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1.
Br J Oral Maxillofac Surg ; 60(2): 174-182, 2022 02.
Artigo em Inglês | MEDLINE | ID: mdl-34955330

RESUMO

The purpose of this study was to explore the treatment efficacy of botulinum-A (BTX-A) in nocturnal bruxism. Five electronic databases (PubMed, Web of Science, Cochrane, Embase and Clinical Trials) were searched to identify related randomised controlled trials up to September 1, 2020. Five evaluation indices were extracted, namely, the pain at rest and at chewing (PR and PC), the number of bruxism events (NBE) and the self-assessment by patients (SA), to assess the treatment efficacy of BTX-A in bruxism. All data analyses were conducted using Review Manager (Version 5.3; The Cochrane Collaboration, London, United Kingdom). Six studies were included in this review. The sample was composed of 148 participants. Compared with the placebo group, the BTX-A group showed the significantly improved the PR index scores (MD, 1.16 cm; 95%CI, 0.65 to 1.67 cm; p < 0.00001), slightly improved the PC index scores (SMD, 0.25; 95%CI -0.14 to 0.64; p = 0.21), and the NBEs were significantly decreased in the before-injection group compared with that in the after-injection group (MD, 1.72; 95%CI, 0.60 to 2.85; p = 0.003). The results of this study suggest that BTX-A possesses significant therapeutic efficiency for the relief of pain and events of bruxism. However, whether the events of bruxism would recur or rebound after botulinum toxin injection needs more follow-up clinical evidence.


Assuntos
Toxinas Botulínicas Tipo A , Bruxismo , Clostridium botulinum , Fármacos Neuromusculares , Bruxismo do Sono , Toxinas Botulínicas Tipo A/uso terapêutico , Bruxismo/complicações , Bruxismo/tratamento farmacológico , Humanos , Fármacos Neuromusculares/uso terapêutico , Dor/tratamento farmacológico , Bruxismo do Sono/tratamento farmacológico
2.
Oral Dis ; 25(4): 1076-1083, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30746817

RESUMO

OBJECTIVES: Salivary adenoid cystic carcinoma (SACC) is one of the most common malignant salivary gland tumors. Our study aims to investigate whether hypoxia-induced autophagy was up-regulated in the progression of SACC. MATERIALS AND METHODS: We performed differentially expressed gene analysis and pathway enrichment analysis and then calculated the correlation analysis on GSE59701 and GSE28996 datasets. The expression of HIF-1ɑ and MAP1LC3B was analyzed in the paraffin-embedded specimens by immunohistochemical method and in the hypoxic SACC-LM cells by immunofluorescence. TEM microscopy was also performed to observe the formation of autophagosomes in SACC tissue and the hypoxic SACC-LM cells. RESULTS: The autophagy pathway was up-regulated in SACC datasets, and five genes including MAP1LC3B were positively correlated with HIF-1ɑ. Immunohistochemistry results showed that autophagy was activated and the expression of HIF-1ɑ and MAP1LC3B was positively correlated in SACC specimens. In hypoxic SACC-LM cells, we also identified the up-regulation of autophagy and the close correlation between HIF-1ɑ and MAP1LC3B expression. Autophagosomes were observed both in the tissue and the hypoxic SACC-LM cells by TEM microscopy. CONCLUSIONS: Our study showed that autophagy is up-regulated in dataset, SACC tissue, and hypoxic cell line; hypoxia-induced autophagy in SACC might play a vital role in the development of SACC.


Assuntos
Autofagia/genética , Carcinoma Adenoide Cístico , Regulação Neoplásica da Expressão Gênica , Neoplasias das Glândulas Salivares , Linhagem Celular Tumoral , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia , Imuno-Histoquímica
3.
Int J Clin Exp Pathol ; 12(6): 2084-2091, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31934030

RESUMO

Autophagy contributes to head and neck squamous cell carcinoma (HNSCC) development and progression. MiR-17-5p down-regulates Beclin-1 and thus plays an important role in autophagy, but little is known about the function and regulation of miR-17-5p in HNSCC autophagy. This study aimed to investigate the role of miR-17-5p on proliferation, migration, and autophagy under hypoxia in CAL-27 human tongue squamous cell carcinoma cells. CAL-27 cells were transfected with 50 nmol miR-17-5p mimics to overexpress miR-17-5p. Cell proliferation and migration were determined by CCK-8 and wound healing assays, respectively, under hypoxia. Autophagy induced by hypoxia was detected by transmission electron microscope and Beclin-1 mRNA and protein expressions. The miR-17-5p mimics successfully increased the expression of miR-17-5p in CAL-27 cells by almost 700 fold compared with the miRNA mimic negative control. After 3 days, cells transfected with the miR-17-5p mimics showed higher proliferation compared with controls (P < 0.05) under hypoxia. MiR-17-5p transfected CAL-27 cells had a higher migratory capacity compared with the control cells (P < 0.05) under hypoxia. Furthermore, transmission electron microscopy showed that miR-17-5p overexpression inhibited the formation of autophagosomes in hypoxic cells. Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot showed that miR-17-5p overexpression inhibited the mRNA and protein expression of Beclin-1 in CAL-27 cells submitted to hypoxia. MiR-17-5p overexpression promoted the proliferation and migration of the CAL-27 cells, but inhibited autophagy under hypoxia.

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