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1.
Oral Dis ; 25(4): 1175-1184, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30811745

RESUMO

OBJECTIVE: The aim of this study was to investigate the effects of epigallocatechin-3-gallate on the proliferation and apoptosis of odontogenic keratocyst (OKC) keratinocytes in vitro. MATERIALS AND METHODS: Keratinocytes isolated from the epithelial lining of the OKC were cultured in keratinocyte serum-free medium and identified by CK10, CK14, pan-cytokeratin and vimentin immunofluorescence staining. The cells were exposed to EGCG at different concentrations, and proliferation inhibition was measured by cell counting kit 8 assay. Cell cycle and apoptosis were assessed by flow cytometry, and expression of the WNT signalling pathway-related proteins FZD3 and JNK3 was detected by quantitative real-time PCR and Western blotting. Human oral keratinocytes (HOKs) were used as the control. RESULTS: The OKC keratinocytes were successfully cultured. The primary cells were tile-like and expressed the epithelial biomarkers CK10, CK14 and pan-cytokeratin. Epigallocatechin-3-gallate inhibited cell proliferation in a dose- and time-dependent manner, arrested cell cycle in the G1 phase and induced apoptosis of OKC keratinocytes. FZD3 and JNK3 were overexpressed in OKC keratinocytes compared with HOKs and were downregulated by epigallocatechin-3-gallate treatment. CONCLUSION: Epigallocatechin-3-gallate inhibited proliferation and induced apoptosis in OKC keratinocytes, possibly by suppressing the WNT/JNK signalling pathway. It may thus be potentially used for OKC treatment.


Assuntos
Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Catequina/análogos & derivados , Proliferação de Células/efeitos dos fármacos , Catequina/farmacologia , Humanos , Queratinócitos , Sistema de Sinalização das MAP Quinases , Cistos Odontogênicos , Via de Sinalização Wnt
2.
J Mol Model ; 19(12): 5579-86, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-24257902

RESUMO

The geometrical structures, energetics properties, and aromaticity of C(36-n) Si(n) (n ≤ 18) fullerene-based clusters were studied using density functional theory calculations. The geometries of C(36-n) Si(n) clusters undergo strong structural deformation with the increase of Si substitution. For the most energy favorable structures of C(36-n) Si(n) , the silicon and carbon atoms form two distinct homogeneous segregations. Subsequently, the binding energy, HOMO-LUMO energy gap, vertical ionization potential, vertical electron affinity, and chemical hardness for the energetic favorable C(36-n) Si(n) geometries were computed and analyzed. In addition, the aromatic property of C(36-n) Si(n) cagelike clusters was investigated, and the result demonstrate that these C(36-n) Si(n) cagelike structures possess strong aromaticity.

3.
Peptides ; 44: 105-10, 2013 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-23548325

RESUMO

Neuronostatin, a 13-amino acid peptide, is encoded in the somatostatin pro-hormone. I.c.v. administration of neuronostatin produces a significant antinociceptive effect in the mouse tail-flick test, which is mediated by endogenous opioid receptor. However, the direct functional interaction between morphine and neuronostatin has not been characterized. In the present study, effect of neuronostatin on morphine analgesia was investigated in the tail-flick test. Our findings showed that i.c.v. administration of neuronostatin (0.3nmol/mouse i.c.v.) significantly enhanced the antinociceptive effect of morphine (2.5, 5 or 10µg/kg) at the supraspinal level. Results of antagonism experiments suggested that the synergistic analgesia induced by morphine and neuronostatin was mediated by µ- and к-opioid receptors not δ-opioid receptor. In conclusion, there may be a cascade amplification phenomenon when morphine and neuronostatin were co-administered in acute pain model. The above results provide evidence for the potential use of neuronostatin in combination with morphine to control pain and addiction.


Assuntos
Analgésicos Opioides/farmacologia , Morfina/farmacologia , Fragmentos de Peptídeos/farmacologia , Somatostatina/farmacologia , Analgesia , Animais , Sinergismo Farmacológico , Injeções Intraventriculares , Masculino , Naloxona/farmacologia , Antagonistas de Entorpecentes/farmacologia , Nociceptividade/efeitos dos fármacos , Fragmentos de Peptídeos/fisiologia , Receptores Opioides/metabolismo , Somatostatina/fisiologia
4.
Peptides ; 35(1): 31-5, 2012 May.
Artigo em Inglês | MEDLINE | ID: mdl-22465660

RESUMO

Neuronostatin is a 13-amino acid amidated peptide widely distributed in various organs including gastrointestinal tract. However, the effect of neuronostatin on gastrointestinal motility has not been well characterized. In the present work, effects of central administration of neuronostatin on gastric emptying and gastrointestinal transit were investigated. The results indicated that intracerebroventricular (i.c.v.) administration of neuronostatin (1, 5, 10 or 20nmol/mouse) delayed gastric emptying and gastrointestinal transit in a dose-related manner in mice. The effects were significantly reversed by melanocortin 3/4 receptor antagonist SHU9119 or classical opioid receptor antagonist naloxone, suggesting that the central melanocortin system and opioid system may be involved in the gastrointestinal effects elicited by i.c.v. administration of neuronostatin. In addition, we found that C-terminal amidation modification of neuronostatin is essential to exert its gastrointestinal effects. These results indicated that neuronostatin may play an important role in regulating gastrointestinal function.


Assuntos
Ventrículos Cerebrais/fisiologia , Esvaziamento Gástrico , Trânsito Gastrointestinal , Hormônios Peptídicos/fisiologia , Animais , Ventrículos Cerebrais/efeitos dos fármacos , Ventrículos Cerebrais/metabolismo , Esvaziamento Gástrico/efeitos dos fármacos , Trânsito Gastrointestinal/efeitos dos fármacos , Masculino , Hormônios Estimuladores de Melanócitos/farmacologia , Camundongos , Naloxona/farmacologia , Antagonistas de Entorpecentes/farmacologia , Hormônios Peptídicos/administração & dosagem , Receptores de Melanocortina/agonistas
5.
Neurosci Lett ; 506(1): 126-30, 2012 Jan 06.
Artigo em Inglês | MEDLINE | ID: mdl-22075225

RESUMO

Neuronostatin, a newly identified peptide encoded by the somatostatin (SST) gene, was proved to produce significant antinociceptive effect in mouse tail immersion test. However, the effect of neuronostatin on tonic pain was still not clear. The aim of this study was to investigate the effect of neuronostatin in the formalin test and its possible mechanism. We found that intracerebroventricular (i.c.v.) administration of neuronostatin (1, 3, 6, 12nmol/mouse) increased licking in a dose-related manner during the late phase, but did not affect the early phase of formalin test in mice. In addition, the hyperalgesic effect during the late phase was completely reversed by melanocortin 3/4 receptor antagonist SHU9119 (50pmol/mouse) or opioid receptor antagonist naloxone (5nmol/mouse), but not GABAA receptor antagonist bicuculline (1086pmol/mouse). These data suggested that the hyperalgesic response induced by neuronostatin was dependent upon the central melanocortin system and endogenous opioid system. In conclusion, these results indicated that neuronostatin may be a new neuropeptide with important role in the modulation of acute and tonic pain.


Assuntos
Hiperalgesia/induzido quimicamente , Hiperalgesia/tratamento farmacológico , Medição da Dor , Limiar da Dor/efeitos dos fármacos , Fragmentos de Peptídeos/efeitos adversos , Somatostatina/efeitos adversos , Análise de Variância , Animais , Bicuculina/uso terapêutico , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Interações de Medicamentos , Antagonistas de Receptores de GABA-A/uso terapêutico , Injeções Intraventriculares , Masculino , Hormônios Estimuladores de Melanócitos/uso terapêutico , Camundongos , Camundongos Endogâmicos , Fatores de Tempo
6.
Cancer Epidemiol ; 36(1): 73-7, 2012 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-21621497

RESUMO

BACKGROUND: To investigate the feasibility of detecting methylated tissue factor pathway inhibitor (TFPI2) and quantifying human long DNA with fluorescent quantitative Alu PCR in fecal DNA as a non-invasive screening tool for colorectal cancer (CRC). MATERIALS AND METHODS: Methylation-specific PCR (MSP) was performed to analyze TFPI2 gene promoter methylation status in a blinded fashion in stool samples taken from 30 endoscopically diagnosed healthy controls, 20 patients with adenomas, and 60 patients with colorectal cancer. Real-time Alu PCR was used to quantify human long DNA. RESULTS: The specificity of fecal TFPI2 MSP assay and long DNA assay was 100% and 83.3%, respectively. The sensitivity of fecal TFPI2 MSP assay and long DNA assay was 68.3% and 53.3%, respectively. The sensitivity of fecal DNA assay (either marker being positive) was 86.7%, which was high for CRC. CONCLUSIONS: Our results have demonstrated the feasibility of using TFPI2 methylation and quantify human long DNA with fluorescent quantitative Alu PCR in fecal samples as a new noninvasive test for CRC.


Assuntos
Biomarcadores Tumorais/genética , Neoplasias Colorretais/genética , Metilação de DNA , DNA de Neoplasias/análise , Glicoproteínas/genética , Biomarcadores Tumorais/metabolismo , China , Neoplasias Colorretais/metabolismo , DNA de Neoplasias/genética , Detecção Precoce de Câncer/métodos , Fezes/química , Feminino , Glicoproteínas/metabolismo , Humanos , Masculino , Pessoa de Meia-Idade , Sangue Oculto , Reação em Cadeia da Polimerase em Tempo Real
7.
Peptides ; 32(9): 1893-901, 2011 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21839129

RESUMO

Neuronostatin, a recently discovered endogenous bioactive peptide, was encoded by pro-mRNA of somatostatin that contributes to modulation of nociception. However, nociceptive effect of neuronostatin is still not fully known. The aim of this study was to evaluate effect of neuronostatin on nociception and elucidate its possible mechanism of action. Intracerebroventricular (i.c.v.) administration of neuronostatin (0.3, 3, 6, 12nmol/mouse) produced a dose- and time-related antinociceptive effect in the tail immersion assay in mice, an acute pain model. The antinociceptive effect of neuronostatin was significantly antagonized by naloxone, and was strongly inhibited by co-injection with ß-funaltrexamine or nor-binaltorphimine, but not by naltrindole. Also, melanocortin 3/4 receptor antagonist, SHU9119, completely blocked the effect of neuronostatin. These data indicated the involvement of both µ- and κ-opioid receptors and central melanocortin system in the analgesic response induced by neuronostatin. In addition, neuronostatin (6nmol, i.c.v.) increased c-Fos protein expression in the periaqueductal gray (PAG) and the nucleus raphe magnus (NRM) that have a pivotal role in regulating descending pain pathways. Taken together, this study is the first to reveal that neuronostatin produces antinociceptive effect via opioid and central melanocortin systems, which is associated with an increase in neuronal activity the PAG and NRM.


Assuntos
Nociceptividade/efeitos dos fármacos , Hormônios Peptídicos/administração & dosagem , Hormônios Peptídicos/farmacologia , Dor Aguda/tratamento farmacológico , Analgésicos/administração & dosagem , Analgésicos/farmacologia , Animais , Relação Dose-Resposta a Droga , Imuno-Histoquímica , Infusões Intraventriculares , Masculino , Hormônios Estimuladores de Melanócitos/farmacologia , Camundongos , Modelos Animais , Naloxona/farmacologia , Naltrexona/análogos & derivados , Naltrexona/farmacologia , Antagonistas de Entorpecentes , Hormônios Peptídicos/antagonistas & inibidores , Hormônios Peptídicos/síntese química , Substância Cinzenta Periaquedutal/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-fos/metabolismo , Receptor Tipo 3 de Melanocortina/antagonistas & inibidores , Receptor Tipo 4 de Melanocortina/antagonistas & inibidores
8.
Peptides ; 32(9): 1948-52, 2011 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21871935

RESUMO

Neuronostatin is a recently discovered endogenous bioactive peptide that is encoded by pro-mRNA of somatostatin. In the present study, we investigated the effect of neuronostatin on mood regulation in the forced swim test of mice. Our results showed intracerebroventricular (i.c.v.) administration of neuronostatin produced an increase in the immobility time, suggesting that neuronostatin induced depression-like effect. In order to rule out the possibility that neuronostatin had increased immobility time by a non-specific reduction in general activity, the effect of neuronostatin on locomotor activity was examined. Neuronostatin had no influence on locomotor activity in mice. In addition, the depression-like effect of neuronostatin was completely reversed by melanocortin 3/4 receptor antagonist SHU9119 or GABAA receptor antagonist bicuculline, but not by opioid receptor antagonist naloxone. These data suggested that the depression-like effect induced by i.c.v. administered neuronostatin was dependent upon the central melanocortin system and GABAA receptor. In conclusion, the results of this study report that neuronostatin induces depression-like effect. These findings reveal that neuronostatin is a new neuropeptide with an important role in regulating depressive behavior.


Assuntos
Afeto/efeitos dos fármacos , Depressão/induzido quimicamente , Hormônios Peptídicos/administração & dosagem , Hormônios Peptídicos/farmacologia , Animais , Bicuculina/administração & dosagem , Bicuculina/farmacologia , Antagonistas de Receptores de GABA-A/farmacologia , Infusões Intraventriculares , Masculino , Hormônios Estimuladores de Melanócitos/farmacologia , Camundongos , Atividade Motora , Naloxona/administração & dosagem , Naloxona/farmacologia , Antagonistas de Entorpecentes , Hormônios Peptídicos/síntese química , Receptor Tipo 3 de Melanocortina/antagonistas & inibidores , Receptores de GABA-A/metabolismo , Técnicas de Síntese em Fase Sólida , Natação/fisiologia , Fatores de Tempo
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