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[PMID]:28766982
[Au] Autor:Ludwig MD; Zagon IS; McLaughlin PJ
[Ad] Endereço:Department of Neural & Behavioral Sciences, College of Medicine, Pennsylvania State University, PA 17033, USA.
[Ti] Título:Featured Article: Serum [Met ]-enkephalin levels are reduced in multiple sclerosis and restored by low-dose naltrexone.
[So] Source:Exp Biol Med (Maywood);242(15):1524-1533, 2017 Sep.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Low-dose naltrexone is a widely used off-label therapeutic prescribed for a variety of immune-related disorders. The mechanism underlying low-dose naltrexone's efficacy for fatigue, Crohn's disease, fibromyalgia, and multiple sclerosis is, in part, intermittent blockade of opioid receptors followed by upregulation of endogenous opioids. Short, intermittent blockade by naltrexone specifically blocks the opioid growth factor receptor resulting in biofeedback events that increase production of the endogenous opioid growth factor (OGF) (chemically termed [Met ]-enkephalin) facilitating interactions between opioid growth factor and opioid growth factor receptor that ultimately, result in inhibited cell proliferation. Preclinical studies have reported that enkephalin levels are deficient in animal models of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. Our hypothesis is that serum enkephalin levels are diminished in humans with multiple sclerosis and experimental autoimmune encephalomyelitis mice, and that change in serum opioid growth factor levels may serve as a reasonable candidate biomarker for the onset of experimental autoimmune encephalomyelitis and response to therapy. To address this, we designed a two-part study to measure endogenous opioids in multiple sclerosis patients, and to investigate the temporal pattern of decline in serum enkephalin concentrations in mice with chronic progressive experimental autoimmune encephalomyelitis and treated with low-dose naltrexone. For comparison, we investigated whether low-dose naltrexone exposure in normal mice also resulted in altered enkephalin levels. In both animal models, we monitored tactile and heat sensitivity, as well as differential white blood cell counts as indicators of inflammation. Serum [Met ]-enkephalin levels were lower in humans with multiple sclerosis relative to non-multiple sclerosis patients, and low-dose naltrexone restored their levels. In experimental autoimmune encephalomyelitis mice, [Met ]-enkephalin levels were depressed prior to the appearance of clinical disease, and were restored with low-dose naltrexone treatment. Low-dose naltrexone therapy had no effect on serum [Met ]-enkephalin or ß-endorphin in normal mice. Thus, [Met ]-enkephalin (i.e. opioid growth factor) may be a reasonable candidate biomarker for multiple sclerosis, and may signal new pathways for treatment of autoimmune disorders. Impact statement This report presents human and animal data identifying a novel biomarker for the onset and progression of multiple sclerosis (MS). Humans diagnosed with MS have reduced serum levels of OGF (i.e. [Met ]-enkephalin) relative to non-MS neurologic patients, and low-dose naltrexone (LDN) therapy restored their enkephalin levels. Serum OGF levels were reduced in mice immunized with MOG prior to any clinical behavioral sign of experimental autoimmune encephalomyelitis, and LDN therapy restored their serum OGF levels. ß-endorphin concentrations were not altered by LDN in humans or mice. Thus, blood levels of OGF may serve as a new, selective biomarker for the progression of MS, as well as response to therapy.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Encefalomielite Autoimune Experimental/patologia
Encefalina Metionina/sangue
Esclerose Múltipla/tratamento farmacológico
Esclerose Múltipla/patologia
Naltrexona/uso terapêutico
Fármacos Neuroprotetores/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Feminino
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Meia-Idade
Soro/química
Resultado do Tratamento
Voluntários
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Neuroprotective Agents); 58569-55-4 (Enkephalin, Methionine); 5S6W795CQM (Naltrexone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.1177/1535370217724791


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[PMID]:28115487
[Au] Autor:Yorgason JT; Zeppenfeld DM; Williams JT
[Ad] Endereço:Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239.
[Ti] Título:Cholinergic Interneurons Underlie Spontaneous Dopamine Release in Nucleus Accumbens.
[So] Source:J Neurosci;37(8):2086-2096, 2017 Feb 22.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The release of dopamine from terminals in the NAc is regulated by a number of factors, including voltage-gated ion channels, D2-autoreceptors, and nAChRs. Cholinergic interneurons (CINs) drive dopamine release through activation of nAChRs on dopamine terminals. Using cyclic voltammetry in mouse brain slices, nAChR-dependent spontaneous dopamine transients and the mechanisms underlying the origin were examined in the NAc. Spontaneous events were infrequent (0.3 per minute), but the rate and amplitude were increased after blocking Kv channels with 4-aminopyridine. Although the firing frequency of CINs was increased by blocking glutamate reuptake with TBOA and the Sk blocker apamin, only 4-aminopyridine increased the frequency of dopamine transients. In contrast, inhibition of CIN firing with the µ/δ selective opioid [Met ]enkephalin (1 µm) decreased spontaneous dopamine transients. Cocaine increased the rate and amplitude of dopamine transients, suggesting that the activity of the dopamine transporter limits the detection of these events. In the presence of cocaine, the rate of spontaneous dopamine transients was further increased after blocking D2-autoreceptors. Blockade of muscarinic receptors had no effect on evoked dopamine release, suggesting that feedback inhibition of acetylcholine release was not involved. Thus, although spontaneous dopamine transients are reliant on nAChRs, the frequency was not strictly governed by the activity of CINs. The increase in frequency of spontaneous dopamine transients induced by cocaine was not due to an increase in cholinergic tone and is likely a product of an increase in detection resulting from decreased dopamine reuptake. The actions of dopamine in the NAc are thought to be responsible for endogenous reward and the reinforcing properties of drugs of abuse, such as psychostimulants. The present work examines the mechanisms underlying nAChR-induced spontaneous dopamine release. This study demonstrates that spontaneous dopamine release is (1) dependent of the activation of nicotinic receptors, (2) independent on the spontaneous activity of cholinergic interneurons, and (3) that cocaine increased the detection of dopamine transients by prolonging the presence and increasing the diffusion of dopamine in the extracellular space. The release of acetylcholine is therefore responsible for spontaneous dopamine transients, and cocaine augments dopamine tone without altering activity of cholinergic interneurons.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Dopamina/metabolismo
Interneurônios/metabolismo
Núcleo Accumbens/citologia
[Mh] Termos MeSH secundário: 4-Aminopiridina/farmacologia
Acetilcolina/farmacologia
Potenciais de Ação/efeitos dos fármacos
Análise de Variância
Animais
Apamina/farmacologia
Ácido Aspártico/farmacologia
Cocaína/farmacologia
Inibidores da Captação de Dopamina/farmacologia
Estimulação Elétrica
Encefalina Metionina/farmacologia
Feminino
Técnicas In Vitro
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Técnicas de Patch-Clamp
Bloqueadores dos Canais de Potássio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Uptake Inhibitors); 0 (Potassium Channel Blockers); 0 (benzyloxyaspartate); 24345-16-2 (Apamin); 30KYC7MIAI (Aspartic Acid); 58569-55-4 (Enkephalin, Methionine); BH3B64OKL9 (4-Aminopyridine); I5Y540LHVR (Cocaine); N9YNS0M02X (Acetylcholine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3064-16.2017


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[PMID]:28088065
[Au] Autor:Meng Y; Gao X; Chen W; Plotnikoff NP; Griffin N; Zhang G; Shan F
[Ad] Endereço:Department of Immunology, School of Basic Medical Science, China Medical University, No. 77, Puhe Road, Shenyang 110122, China; Center of Biological Therapy, Cancer Hospital of China Medical University, No. 44, Xiaoheyan Road, Shenyang 110042, Liaoning Province, China.
[Ti] Título:Methionine enkephalin (MENK) mounts antitumor effect via regulating dendritic cells (DCs).
[So] Source:Int Immunopharmacol;44:61-71, 2017 Mar.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:MENK, an endogenous opioid peptide has been reported to have many immunological and antitumor activities. So far the detailed mechanisms of antitumor through regulating DCs by MENK have not been elucidated yet. The aim of this work was to investigate the antitumor mechanisms of MENK via regulating DC. The monitoring methods, such as ELISA, MTS assay, CFSE, Real-time PCR and Western blot were included in our research. We found bone marrow derived dendritic cells (BMDCs) in 36 female C57BL/6 mice treated with MENK enhanced expression of key surface molecules, increased production of critical cytokines reduced endocytosis of FITC-dextran, upregulated TLR4 through MyD88/NF-κB signaling pathway and mounted higher antitumor activity. These observations were further supported by an enhancement of nuclear translocation of the p65NF-κB subunit involved in this process. Surprisingly, mu-opioid receptors were the main participants of this kind of activation, not delta-opioid receptors nor kappa-opioid receptors, and these interactions could be partly blocked by Naltrexone (a kind of opioid antagonist). In vivo study the activated CD4 , CD8 T cells and decreased ability to induce differentiation of Foxp3 regulatory T cells were detected post treatment of MENK. Thus, it is concluded that MENK could exert antitumor effect through precisely regulating opioid receptor mediated functions of DCs. In addition, MENK treated DCs may serve as a new immunotherapy approach against tumor.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Células Dendríticas/efeitos dos fármacos
Encefalina Metionina/uso terapêutico
Imunoterapia/métodos
Neoplasias/terapia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Citocinas/metabolismo
Células Dendríticas/imunologia
Feminino
Seres Humanos
Ativação Linfocitária/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/metabolismo
Neoplasias/imunologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytokines); 0 (NF-kappa B); 58569-55-4 (Enkephalin, Methionine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE


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[PMID]:28039905
[Au] Autor:Hiramoto K; Yokoyama S; Yamate Y
[Ad] Endereço:Department of Pharmaceutical Science, Suzuka University of Medical Science, Mie, Japan.
[Ti] Título:Ultraviolet A eye irradiation ameliorates colon carcinoma induced by azoxymethane and dextran sodium sulfate through ß-endorphin and methionine-enkephalin.
[So] Source:Photodermatol Photoimmunol Photomed;33(2):84-91, 2017 Mar.
[Is] ISSN:1600-0781
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We previously reported that ultraviolet (UV) A eye irradiation reduces the ulcerative colitis induced by dextran sodium sulfate (DSS). This study examined the effects of UVA on colon carcinoma induced by azoxymethane (AOM) and DSS. METHODS: We irradiated the eyes of ICR mice with UVA at a dose of 110 kJ/m using an FL20SBLB-A lamp for the experimental period. RESULTS: In mice treated with these drugs, the symptom of colon carcinoma was reduced by UVA eye irradiation. The levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in the blood were increased in AOM + DSS-treated mice; however, those levels were reduced by UVA eye irradiation. The expression of ß-endorphin, methionine-enkephalin (OGF), µ-opioid receptor, and opioid growth factor receptor (OGFR) of the colon was increased in the AOM + DSS-treated mice, and these levels were increased further following UVA eye irradiation. When ß-endorphin inhibitor was administered, the ameliorative effect of UVA eye irradiation was reduced, and the effect of eye irradiation disappeared entirely following the administration of naltrexone (inhibitor of both opioid receptor and OGFR). CONCLUSIONS: These results suggested that UVA eye irradiation exerts major effects on AOM + DSS-induced colon carcinoma.
[Mh] Termos MeSH primário: Colo/metabolismo
Neoplasias do Colo/metabolismo
Encefalina Metionina/metabolismo
Olho/efeitos da radiação
Raios Ultravioleta
beta-Endorfina/metabolismo
[Mh] Termos MeSH secundário: Aminoquinolinas/farmacologia
Animais
Azoximetano
Benzamidas/farmacologia
Neoplasias do Colo/induzido quimicamente
Neoplasias do Colo/patologia
Sulfato de Dextrana
Feminino
Interleucina-6/sangue
Antígeno Ki-67/metabolismo
Camundongos Endogâmicos ICR
Naltrexona/farmacologia
Receptores Opioides/metabolismo
Receptores Opioides mu/antagonistas & inibidores
Receptores Opioides mu/metabolismo
Fator de Necrose Tumoral alfa/sangue
beta-Endorfina/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Benzamides); 0 (Interleukin-6); 0 (Ki-67 Antigen); 0 (N-(4-amino-2-methylquinolin-6-yl)-2-(4-ethylphenoxymethyl)benzamide); 0 (Receptors, Opioid); 0 (Receptors, Opioid, mu); 0 (Tumor Necrosis Factor-alpha); 0 (methionine-enkephalin receptor); 58569-55-4 (Enkephalin, Methionine); 5S6W795CQM (Naltrexone); 60617-12-1 (beta-Endorphin); 9042-14-2 (Dextran Sulfate); MO0N1J0SEN (Azoxymethane)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170322
[Lr] Data última revisão:
170322
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1111/phpp.12290


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[PMID]:27759693
[Au] Autor:Yazdani Abyaneh MA; Engel P; Slominski A; Ragsdale B; Agag R; Cramer D; Carlson JA
[Ad] Endereço:*Albany Medical College, Albany, NY; †Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; ‡VA Boston Healthcare System Geriatric Research, Education and Clinical Center, Boston, MA; §Department of Dermatology, University of Alabama at Birmingham, VA Medical Center, Birmingham, AL; ¶Western Pathology, Inc., San Luis Obispo, CA; ‖Department of Plastic Surgery, Albany Medical College, Albany, NY; **Loyola Stritch School of Medicine, Maywood, IL; and ††Department of Pathology, Albany Medical College, Albany, NY.
[Ti] Título:Giant Basal Cell Carcinomas Express Neuroactive Mediators and Show a High Growth Rate: A Case-Control Study and Meta-Analysis of Etiopathogenic and Prognostic Factors.
[So] Source:Am J Dermatopathol;39(3):189-194, 2017 Mar.
[Is] ISSN:1533-0311
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Giant basal cell carcinomas (GBCCs), (BCC ≥ 5 cm), are often painless, destructive tumors resulting from poorly understood patient neglect. OBJECTIVES: To elucidate etiopathogenic factors distinguishing GBCC from basal cell carcinoma (BCC) and identify predictors for disease-specific death (DSD). METHODS: Case-control study examining clinicopathologic and neuroactive factors (ß-endorphin, met-enkephalin, serotonin, adrenocorticotropic hormone, and neurofilament expression) in GBCC and BCC. Systematic literature review to determine DSD predictors. RESULTS: Thirteen GBCCs (11 patients) were compared with 26 BCCs (25 patients). GBCC significantly differed in size, disease duration, and outcomes; patients were significantly more likely to live alone, lack concern, and have alcoholism. GBCC significantly exhibited infiltrative/morpheic phenotypes, perineural invasion, ulceration, and faster growth. All neuromediators were similarly expressed. Adenoid phenotype was significantly more common in GBCC. Adenoid tumors expressed significantly more ß-endorphin (60% vs. 18%, P = 0.01) and serotonin (30% vs. 4%, P = 0.02). In meta-analysis (n ≤ 311: median age 68 years, disease duration 90 months, tumor diameter 8 cm, 18.4% disease-specific mortality), independent DSD predictors included tumor diameter (cm) (hazard ratio (HR): 1.12, P = 0.003), bone invasion (HR: 4.19, P = 0.015), brain invasion (HR: 8.23, P = 0.001), and distant metastases (HR: 14.48, P = 0.000). CONCLUSIONS: GBCC etiopathogenesis is multifactorial (ie, tumor biology, psychosocial factors). BCC production of paracrine neuromediators deserves further study.
[Mh] Termos MeSH primário: Carcinoma Basocelular/patologia
Serotonina/biossíntese
Neoplasias Cutâneas/patologia
beta-Endorfina/biossíntese
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/análise
Hormônio Adrenocorticotrópico/biossíntese
Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Basocelular/metabolismo
Carcinoma Basocelular/psicologia
Estudos de Casos e Controles
Encefalina Metionina/análise
Encefalina Metionina/biossíntese
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Prognóstico
Estudos Retrospectivos
Serotonina/análise
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/psicologia
Adulto Jovem
beta-Endorfina/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
333DO1RDJY (Serotonin); 58569-55-4 (Enkephalin, Methionine); 60617-12-1 (beta-Endorphin); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1097/DAD.0000000000000640


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[PMID]:27878237
[Au] Autor:Wang DM; Wang GC; Yang J; Plotnikoff NP; Griffin N; Han YM; Qi RQ; Gao XH; Shan FP
[Ad] Endereço:Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, Liaoning 110122, P.R. China.
[Ti] Título:Inhibition of the growth of human melanoma cells by methionine enkephalin.
[So] Source:Mol Med Rep;14(6):5521-5527, 2016 Dec.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Melanoma is an aggressive cancer, the incidence of which is increasing worldwide. Limited therapies are currently available, particularly following metastasis. The aim of the present study was to investigate the inhibiting effect of methionine enkephalin (MENK) on human melanoma via opioid receptors. The results of the present study revealed that MENK markedly regulates the proliferation of A375 cells, causing cell cycle arrest in G0/G1 phase and a decrease in the percentage of cells in S and G2/M phases. Reverse transcription­quantitative polymerase chain reaction demonstrated that MENK treatment increased opioid receptor expression in A375 cells. Furthermore, the expression level of survivin, an inhibitory apoptotic protein, was 1.1% of the level in the control group in the MENK group following 48 h of treatment. In conclusion, the results of the present study revealed, to the best of our knowledge for the first time, that MENK may inhibit growth and induce apoptosis of A375 cells, and describes a potential mechanism underlying these effects. Therefore, MENK should be investigated as a primary therapy for human melanoma cancer and as an adjuvant to other chemotherapies. Further studies are required to develop an optimal strategy for the use of MENK for the treatment of human cancers.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Encefalina Metionina/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Expressão Gênica
Seres Humanos
Melanoma/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores Opioides/genética
Receptores Opioides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (RNA, Messenger); 0 (Receptors, Opioid); 58569-55-4 (Enkephalin, Methionine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170407
[Lr] Data última revisão:
170407
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.5941


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[PMID]:27703986
[Au] Autor:Sassani JW; Mc Laughlin PJ; Zagon IS
[Ad] Endereço:Departments of Ophthalmology and Pathology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA.
[Ti] Título:The Yin and Yang of the Opioid Growth Regulatory System: Focus on Diabetes-The Lorenz E. Zimmerman Tribute Lecture.
[So] Source:J Diabetes Res;2016:9703729, 2016.
[Is] ISSN:2314-6753
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:The Opioid Growth Regulatory System consists of opioid growth factor (OGF), [Met ]-enkephalin, and its unique receptor (OGFr). OGF inhibits cell division when bound to OGFr. Conversely, blockade of the interaction of OGF and OGFr, using the potent, long-acting opioid receptor antagonist, naltrexone (NTX), results in increased DNA synthesis and cell division. The authors have demonstrated both and that the addition of exogenous OGF or an increase in available OGFr decreases corneal epithelial cell division and wound healing. Conversely, blockade of the OGF-OGFr interaction by NTX or a decrease in the production of the OGFr increases corneal epithelial cell division and facilitates corneal epithelial wound healing. The authors also have demonstrated that depressed corneal and cutaneous wound healing, dry eye, and abnormal corneal sensitivity in type 1 and type 2 diabetes in animals can be reversed by OGF-OGFr blockade by NTX. Thus, the function of the Opioid Growth Regulatory System appears to be disordered in diabetic animals, and its function can be restored with NTX treatment. These studies suggest a fundamental role for the Opioid Growth Regulatory System in the pathobiology of diabetic complications and a need for studies to elucidate this role further.
[Mh] Termos MeSH primário: Diabetes Mellitus/metabolismo
Encefalina Metionina/metabolismo
Receptores Opioides/metabolismo
[Mh] Termos MeSH secundário: Animais
Divisão Celular/fisiologia
Seres Humanos
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Opioid); 0 (methionine-enkephalin receptor); 58569-55-4 (Enkephalin, Methionine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161006
[St] Status:MEDLINE


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[PMID]:27584058
[Au] Autor:Xu X; Gao Y; Wen L; Zhai Z; Zhang S; Shan F; Feng J
[Ad] Endereço:Department of Neurology, Shengjing Hospital, Affiliated Hospital of China Medical University, Shenyang 110004, PR China.
[Ti] Título:Methionine enkephalin regulates microglia polarization and function.
[So] Source:Int Immunopharmacol;40:90-97, 2016 Nov.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Methionine enkephalin (MENK), an opioid peptide, is known to function as a regulator in the immune system. As microglia are considered the most important immune cells in the central nervous system (CNS), we aimed to assess the function of MENK on microglia polarization and tumoricidal responses. Initially, we chose the most optimal condition of 10 M for 48h; however, MENK had no function on the viability and apoptosis of microglia under this treatment. However, MENK treatment markedly increased levels of M1-associated genes, such as CD86, CD40, IL-12, and TNF-α, but had no effect on M2 markers, including CD163, IL-10, and TGF-ß. Moreover, microglia in the MENK-treated group showed high phagocytosis capacity, which coincided with characteristics of M1 microglia. MENK stimulation also induced up-regulation of reactive oxygen species (ROS) expression, which contributed to maintaining homeostasis. We also detected NO production by measuring the end product nitrite, and found that MENK treatment increased expression of nitrite and inducible NO synthase (iNOS), but did not influence arginase-1 (Arg1) expression. Furthermore, treatment of microglia with MENK led to a significant increase in cytotoxicity against glioblastoma cells, indicating that MENK possessed anti-tumor ability. Overall, MENK treatment could induce microglia to an M1 phenotype, modulating Th1 responses in the immune system. Additionally, microglia treated with MENK had tumoricidal activity, which provides new insight into anti-tumor immunity.
[Mh] Termos MeSH primário: Encefalina Metionina/farmacologia
Microglia/efeitos dos fármacos
Microglia/imunologia
[Mh] Termos MeSH secundário: Antígenos CD/genética
Apoptose/efeitos dos fármacos
Arginase/genética
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citocinas/genética
Citocinas/metabolismo
Glioblastoma
Seres Humanos
Microglia/metabolismo
Óxido Nítrico Sintase Tipo II/genética
Fagocitose/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cytokines); 0 (Reactive Oxygen Species); 58569-55-4 (Enkephalin, Methionine); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160902
[St] Status:MEDLINE


  9 / 4343 MEDLINE  
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[PMID]:27531857
[Au] Autor:Sánchez ML; Díaz-Cabiale Z; Narváez JA; Manso B; Salinas P; Rivada E; Smith V; Coveñas R
[Ad] Endereço:University of Salamanca, Institute of Neurosciences of Castilla y León (INCYL), Laboratory of Neuroanatomy of the Peptidergic Systems (Lab. 14), Salamanca, Spain. Electronic address: lisardosanchez8@gmail.com.
[Ti] Título:Mapping of methionine-enkephalin-arg -gly -leu in the human diencephalon.
[So] Source:Neuroscience;334:245-258, 2016 Oct 15.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using an immunohistochemical technique, we mapped the immunoreactive structures containing methionine-enkephalin-Arg -Gly -Leu (Met-8) (a marker for the pro-enkephalin system) in the human diencephalon. Compared with previous studies, we observed a more widespread distribution of Met-8 in the human diencephalon. Met-8-immunoreactive cell bodies and fibers exhibited a more widespread distribution in the hypothalamus than in the thalamus. We observed six populations of Met-8-immunoreactive cell bodies. These perikarya were observed in the paratenial thalamic nucleus, ventromedial and dorsomedial hypothalamic nuclei, lateral hypothalamic area, pallidohypothalamic nucleus and in the paraventricular hypothalamic nucleus (posterior part). In the thalamus, Met-8-immunoreactive fibers were primarily observed in the midline region, whereas in the hypothalamus, these fibers were widely distributed. In general, a moderate/low density of Met-8-immunoreactive fibers was observed in the diencephalic nuclei. A moderate density was observed in the paraventricular thalamic nucleus, reuniens thalamic nucleus, lateral and medial geniculate nuclei, dorsomedial hypothalamic nucleus, paraventricular hypothalamic nucleus (posterior part) and ventromedial hypothalamic nucleus. The present study is the first to demonstrate the presence of clusters of Met-8-immunoreactive cell bodies in the human thalamus and hypothalamus, the distribution of fibers containing neuropeptides in the hypothalamus and the presence of these fibers in several thalamic nuclei. This neuroanatomical study will serve to elucidate the physiological roles of Met-8 in future studies of the human diencephalon.
[Mh] Termos MeSH primário: Diencéfalo/citologia
Diencéfalo/metabolismo
Encefalina Metionina/análogos & derivados
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Encefalina Metionina/metabolismo
Encefalinas/metabolismo
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Precursores de Proteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enkephalins); 0 (Protein Precursors); 0 (proenkephalin); 58569-55-4 (Enkephalin, Methionine); 80501-44-6 (enkephalin-Met, Arg(6)-Gly(7)-Leu(8)-)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160818
[St] Status:MEDLINE


  10 / 4343 MEDLINE  
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[PMID]:27498137
[Au] Autor:Estrada JA; Barlow MA; Yoshishige D; Williams AG; Downey HF; Mallet RT; Caffrey JL
[Ad] Endereço:Institute of Cardiovascular and Metabolic Diseases, University of North Texas Health Science Center, Fort Worth, TX, USA.
[Ti] Título:δ-Opioid receptors: Pivotal role in intermittent hypoxia-augmentation of cardiac parasympathetic control and plasticity.
[So] Source:Auton Neurosci;198:38-49, 2016 Jul.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Intermittent hypoxia training (IHT) produces robust myocardial protection against ischemia-reperfusion induced infarction and arrhythmias. Blockade of this cardioprotection by antagonism of either ß1-adrenergic or δ-opioid receptors (δ-OR) suggests autonomic and/or opioidergic adaptations. PURPOSE: To test the hypothesis that IHT shifts cardiac autonomic balance toward greater cholinergic and opioidergic influence. METHODS: Mongrel dogs completed 20d IHT, non-hypoxic sham training, or IHT with the δ-OR antagonist naltrindole (200µg/kgsc). The vagolytic effect of the δ-OR agonist met-enkephalin-arg-phe delivered by sinoatrial microdialysis was evaluated following IHT. Sinoatrial, atrial and left ventricular biopsies were analyzed for changes in δ-OR, the neurotrophic monosialoganglioside, GM-1, and cholinergic and adrenergic markers. RESULTS: IHT enhanced vagal bradycardia vs. sham dogs (P<0.05), and blunted the δ2-OR mediated vagolytic effect of met-enkephalin-arg-phe. The GM-1 labeled fibers overlapped strongly with cholinergic markers, and IHT increased the intensity of both signals (P<0.05). IHT increased low and high intensity vesicular acetylcholine transporter labeling of sinoatrial nodal fibers (P<0.05) suggesting an increase in parasympathetic arborization. IHT reduced select δ-OR labeled fibers in both the atria and sinoatrial node (P<0.05) consistent with moderation of the vagolytic δ2-OR signaling described above. Furthermore, blockade of δ-OR signaling with naltrindole during IHT increased the protein content of δ-OR (atria and ventricle) and vesicular acetylcholine transporter (atria) vs. sham and untreated IHT groups. IHT also reduced the sympathetic marker, tyrosine hydroxylase in ventricle (P<0.05). SUMMARY: IHT shifts cardiac autonomic balance in favor of parasympathetic control via adaptations in opioidergic, ganglioside, and adrenergic systems.
[Mh] Termos MeSH primário: Átrios do Coração/metabolismo
Hipóxia/tratamento farmacológico
Plasticidade Neuronal
Receptores Opioides delta/metabolismo
[Mh] Termos MeSH secundário: Animais
Cães
Encefalina Metionina/farmacologia
Átrios do Coração/efeitos dos fármacos
Átrios do Coração/fisiopatologia
Microdiálise/métodos
Naltrexona/análogos & derivados
Naltrexona/farmacologia
Antagonistas de Entorpecentes/farmacologia
Plasticidade Neuronal/efeitos dos fármacos
Norepinefrina/metabolismo
Norepinefrina/farmacologia
Nó Sinoatrial/efeitos dos fármacos
Nervo Vago/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Narcotic Antagonists); 0 (Receptors, Opioid, delta); 58569-55-4 (Enkephalin, Methionine); 5S6W795CQM (Naltrexone); G167Z38QA4 (naltrindole); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160808
[St] Status:MEDLINE



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