{"content"=>"Emodin successfully inhibited invasion of via modulating adherence, microtubule dynamics and ERK signaling pathway in RAW 264.7 cells.", "i"=>{"content"=>"Brucella abortus"}} (original) (raw)

Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) inhibits TNF-induced NF-κB activation, IκB degradation, and expression of cell surface adhesion proteins in human vascular endothelial cells

Oncogene, 1998

Most in¯ammatory agents activate nuclear transcription factor-kB (NF-kB) which results in expression of genes for cytokines, adhesion molecules, and enzymes involved in ampli®cation and perpetuation of in¯ammation. Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is an active component from the roots of Polygonum cuspidatum that has been reported to exhibit antiinammatory properties but the mechanism is not known. In the present study we investigated the eects of emodin on the activation of NF-kB in human umbelical vein endothelial cells (EC). Treatment of EC with TNF activated NF-kB; preincubation with emodin inhibited this activation in a dose-and time-dependent manner. Emodin did not chemically modify NF-kB subunits but rather inhibited degradation of IkB, an inhibitory subunit of NF-kB. Since the promoter regions of ICAM-1, VCAM-1, and ELAM-1 contain NF-kB binding sites and these adhesion molecules are involved in the attachment of leukocytes to EC, the eect of emodin on the adhesion of monocytes to EC and the expression of these adhesion molecules was also studied. Treatment of EC with TNF for 6 h increased the adhesion of monocytes to EC, which correlated with increases in cell surface expression of ICAM-1, VCAM-1 and ELAM-1. Pretreatment of EC for 1 h with emodin inhibited both monocyte-EC attachment and expression of ICAM-1, ELAM-1 and VCAM-1. These results indicate that emodin is a potent inhibitor of NF-kB activation and expression of adhesion molecules and thus could be useful in treating various in¯ammatory diseases.

Antimicrobial and morphogenic effects of emodin produced by Aspergillus awamori WAIR120

The antimicrobial activity of anthraquinone emodin isolated from Aspergillus awamori WAIR120 (LC032125) culture was investigated against some clinical, phytopathogenic and foodborne pathogenic microorganisms using an agar diffusion method. Among bacterial and fungal strains tested, the highest activity was obtained against Enterococcus faecalis AHR7 as well as Aspergillus niger OC20 with minimal inhibitory emodin concentration of 125 and 85 µg/mL, respectively. Emodin was found to induce morphogenic effects including swelling and elongation of bacterial cell and conidiation decrease, pigmentation loss, and cytoplasmic retraction of fungal cell, as was shown by light microscopy. Additionally, cellular effects were also resulted, in which emodin caused considerable changes in the nature of cell membrane and submicroscopic structure of bacterial and fungal cell, as was shown by transmission electron microscopy. Furthermore, there was an evidence of a disruption of lipid metabolism of fungal cell. These findings thus indicate the future possibility of exploiting emodin as an effective inhibitor of clinical, phytopathogenic and foodborne pathogenic microorganisms.

Emodin inhibits the proliferation and migration of B16F10 cells and induces their apoptosis

Translational Cancer Research

Background: Emodin, extracted from the rhizomes of various Chinese herbs, is a natural anthraquinone derivative with the formula C15H10O5. Many recent studies have shown that emodin has an antitumour effect. In this study, emodin was investigated in vitro to observe its effect on the proliferation, migration, and apoptosis of the B16F10 melanoma cell line. Methods: B16F10 cells were treated with 20, 40, 60, or 80 μM emodin for 24 h. A Cell Counting Kit-8 (CCK-8) was used to measure the effect of emodin on cell proliferation. After 24 h of emodin treatment, a scratch test was used to detect the wound healing rate of each group. A Transwell test was used to measure the effect of emodin on cell migration ability. The apoptosis rate of the B16F10 cells was determined by a TUNEL assay. The expression of caspase-3 was measured by western blot analysis. Results: Compared with the control group, emodin significantly inhibited the proliferation and migration of the B16F10 cells in a concentration-dependent manner. Emodin also inhibited the migration of the B16F10 cells and induced their apoptosis. Conclusions: Emodin can effectively suppress the viability and migration of B16F10 cells and may induce apoptosis through the mitochondrial pathway or death receptor-mediated pathway.

‘Old Wine in a New Bottle’: Harnessing the Therapeutic Properties of Emodin Derivatives

Journal of Biomedical Engineering and Medical Devices

Studies involving mechanism of emodin, an herbal extract, has revealed its potential as anti-inflammatory, antioxidant and anti-cancer agent. Emodin has been shown to successfully induce apoptosis, down-regulate cancer inducing genes, proving it to be a therapeutically significant pharmacophore. Modification of emodin and synthesis of various derivatives have successfully increased efficacy of the molecule in regulating various cellular pathway like MAPK signaling pathway, NF-κβ signaling pathway, ROS mediated pathways and apoptotic pathways. With the advent of various, anti-bacterial properties of emodin may come in rescue to combat emerging drug resistant microbial and parasitic strains. Different emodin derivatives, including the recently reported haloemodin, which inhibits bacterial topoisomerases, can be designed to generate future drugs against resistant pathogens. Emodin derivatives can also inhibit proteases and microtubule-associated proteins, which play an important role in Alzheimer's disease. Properly designed drug delivery systems like liposomes and nanoparticles have been reported as efficient emodin carriers and to enhance emodin activity in cancer cell inhibition. Exploitation of these newly reported properties of this age-old drug could prove to be a promising solution for anti-microbial chemoresistance menace and other prevalent non-communicable diseases.

The effects of red ginseng saponin fraction-A (RGSF-A) on phagocytosis and intracellular signaling in Brucella abortus infected RAW 264.7 cells

This study indicated that RGSF-A caused a marked reduction in the adherence, internalization and intracellular growth of Brucella abortus in RGSF-A-treated cells. Furthermore, a decline in the intensity of F-actin fluorescence was observed in RGSF-A-treated cells compared with untreated B. abortus-infected cells. In addition, an evaluation of phagocytic signaling proteins by Western blot analysis revealed an apparent reduction of ERK and p38¥á phosphorylation levels in B. abortus-infected RGSF-A-treated cells compared with the control. Upon intracellular trafficking of the pathogen, a higher number of B. abortus-containing phagosomes colocalized with LAMP-1 in RGSF-A-treated cells compared with control cells. These results strongly suggest that inhibition of B. abortus uptake could be mediated by suppression in the activation of MAPKs signaling proteins phospho-ERK 1/2, and p38 levels. On the other hand, inhibition of intracellular replication results from the enhancement of phagolysosome fusion in host macrophages. This study highlights the phagocytic and intracellular modulating effect of RGSF-A and its potential as an alternative remedy to control B. abortus infection.

Emodin, a natural inhibitor of protein kinase CK2, suppresses growth, hyphal development, and biofilm formation of Candida albicans

Yeast (Chichester, England), 2017

Emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) is a natural secondary plant product, originally isolated from the rhizomes of Rheum palmatum. Many reports show its diuretic, vasorelaxant, antibacterial, antiviral, anti-ulcerogenic, immunosuppressive, hepatoprotective, anti-inflammatory and anticancer potential. Emodin is a pleiotropic molecule capable of interacting with several major molecular targets, e.g. NF-κB, AKT/mTOR and STAT3. The compound can also act as an inhibitor of some protein kinases, with special affinity to protein kinase CK2. The aim of the presented report was to evaluate antifungal properties of emodin and its activity towards CK2 isolated from Candida cells. Our studies revealed that the compound suppressed growth of the cells of reference strains as well as clinical Candida strains, with minimal inhibitory concentration and minimal fungicidal concentration values between 12.5 and 200 μg/mL. Moreover, at a low concentration, the compound was able to effective...

Membrane-related effects underlying the biological activity of the anthraquinones emodin and barbaloin

Biochemical Pharmacology, 2004

Commercial plant extracts containing anthraquinones are being increasingly used for cosmetics, food and pharmaceuticals due to their wide therapeutic and pharmacological properties. In this work, the interaction with model membranes of two representative 1,8dihydroxyanthraquinones, barbaloin (Aloe) and emodin (Rheum, Polygonum), has been studied in order to explain their effects in biological membranes. Emodin showed a higher affinity for phospholipid membranes than barbaloin did, and was more effective in weakening hydrophobic interactions between hydrocarbon chains in phospholipid bilayers. Whereas emodin induced the formation of hexagonal-H II phase, barbaloin stabilized lamellar structures. Barbaloin promoted the formation of gel-fluid intermediate structures in phosphatidylglycerol membranes at physiological pH and ionic strength values. It is proposed that emodin's chromophore group is located at the upper half of the membrane, whereas barbaloin's one is in a deeper position but having its glucopyranosyl moiety near the phospholipid/water interface. Moreover, membrane disruption by emodin or barbaloin showed specificity for the two major phospholipids present in bacterial membranes, phosphatidylethanolamine and phosphatidylglycerol. In order to relate their strong effects on membranes to their biological activity, the capacity of these compounds to inhibit the infectivity of the viral haemorrhagic septicaemia rhabdovirus (VHSV), a negative RNA enveloped virus, or the growth of Escherichia coli was tested. Anthraquinone-loaded liposomes showed a strong antimicrobial activity whereas these compounds in their free form did not. Both anthraquinones showed antiviral activity but only emodin was a virucidal agent. In conclusion, a molecular mechanism based on the effect of these compounds on the structure of biological membranes is proposed to account for their multiple biological activities. Anthraquinone-loaded liposomes may suppose an alternative for antimicrobial, pharmaceutical or cosmetic applications. #

Modulation of Activated Murine Peritoneal Macrophages Functions by Emodin, Aloe-emodin and Barbaloin Isolated from Aloe barbadensis

Journal of Food and Drug Analysis, 2006

Activated murine macrophages produce high level of nitric oxide by inducible nitric oxide synthase (iNOS), which is an important mechanism in macrophage-induced inflammation. In the present study, we isolated emodin, aloe-emodin and barbaloin compounds from Aloe barbadensis and investigated their inhibitory effects on the production of nitric oxide (NO), tumor necrosis factor-α (TNFα) and interleukin (IL-12) from murine macrophages activated by lipopolysaccharide (LPS) and interferon-gamma (IFN-γ).

A potential antibacterial agent Embelin, a natural benzoquinone extracted from Embelia ribes

2011

Herbal medicine has been used for the prevention and treatment of various health aliments from time immemorial. In the present work, embelin from Embelia ribes berries of Indian origin was extracted and characterized by UV, NMR, thermal and X-ray diffraction analyses. Minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of embelin against both Gram +ve and Gram -ve bacteria were studied using micro dilution method and agar plate method by sub-culturing 10 µl of the test dilutions from MIC tubes on to fresh Mueller-Hinton agar plates. About 1.9± 0.1 gram of pure embelin was obtained from 100 gram of powdered berries (E.ribes). The characteristics studied reveal the properties are on par with the standard embelin received from Sigma (USA). With regard to antibacterial activity, embelin showed bactericidal activity against Gram +ve organisms, and bacteriostatic against Gram –ve organisms. Thus, embelin finds application as potent antibacterial agent.

Molecular mechanism of emodin action: Transition from laxative ingredient to an antitumor agent

Medicinal Research Reviews, 2007

Anthraquinones represent a large family of compounds having diverse biological properties. Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a naturally occurring anthraquinone present in the roots and barks of numerous plants, molds, and lichens, and an active ingredient of various Chinese herbs. Earlier studies have documented mutagenic/genotoxic effects of emodin, mainly in bacterial system. Emodin, first assigned to be a specific inhibitor of the protein tyrosine kinase p65lck, has now a number of cellular targets interacting with it. Its inhibitory effect on mammalian cell cycle modulation in specific oncogene overexpressed cells formed the basis of using this compound as an anticancer agent. Identification of apoptosis as a mechanism of elimination of cells treated with cytotoxic agents initiated new studies deciphering the mechanism of apoptosis induced by emodin. At present, its role in combination chemotherapy with standard drugs to reduce toxicity and to enhance efficacy is pursued vigorously. Its additional inhibitory effects on angiogenic and metastasis regulatory processes make emodin a sensible candidate as a specific blocker of tumor-associated events. Additionally, because of its quinone structure, emodin may interfere with electron transport process and in altering cellular redox status, which may account for its cytotoxic properties in different systems. However, there is no documentation available which reviews the biological activities of emodin, in particular, its growth inhibitory effects. This review is an attempt to analyze the biological properties of emodin, a molecule offering a broad therapeutic window, which in future may become a member of anticancer armamentarium. © 2006 Wiley Periodicals, Inc. Med Res Rev, 27, No. 5, 591–608, 2007