Inhibitory Effect of Myricetin on Melanoma Cells (A375)

Background: Cancer, a major cause of mortality worldwide, is a group of diseases distinguished by uncontrolled growth and expansion of abnormal cells. According to American Cancer Society, melanoma, a kind of skin cancer, is one of the most prevalent cancers. The side effects of chemical treatment developed more demands on natural products. Flavonoids, polyphenol compounds, with anticancer and antioxidant activity attracted more attention to themselves.Materials and Methods: Through this investigation the effect of myricetin on cell proliferation was determined by MTT (Methylthiazolyl diphenyl-tetrazolium bromide) assay. A375 cell lines were seeded in a 96 wells plate and were exposed to different concentrations of myricetin (10, 15, 20, 40, 60, 80, and 100µΜ). After considered times, the MTT solution was added, then the viability of cells was detected by measuring the absorbance on 570 and 630 nm.Results: Our finding showed that low concentration of myricetin (up to 25µM) has no toxicity effect. Also the result confirmed the IC50 of myricetin on melanoma cells for three ordered period (24, 48, 72 hours) as following: 50, 40, 35µΜ, respectively.Conclusion: According to this research, myricetin has anti-proliferative effect on melanoma cells, which can be used as a therapeutic agent. We hope that this study could be used as a mile stone in future researches to acquire confirmative results

The Effect of Myricetin Flavonoid on the Expression of Fyn Gene in Melanoma Cells (A375)

Background: Malignant melanoma as one of the most common cancers is currently spreading worldwide. Regarding after-effect of advanced treatments, using natural products has attracted much attention. Flavonoids, polyphenol compounds rich in diet, are being considered for their therapeutic preventive features. Fyn gene, a member of the protein tyrosine kinase oncogene family, has become an important target for therapy goals. Objectives: The aim of this study was to assess Fyn gene expression after treatment of melanoma cells with myricetin. Methods: In this study, the melanoma cells were treated with different concentrations of myricetin (0 to 100 �M) and their viability was determined by the methylthiazolyl diphenyl-tetrazolium bromide (MTT) assay, also the expression of Fyn gene in treated cells with selected concentrations of myricetin (0, 20, 40, 50, and 60 �M) was detected by real time quantitative polymerase chain reaction (qPCR). Results: The current investigation showed that treatment of A375 melanoma cells with the dietary flavonoid myricetin (3, 5, 7- trihydroxy-2-(3, 4, 5,-trihydroxy phenyl)-4- chromenone), resulted in decreased cell viability and increased expression of Fyn gene. The MTT assay analysis of exposed cells with different concentrations of myricetin showed that up to 25 �Mof myricetin had no cytotoxicity effect on A375 cells, also with increasing of myricetin concentration, the repression of cell proliferation developed as well. Conclusions: Real time qPCR analysis of Fyn expression in exposed cells with various concentration of myricetin leads to overexpression of this gene, dose dependently. Through this research, it was determined that myricetin with its anti-proliferative potential could suppress the development of cancer cells. On the other hand, since Fyn kinase could be involved in tumorigenesis of some cancer cells, it could be concluded that myricetin could effect the carcinogenicity of Fyn function in melanoma cells. Keywords: Melanoma, A375, Myricetin, Fyn Gen

Inhibitory Effect of Myricetin on Melanoma Cells (A375)

Background: Cancer, a major cause of mortality worldwide, is a group of diseases distinguished by uncontrolled growth and expansion of abnormal cells. According to American Cancer Society, melanoma, a kind of skin cancer, is one of the most prevalent cancers. The side effects of chemical treatment developed more demands on natural products. Flavonoids, polyphenol compounds, with anticancer and antioxidant activity attracted more attention to themselves. Materials and Methods: Through this investigation the effect of myricetin on cell proliferation was determined by MTT (Methylthiazolyl diphenyl-tetrazolium bromide) assay. A375 cell lines were seeded in a 96 wells plate and were exposed to different concentrations of myricetin (10, 15, 20, 40, 60, 80, and 100μΜ). After considered times, the MTT solution was added, then the viability of cells was detected by measuring the absorbance on 570 and 630 nm. Results: Our finding showed that low concentration of myricetin (up to 25μM) has no toxicity effect. Also the result confirmed the IC50 of myricetin on melanoma cells for three ordered period (24, 48, 72 hours) as following: 50, 40, 35μΜ, respectively. Conclusion: According to this research, myricetin has anti-proliferative effect on melanoma cells, which can be used as a therapeutic agent. We hope that this study could be used as a mile stone in future researches to acquire confirmative results. Keywords: Melanoma, Flavonoids, Polyphenol, A375 cell line, Myricetin, Anti-proliferativ

The effect of myricetin on the expression of b-catenin gene in melanoma cells (A375)

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Atherosclerosis is an inflammatory and multifaceted disorder resulting from the accumulation of lipid droplets and several types of immune cells, including macrophages, T and B lymphocytes in the arterial walls. A wide variety of macrophage subtypes with different functions is implicated in the development and progression of atherosclerotic lesions. The prevalence of specific macrophage subtypes, which is influenced by cytokines, mediators, and substances composing atherosclerotic lesions, has been suggested to be an appropriate indicator of transition from a stable to an unstable plaque phenotype. Thus, a better understanding of the mechanisms underlying the differentiation of macrophage subpopulations in relation to the plaque phenotype would help to develop novel approaches aiming at slowing-down the progression of atherosclerotic disease by modulating the polarization of these cells. In addition, many arms of the adaptative immune system, which are regulated by different subtypes of T and B lymphocytes, are involved in atherosclerosis progression and there is an increasing effort to identify immune-modulating therapies targeting either T or B cells with a potential anti-atherosclerotic impact. This paper summarizes the pathophysiology of atherosclerotic disease as it relates to the contribution from the immune system, reviewing the crucial role of macrophages, T and B lymphocytes. Keywords: Atherosclerosis,Macrophages, Atherosclerotic ,lesion,Plaque,Immunit

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The Wnt signaling pathway appears to activate intracellular signaling transduction in embryonic development, cell migration, hematopoiesis, and several diseases. Wnt signaling is basically recognized as a canonical beta-catenindependent signaling pathway. However, in recent years, generally three Wnt-mediated pathways have been investigated, which operate independently of beta-catenin and include calcium/calmodulin-dependent kinase II and protein kinase C, planar cell polarity, and a third one recruits hetrotrimeric GTP-binding proteins to stimulate phospholipase C and phosphodiesterase. We provide an overview of the noncanonical Wnt signaling pathway and then will focus on canonical Wnt signaling components, Wnt ligands, agonists, and antagonist. This review will also discuss beta-catenin, both cytoplasmic and nuclear mechanisms, through signaling transduction, and, as a consequence, we have briefly highlighted potential implications of Wnt/beta-catenin in some cancers

The Role of Efferocytosis in Autoimmune Diseases

Apoptosis happens continuously for millions of cells along with the active removal of apoptotic debris in order to maintain tissue homeostasis. In this respect, efferocytosis, i.e., the process of dead cell clearance, is orchestrated through cell exposure of a set of “find me,” “eat me,” and “tolerate me” signals facilitating the engulfment of dying cells through phagocytosis by macrophages and dendritic cells. The clearance of dead cells via phagocytes is of utmost importance to maintain the immune system tolerance to self-antigens. Accordingly, this biological activity prevents the release of autoantigens by dead cells, thus potentially suppressing the undesirable autoreactivity of immune cells and the appearance of inflammatory autoimmune disorders as systemic lupus erythematous and rheumatoid arthritis. In the present study, the apoptosis pathways and their immune regulation were reviewed. Moreover, efferocytosis process and its impairment in association with some autoimmune diseases were discussed. Keywords: apoptosis, efferocytosis, autoimmune disease, phagocytosis, systemic lupus erythematou

The Role of Efferocytosis in Autoimmune Diseases

Apoptosis happens continuously for millions of cells along with the active removal of apoptotic debris in order to maintain tissue homeostasis. In this respect, efferocytosis, i.e., the process of dead cell clearance, is orchestrated through cell exposure of a set of “find me,” “eat me,” and “tolerate me” signals facilitating the engulfment of dying cells through phagocytosis by macrophages and dendritic cells. The clearance of dead cells via phagocytes is of utmost importance to maintain the immune system tolerance to self-antigens. Accordingly, this biological activity prevents the release of autoantigens by dead cells, thus potentially suppressing the undesirable autoreactivity of immune cells and the appearance of inflammatory autoimmune disorders as systemic lupus erythematous and rheumatoid arthritis. In the present study, the apoptosis pathways and their immune regulation were reviewed. Moreover, efferocytosis process and its impairment in association with some autoimmune diseases were discussed. Keywords: apoptosis, efferocytosis, autoimmune disease, phagocytosis, systemic lupus erythematou