Disease relevance of emodin

• Aloe-emodin is a new type of anticancer agent with selective activity against neuroectodermal tumors [1].
• Based on these reasons, we were interested in the change of aloe-emodin-induced total protein expression by the proteomics technique during aloe-emodin-induced lung cancer cell apoptosis [2].
• The results showed that aloe emodin inactivated all of the viruses tested except adenovirus and rhinovirus [3].
• 1. This study demonstrated aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell lines CH27 (human lung squamous carcinoma cell) and H460 (human lung non-small cell carcinoma cell) [4].
• In VACO235 adenoma cells, sennidine and aloe-emodin did not affect urokinase secretion, but stimulated growth [5].

High impact information on emodin

• The in vivo treatment of primary rat hepatocytes with danthron, aloe-emodin, chrysophanol, and rhein resulted in a 2-3-fold increase of DNA synthesis, lucidin and purpurin were less active, and emodin, purpuroxanthin, and alizarin were essentially inactive [6].
• We determined that incubation of human skin fibroblasts with 20 microM aloe emodin for 18 h followed by irradiation with UV or visible light resulted in significant photocytotoxicity [7].
• In an attempt to explain the different photobiological properties of aloin A and aloe emodin, laser flash photolysis experiments were performed [7].
• The present study identified aloe-emodin (AE, a hydroxyanthraquinone from Aloe vera and other plants) as a new anti-angiogenic compound with inhibitory effects in an in vivo angiogenesis assay and evaluates its effects on specific key steps of the angiogenic process [8].
• Our study also demonstrated that the gene expression of nucleophosmin remained unchanged after treatment with aloe-emodin [2].

Chemical compound and disease context of emodin

• All three tested anthraquinones, emodin, aloe-emodin, and danthron, showed capabilities to inhibit the non-covalent binding of bisbenzimide Hoechst 33342 to isolated DNA and in mouse lymphoma L5178Y cells comparable to the topoisomerase II inhibitor and intercalator m-amsacrine [9].
• To establish the cell cycle effects of aloe-emodin on brain cells [transformed glia cell line (SVG) and human glioma U-373MG cell line (U-373MG)], cells were treated with either dimethylsulfoxide (DMSO; control) or aloe-emodin (40 microM) [10].

Biological context of emodin

• Our study applied 2D electrophoresis to analyze the proteins involved in aloe-emodin-induced apoptosis in H460 cells [2].
• Aloe-emodin prevents cytokine-induced tumor cell death: the inhibition of auto-toxic nitric oxide release as a potential mechanism [11].
• When uptake was normalised to cell number, danthrone and sennidine doubled BrdU uptake/10(6) cells, 18 microM rhein and 0.7 microM aloe-emodin induced increases of 37 and 50%, respectively [5].
• Hepatocytes of aloeemodin-treated male Wistar rats did not show DNA damage via repair synthesis [12].
• In in vivo studies (micronucleus assay in bone marrow cells of NMRI mice; chromosome aberration assay in bone marrow cells of Wistar rats; mouse spot text [DBA/2JxNMRI]) no indication of a mutagenic activity of aloeemodin was found [12].

Anatomical context of emodin

• Our study investigated the mechanisms of aloe-emodin-induced cell death in the human lung nonsmall cell carcinoma cell line H460 [13].
• We found that the release of nucleophosmin from the nucleus to the cytosol and the degradation of nucleophosmin were associated with aloe-emodin-induced H460 cell apoptosis [2].
• The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 microM aloe-emodin for 12, 24, 48, and 72 hours [14].
• The relevance of the absence of a mutagenic potential in in vivo test systems was strengthened by the fact that aloe-emodin could be found in the blood serum after oral administration [15].
• Among them, emodin and aloe-emodin showed higher cytotoxic activities against human oral squamous cell carcinoma (HSC-2) and salivary gland tumor (HSG) cell lines than against normal human gingival fibroblasts (HGF) [16].

Associations of emodin with other chemical compounds

• The separation of four major anthraquinones (aloe-emodin, emodin, chrysophanol, and physcion) was optimized with respect to pH and concentration of buffers, addition of acetonitrile, applied voltage, and column temperature [17].
• Protein kinase C involvement in aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell [4].
• A cytotoxicity profile of rhein, aloe emodin and danthron was established in related cell lines exhibiting different levels of topoisomerases, multidrug resistance-associated protein 1 and P-glycoprotein [18].
• Ethanol and aloe emodin alter the p53 mutational spectrum in ultraviolet radiation-induced murine skin tumors [19].
• A simple and rapid method for the simultaneous determination of five anthraquinone derivatives including aloe-emodin, emodin, chrysophanol, physcoin and rhein in Rheum species and Polygonum cuspidatum was established by capillary zone electrophoresis (CZE) using beta-cyclodextrin (CD) as modifier and urea to enhance its solubility [20].

Gene context of emodin

• Aloe-emodin induces apoptosis in T24 human bladder cancer cells through the p53 dependent apoptotic pathway [21].
• The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines [22].
• Release of nucleophosmin from the nucleus: Involvement in aloe-emodin-induced human lung non small carcinoma cell apoptosis [2].
• 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 aloe-emodin in HL-60 cells [14].
• In addition, aloe-emodin had a marked increase in Fas/APO1 receptor and Bax expression [22].

Analytical, diagnostic and therapeutic context of emodin

• 3. To elucidate whether the expression of protein kinase C (PKC) isozymes are involved in aloe-emodin- and emodin-induced apoptosis, this study examined the changes of PKC isozymes by Western blotting techniques during aloe-emodin- and emodin-induced apoptosis [4].
• Since aloe-emodin and emodin occur in senna in the free form as well as their glucosides and dianthrone glucosides, a HPLC method was established to allow the quantification of all free and glycosidic 1,8-dihydroxy anthranoids [23].
• Determination of the anthraquinones aloe-emodin and aloin-A by liquid chromatography with mass spectrometric and diode array detection [24].
• Aloe-emodin (40microM)-induced DNA single strand breaks were observed by comet assay [25].
• Genotoxicity tests were performed by several laboratories with the drug fructus sennae, senna extract, sennosides, rhein and aloe-emodin [15].

References