Inhibitory effects of melatonin on the lipopolysaccharide‐induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt‐induced NF‐κB and STAT/GAS activity

Min, Kyoung‐jin; Jang, Ji Hoon; Kwon, Taeg Kyu

doi:10.1111/j.1600-079x.2011.00943.x

Cited by 52 publications

(41 citation statements)

References 58 publications

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“…Melatonin reduces nf-κB binding in spleen [89]. a number of laboratories report melatonin-induced inhibition of nK-κB activity or inhibition of nf-κB activation [90][91][92][93][94][95][96][97][98][99][100]. these results suggest an interaction of melatonin and the ubiquitin-proteasome system in the activation of nf-κB.…”

Section: Melatonin/ubiquitin Interaction In Brown Fatmentioning

confidence: 49%

Melatonin and ubiquitin: what’s the connection?

Vriend

Reíter

2014

Cell. Mol. Life Sci.

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Section: Melatonin/ubiquitin Interaction In Brown Fatmentioning

confidence: 49%

Melatonin and ubiquitin: what’s the connection?

Vriend

Reíter

2014

Cell. Mol. Life Sci.

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“…For example, a previous study found that treatment with 1 mM melatonin for 24 h inhibited activation of NF-κB in the human prostate cancer LNCaP cell line (21). In addition, several prior reports have revealed that melatonin inhibits NF-κB activity (34,35), supporting the hypothesis that melatonin is a proteasome inhibitor and a natural NF-κB inhibitor. NF-κB inhibition serves an important role in the treatment of leukemia and lymphoma (36).…”

Section: Discussionmentioning

confidence: 66%

Melatonin treatment induces apoptosis through regulating the nuclear factor-κB and mitogen-activated protein kinase signaling pathways in human gastric cancer SGC7901 cells

et al. 2017

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Abstract. Melatonin, which is synthesized by the pineal gland and released into the blood, exhibits antitumor properties. However, the mechanisms underlying these effects, particularly in stomach cancer, remain unknown. In the present study, the effect of melatonin on the nuclear factor (NF)-κB signaling pathway and the mitogen-activated protein kinase signaling pathway, involving p38 and c-Jun-N-terminal kinase (JNK), were investigated in SGC7901 gastric cancer cells. In addition, the effect of melatonin on the survival, migration and apoptosis of these cells was investigated in vitro in order to evaluate the use of melatonin for the treatment of gastric cancer. The results of the present study revealed that melatonin decreased the viability and migration of SGC7901 cells. Furthermore, melatonin induced apoptosis. Melatonin was identified to elevate the expression levels of phosphorylated (p)-p38 and p-JNK protein, and decrease the expression level of nucleic p-p65. These results suggest that the protein levels of p65, p38 and JNK are associated with the survival of SGC7901 cells following treatment with melatonin. The optimal concentration of melatonin was demonstrated to be 2 mM, which significantly induced apoptosis following a 24 h treatment period. These findings suggest that conflicting growth signals in cells may inhibit the efficacy of melatonin in the treatment of gastric cancer. Therefore, adjunct therapy would be required to improve the efficacy of melatonin in the treatment of cancer. IntroductionGastric carcinoma is one of the most common types of malignancy, worldwide (1). In Asia, patients tend to be diagnosed at an average age of 66.8 years, and exhibit poor rates of survival (1). Gastric cancer is a refractory cancer and the third-leading cause of cancer-associated mortality in China (2). Gastric adenocarcinoma is the predominant type of gastric cancer and has limited treatment options (3). The typical treatments for gastric cancer, surgery and chemotherapy, only partially improve the overall survival of patients with this disease (4,5). Therefore, more effective drugs or comprehensive therapies are required (6).Melatonin is an indole hormone secreted by the pineal gland and was first identified in 1958 (7). Melatonin serves a significant role in a wide variety of biological processes, including sleep, immunomodulation, anti-inflammation and antioxidative stress (8-11). In addition, melatonin is an anticancer hormone and a potential target for cancer treatments (12). Several studies have revealed that melatonin is useful for the prevention of cancer (13,14). The antitumor ability of melatonin may be mediated by numerous mechanisms, including the activation of antioxidative stress, inhibition of migration and induction of apoptosis (15)(16)(17). Melatonin has also been demonstrated to suppress the growth, migration and invasion of SGC7901 gastric cancer cells in vitro (18), and to exert an apoptotic effect in the hepatocellular carcinoma HepG2 cell line (19). Additionally, the use of melatonin h...

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“…96 A nivel molecular, la MEL inhibe la expresión del ARNm de quimiocinas como CCL2 (MCP-1), CCL5 y CCL9 (MIP-1γ) inducidas por LPS en una línea celular de microglia. 97 Este efecto fue mediado por la inhibición de la actividad transcripcional de NF-κB y STAT/GAS. 97 En cultivos organotípicos de cerebro de ratón 98 y de hipocampo de rata 44 estimulados con los pép-tidos Aβ1-40 y Aβ25-35, respectivamente, la MEL disminuye la secreción de citocinas pro-inflamatorias y previene la activación de la microglia y de los astrocitos que se inducen por la exposición al péptido Aβ25-35.…”

Section: La Melatonina Tiene Efectos Anti-inflamatorios En El Sistemaunclassified

La melatonina como un factor promotor de la diferenciación neuronal: implicaciones en el tratamiento de las demencias

et al. 2013

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SUMMARYDementias are progressive and neurodegenerative neuropsychiatric disorders, with a high worldwide prevalence. These disorders affect memory and behavior, causing impairment in the performance of daily activities and general disability in the elders. Cognitive impairment in these patients is related to anatomical and structural alterations at cellular and sub-cellular levels in the Central Nervous System. In particular, amyloid plaques and neurofibrillar tangles have been defined as histopathological hallmarks of Alzheimer's disease. Likewise, oxidative stress and neuroinflammation are implicated in the etiology and progression of the disease.Neuronal precursors from human olfactory neuroepithelium have been recently characterized as an experimental model to identify neuropsychiatric disease biomarkers. Moreover, this model not only allows the study of neuropsychiatric physiopathology, but also the process of neurodevelopment at cellular, molecular and pharmacological levels.This review gathers the evidence to support the potential therapeutic use of melatonin for dementias, based on its antioxidant properties, its anti-inflammatory effect in the brain, and its ability to inhibit both tau hyper-phosphorylation and amyloid plaque formation. Furthermore, since melatonin stimulates neurogenesis, and promotes neuronal differentiation by inducing the early stages of neuritogenesis and dendrite formation, it has been suggested that melatonin could be useful to counteract the cognitive impairment in dementia patients.Key words: Melatonin, dementia, biomarkers, neuroepithelium, neuritogenesis. RESUMENLas demencias son enfermedades neuropsiquiátricas, progresivas, neurodegenerativas y con una alta prevalencia a nivel mundial. Ocupan uno de los primeros lugares como enfermedades que causan incapacidad en los adultos mayores. En estos pacientes el Sistema Nervioso Central presenta alteraciones anatómico-estructurales a nivel celular y subcelular que se asocian con deficiencias cognitivas. En particular, en la enfermedad de Alzheimer se han caracterizado marcadores histopatológicos como las placas amiloides y las marañas neurofibrilares. Se sabe que el estrés oxidativo y la neuroinflamación participan en la etiología y el desarrollo de la enfermedad. Recientemente se caracterizó a los precursores neuronales del neuroepitelio olfatorio humano como un modelo experimental adecuado para identificar biomarcadores de rasgo y para estudiar la fisiopatología de diversas enfermedades neuropsiquiátricas, así como el proceso del neurodesarrollo, a nivel celular, molecular y farmacológico. En este trabajo se presenta la evidencia que sustenta que la melatonina puede ser útil en el tratamiento de las demencias, por su capacidad antioxidante, por su efecto anti-inflamatorio, así como por el efecto inhibidor de la hiperfosforilación de la proteina tau y de la formación de placas amiloides. Además, al estimular la formación de nuevas neuronas, la neuritogénesis en sus etapas tempranas y la formación de dendritas, la melatonina podría...

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Inhibitory effects of melatonin on the lipopolysaccharide‐induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt‐induced NF‐κB and STAT/GAS activity

Cited by 52 publications

References 58 publications

Melatonin and ubiquitin: what’s the connection?

Melatonin and ubiquitin: what’s the connection?

Melatonin treatment induces apoptosis through regulating the nuclear factor-κB and mitogen-activated protein kinase signaling pathways in human gastric cancer SGC7901 cells

La melatonina como un factor promotor de la diferenciación neuronal: implicaciones en el tratamiento de las demencias

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