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1.
Eur Rev Med Pharmacol Sci ; 23(14): 6371-6378, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31364145

RESUMO

OBJECTIVE: To investigate the influences of probiotics combined with sulfasalazine (SASP) on the expression of the Wnt/ß-catenin signaling pathway in rats with ulcerative colitis (UC). MATERIALS AND METHODS: A total of 60 clean level and healthy Sprague-Dawley (SD) rats were randomly divided into the normal group, model group, SASP group and combination therapy group, with 15 rats in each group. The rats in the normal group were given normal feeding, and those in the remaining three groups were subjected to the establishment of the UC model. During the modeling, the rats underwent daily gavage and were sacrificed after 4 weeks. Clinical symptoms and pathological changes in ulcer indexes and colon tissues were observed in each group. The expression levels of relative genes in the Wnt/ß-catenin signaling pathway were detected by Polymerase Chain Reaction (PCR). RESULTS: Compared with those in the model group, the pathological sections of rats in the SASP group and combination therapy group showed significant improvement in the inflammatory response. The expression levels of relative genes in the Wnt/ß-catenin signaling pathway were downregulated in rats of the SASP group and combination therapy group relative to those in the model group. CONCLUSIONS: SASP and probiotics alleviate UC by reducing inflammation by inhibiting the activation of the Wnt/ß-catenin signaling pathway, thereby improving intestinal function and restoring the intestinal structure.


Assuntos
Colite Ulcerativa/tratamento farmacológico , Probióticos/administração & dosagem , Sulfassalazina/administração & dosagem , Via de Sinalização Wnt/efeitos dos fármacos , Animais , Colite Ulcerativa/metabolismo , Modelos Animais de Doenças , Quimioterapia Combinada , Regulação da Expressão Gênica/efeitos dos fármacos , Masculino , Probióticos/farmacologia , Ratos , Ratos Sprague-Dawley , Sulfassalazina/farmacologia , Resultado do Tratamento
2.
Eur Rev Med Pharmacol Sci ; 23(5): 2151-2157, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30915760

RESUMO

OBJECTIVE: To study the effect of micro ribonucleic acid (miR)-146a on the development of ulcerative colitis (UC) and to explore its regulatory effect on the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) and nuclear factor-kappa B (NF-κB) signaling pathways. MATERIALS AND METHODS: The UC model in rats was established using 2,4,6-trinitrobenzenesulfonic acid (TNBS)/ethanol. A total of 30 male rats were randomly divided into control group, model group and miR-146a inhibitor group, with 10 rats in each group. The disease activity index (DAI) and the macroscopic score of colonic mucosa were measured in each rat. MiR-146a expression in rat intestinal tissues was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Serum levels of interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Additionally, Western blotting assay was performed to detect protein levels of TLR4, MyD88, and NF-κB in rat intestinal tissues. RESULTS: Compared with those in control group, rats in model group had notably increased DAI, inflammation score, upregulated expression levels of TLR4, MyD88, NF-κB, and miR-146a, as well as increased serum levels of IL-1ß and TNF-α. However, rats in miR-146a inhibitor group exhibited substantially decreased DAI, inflammation score, lowered content of IL-1ß and TNF-α and levels of TLR4, MyD88, and NF-κB compared with those in model group. CONCLUSIONS: We found that miR-146a inhibitor alleviates UC by reducing the release of inflammatory factors through suppressing the TLR4/MyD88/NF-κB signaling pathway.


Assuntos
Colite Ulcerativa/genética , MicroRNAs/genética , Transdução de Sinais , Ácido Trinitrobenzenossulfônico/efeitos adversos , Animais , Colite Ulcerativa/induzido quimicamente , Colite Ulcerativa/metabolismo , Modelos Animais de Doenças , Regulação da Expressão Gênica , Masculino , Fator 88 de Diferenciação Mieloide/metabolismo , NF-kappa B/metabolismo , Distribuição Aleatória , Ratos , Receptor 4 Toll-Like/metabolismo
4.
HLA ; 91(4): 303-305, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29292580

RESUMO

HLA-B*40:338N differs from HLA-B*40:01:01 by a single nucleotide substitution at position 843C>A.


Assuntos
Alelos , Povo Asiático/genética , Antígenos HLA-B/genética , Leucemia/genética , Sequência de Bases , Éxons/genética , Humanos , Alinhamento de Sequência
5.
HLA ; 91(2): 136-137, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-29193787

RESUMO

HLA-B*27:04:06 differs from HLA-B*27:04:01 by a single-nucleotide substitution at position 396 C > A.


Assuntos
Alelos , Povo Asiático/genética , Medula Óssea/metabolismo , Antígenos HLA-B/genética , Doadores de Tecidos , Sequência de Bases , Éxons/genética , Humanos
6.
HLA ; 91(2): 142-143, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-29220119

RESUMO

HLA-DQB1*03:181 has one nucleotide change from HLA-DQB1*03:05:01 at position 470C>G.


Assuntos
Alelos , Povo Asiático/genética , Cadeias beta de HLA-DQ/genética , Leucemia/genética , Sequência de Bases , Éxons/genética , Humanos
7.
HLA ; 91(2): 133-134, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-29243881

RESUMO

HLA-B*13:98 differs from HLA-B*13:02:01 by a single nucleotide substitution at position 193 A>G.


Assuntos
Alelos , Povo Asiático/genética , Antígenos HLA-B/genética , Sequência de Bases , Éxons/genética , Humanos
8.
HLA ; 90(2): 118-120, 2017 08.
Artigo em Inglês | MEDLINE | ID: mdl-28371366

RESUMO

HLA-B*40:01:41 differs from HLA-B*40:01:01 by a single nucleotide substitution at position 195 G>A.


Assuntos
Alelos , Técnicas de Genotipagem , Antígeno HLA-B40/genética , Reação em Cadeia da Polimerase , Povo Asiático , Doadores de Sangue , Sangue Fetal , Humanos
11.
HLA ; 89(1): 64-65, 2017 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-27885833

RESUMO

HLA-DRB1*08:69 has one nucleotide change from HLA-DRB1*08:03:02 at position 262 G>A.

15.
Zhonghua Nei Ke Za Zhi ; 55(7): 541-3, 2016 Jul 01.
Artigo em Chinês | MEDLINE | ID: mdl-27373290

RESUMO

Based on high throughput sequencing and PCR detection technology, this study has found out that intestinal microbial diversity was impaired and the quantities of two main bacteria flora (Bacteroidetes and Clostridium) were significantly reduced in patients with diarrhea-predominant irritable bowel syndrome (D-IBS). Meanwhile mucosal expression of toll-like receptor (TLR) 2 and TLR4 were significantly enhanced, which was inversely correlated with the reduction of Bacteroidetes and Clostridium. Thus, it suggests that D-IBS may be associated with TLR signal transduction triggered by the intestinal dysbacteriosis.


Assuntos
Diarreia/genética , Mucosa Intestinal/metabolismo , Síndrome do Intestino Irritável/genética , Receptor 2 Toll-Like/genética , Receptor 4 Toll-Like/genética , Adulto , Sequência de Bases , Estudos de Casos e Controles , Diarreia/metabolismo , Feminino , Expressão Gênica/genética , Humanos , Masculino , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase , Análise de Sequência de RNA/métodos , Transdução de Sinais , Receptor 2 Toll-Like/metabolismo , Receptor 4 Toll-Like/metabolismo
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