEmodin for 12, 24, 48, and 72 hours. Taken together, AloeEmodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.

Hong-zin Lee – One of the best experts on this subject based on the ideXlab platform.

  • Photodynamic activity of AloeEmodin induces resensitization of lung cancer cells to anoikis.
    European journal of pharmacology, 2010
    Co-Authors: Hong-zin Lee, Wen-hui Yang, Mann-jen Hour, Wen-huang Peng, Bo-ying Bao, Ping-hsiu Han, Da-tian Bau

    Abstract:

    AloeEmodin was found to be a photosensitizer and possess anti-tumor activity. However, the detailed mechanism underlying the biological effects of AloeEmodin remains unknown. In this study, we explored the mechanisms of photocytotoxicity induced by AloeEmodin in lung cancer H460 cells. According to the results of the photoactivated AloeEmodin-induced disruption of cytoskeleton, we verify that AloeEmodin with irradiation induces anoikis of H460 cells. Photosensitized AloeEmodin-induced anoikis is associated with the protein expression of α-actinin and mitogen-activated protein (MAP) kinase members. In this study, a rapid opening of the mitochondrial permeability transition pore and the change in apoptosis-related protein expression were involved in photoactivated AloeEmodin-induced cell death. We also demonstrated that anoikis induced by AloeEmodin with irradiation is mediated through the intrinsic and extrinsic death pathways in a caspase-dependent manner in H460 cells.

  • Chaperones are the target in AloeEmodin-induced human lung nonsmall carcinoma H460 cell apoptosis.
    European journal of pharmacology, 2007
    Co-Authors: Miao-ying Lai, Mann-jen Hour, Wen-hui Yang, Henry Wing-cheung Leung, Hong-zin Lee

    Abstract:

    Our previous study has demonstrated that AloeEmodin induced a significant change in the expression of apoptosis-related proteins in H460 cells. However, the molecular mechanisms underlying the biological effects of AloeEmodin still remain unknown. The present study applied 2D electrophoresis (pH range 4-7) to the proteins involved in AloeEmodin (40 muM)-induced H460 cell apoptosis. Eleven proteins were found to markedly change. These altered proteins were identified as ATP synthase, vimentin, HSP60, HSP70 and protein disulfide isomerase. AloeEmodin caused a time-dependent decrease in intracellular ATP levels, which might be related to direct inhibition of ATP synthase. We also observed that the activity of mitochondria was injured by AloeEmodin. These data clearly demonstrated that mitochondria may play a critical role in AloeEmodin-induced H460 cell death. Many reports emphasize that chaperones have a complex role in apoptosis. The present study suggested that the increasing protein expression of HSP60, HSP70, 150 kDa oxygen-regulated protein and protein disulfide isomerase is involved in AloeEmodin-induced H460 cell apoptosis. HSP70, 150 kDa oxygen-regulated protein and protein disulfide isomerase are endoplasmic reticulum chaperone. Therefore, we hypothesized that the increasing endoplasmic reticulum stress serves to promote H460 cell apoptosis after treatment with AloeEmodin. We also demonstrated AloeEmodin-induced H460 cell death through caspase-3 apoptotic pathway, but not apoptosis-inducing factor apoptotic pathway.

  • AloeEmodin induced DNA damage through generation of reactive oxygen species in human lung carcinoma cells.
    Cancer letters, 2005
    Co-Authors: Hong-zin Lee, Wen-hui Yang, Ching-ju Lin, Wing-cheung Leung, Shen-pen Chang

    Abstract:

    The DNA aggregation was found in AloeEmodin-induced H460 cell apoptosis in this study. AloeEmodin (40microM)-induced DNA single strand breaks were observed by comet assay. AloeEmodin induced decreases in the mRNA of DNA repair enzymes such as hMTH1, hOGG1 and APE. Although the activity of the radical-scavenging enzyme SOD was enhanced by AloeEmodin, the effects of AloeEmodin on H460 cell apoptosis were suspected to result from the prooxidant. These results suggest that AloeEmodin induced DNA damage through generation of reactive oxygen species in human lung carcinoma cells.

Bin Zhang – One of the best experts on this subject based on the ideXlab platform.

  • AloeEmodin induces apoptosis in human oral squamous cell carcinoma SCC15 cells.
    BMC complementary and alternative medicine, 2018
    Co-Authors: Jun Wen, Yao Shu, Hongxing Chu, Bin Zhang

    Abstract:

    Oral and pharyngeal cancer is the most common malignant human cancers. Chemotherapy is an effective approach for anti-oral cancer therapy, while the drug tolerance and resistance remain a problem for oral cancer patients. AloeEmodin, rhein and physcion are classified as anthraquinones, which are the main pharmacodynamic ingredients of Rheum undulatum L.. This study was undertaken to investigate whether AloeEmodin, rhein and physcion show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells. We found that AloeEmodin show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells, we also investigated the underlying mechanisms of apoptosis induced by AloeEmodin. Thiazolyl blue tetrazolium bromide (MTT) test was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry. We also used western blot analysis to detect the potential mechanisms of apoptosis. AloeEmodin, rhein and physcion inhibit the proliferation of SCC15 cells and the order of inhibition level are AloeEmodin > Rhein > Physcion, the half maximal inhibitory concentrations (IC50) value of AloeEmodin was 60.90 μM at 48 h of treatment. AloeEmodin treatment resulted in a time- and dose-dependent decrease in cell viability and increased the apoptotic cell ratio. The results of western blotting showed the expression levels of caspase-9 and caspase-3 proteins increased following AloeEmodin treatment. Our results revealed that AloeEmodin treatment could inhibit cell viability of SCC15 cells and the potential mechanism of inhibition might be through the induction of apoptosis by regulation of the expression levels of caspase-9 and caspase-3. This indicates that AloeEmodin may be a good agent for anti-oral cancer drug exploring.

  • AloeEmodin induces apoptosis in human oral squamous cell carcinoma SCC15 cells
    BMC, 2018
    Co-Authors: Jun Wen, Yao Shu, Hongxing Chu, Bin Zhang

    Abstract:

    Abstract Background Oral and pharyngeal cancer is the most common malignant human cancers. Chemotherapy is an effective approach for anti-oral cancer therapy, while the drug tolerance and resistance remain a problem for oral cancer patients. AloeEmodin, rhein and physcion are classified as anthraquinones, which are the main pharmacodynamic ingredients of Rheum undulatum L.. This study was undertaken to investigate whether AloeEmodin, rhein and physcion show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells. We found that AloeEmodin show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells, we also investigated the underlying mechanisms of apoptosis induced by AloeEmodin. Methods Thiazolyl blue tetrazolium bromide (MTT) test was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry. We also used western blot analysis to detect the potential mechanisms of apoptosis. Results AloeEmodin, rhein and physcion inhibit the proliferation of SCC15 cells and the order of inhibition level are AloeEmodin > Rhein > Physcion, the half maximal inhibitory concentrations (IC50) value of AloeEmodin was 60.90 μM at 48 h of treatment. AloeEmodin treatment resulted in a time- and dose-dependent decrease in cell viability and increased the apoptotic cell ratio. The results of western blotting showed the expression levels of caspase-9 and caspase-3 proteins increased following AloeEmodin treatment. Conclusions Our results revealed that AloeEmodin treatment could inhibit cell viability of SCC15 cells and the potential mechanism of inhibition might be through the induction of apoptosis by regulation of the expression levels of caspase-9 and caspase-3. This indicates that AloeEmodin may be a good agent for anti-oral cancer drug exploring