Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Mais filtros

Base de dados
Tipo de documento
Intervalo de ano de publicação
1.
J Biol Regul Homeost Agents ; 34(4): 1317-1324, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32924373

RESUMO

The purpose of this study was to investigate the expression and mechanism of miR-17 in gastric lym-phoma. miR-17mimics, miR-17 inhibitors and negative controls were transfected into human gastric lymphoma cell line cyp6d. The proliferation, invasion and apoptosis of cyp6d cells were detected by CCK-8, Transwell and TUNEL methods, respectively. The expression and clinicopathological features of miR-17 in gastric lymphoma were analyzed by real-time quantitative PCR. The target gene of miR-17 was predicted by targetscan 7.2, and the expression of miR-17 related protein was detected by Western blot. The results showed that the expression of miR-17 in gastric lymphoma was significantly higher than that in normal tissues (P < 0.05), which was closely related to lymph node metastasis, tumor size and distant metastasis (P < 0.05). The high expression of miR-17 significantly promoted the proliferation and invasion of cyp6d cells and inhibited apoptosis (P < 0.05). The high expression of miR-17 can regu¬late the expression of HSP60 and TNFR2. It has been found that miR-17 can promote the development of gastric lymphoma by regulating HSP60/TNFR2 pathway, which is a potential molecular target for the diagnosis and treatment of gastric lymphoma.


Assuntos
MicroRNAs/genética , Neoplasias Gástricas , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Chaperonina 60 , Regulação Neoplásica da Expressão Gênica , Humanos , Linfoma não Hodgkin , Proteínas Mitocondriais , Invasividade Neoplásica/genética , Receptores Tipo II do Fator de Necrose Tumoral , Neoplasias Gástricas/genética
2.
J Biol Regul Homeost Agents ; 32(3): 455-464, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29921370

RESUMO

To observe the effect of Soyisoflavones (SI) on the expression of Wnt/ß-catenin signaling pathway elements, transforming growth factor-ß (THGF-ß) and its related proteins in the renal interstitia of diabetic nephropathic (DN) rats, 48 DN rats were randomly divided into 4 groups: DN model group (group DN), soybean isoflavone treatment group (group DA), DN model group + losartan treatment group (group DL), DN model group + soybean isoflavones combined with losartan treatment group (group SL). Each group comprised 12 rats. Twelve healthy Wistar rats were selected as normal controls (group N). After 12 weeks of continuous administration of soybean isoflavone or losartan or those two combined, the body weight of rats was recorded and serum urea nitrogen (BUN) and creatinine (Scr) were measured. The expression of Wnt4, ß-catenin, and TGF-ß1 proteins, as well as mRNA, in the renal interstitium were detected by immunohistochemistry and real-time quantitative PCR (FQ-PCR). In all the groups, Wnt4, ß-catenin and TGF-ß1 protein were only expressed in renal interstitial and renal tubular epithelial cells. There was no significant difference between group DA and group DL (P>0.05). FQ-PCR results showed that Wnt4, ß-catenin and TGF-ß1 mRNA were consistent with the expression of these proteins in the renal tissue of each group. Soy isoflavones can reduce 24-h urinary protein quantification, alleviate renal interstitial pathological damage, and regulate the expression of Wnt4, ß-catenin and TGF-ß1 in the renal interstitium. This suggests that soybean isoflavones could delay the process of renal interstitial fibrosis in DN rats by decreasing the expression of Wnt4, ß-catenin and TGF-ß1 in the renal interstitium, thus demonstrating that soybean isoflavones plus losartan have the best protective effects against diabetes-induced renal fibrosis.


Assuntos
Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Tipo 2/metabolismo , Nefropatias Diabéticas/metabolismo , Glycine max/química , Isoflavonas/farmacocinética , Rim/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Via de Sinalização Wnt/efeitos dos fármacos , Animais , Diabetes Mellitus Experimental/tratamento farmacológico , Diabetes Mellitus Experimental/patologia , Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/patologia , Nefropatias Diabéticas/tratamento farmacológico , Nefropatias Diabéticas/patologia , Isoflavonas/química , Rim/patologia , Ratos , Ratos Wistar , beta Catenina/metabolismo
4.
Artigo em Zh | MEDLINE | ID: mdl-11236686

RESUMO

AIM: To Investigate the myocardial ultrastructure effects of SMT on the ischemia reperfusion injury (IRI) in the rat heart. METHODS: Eighteen Spraqua-Dawley rats were randomly divided into three groups: ischemia reperfusion group (IR), subjected to 60 min of o-cclusion and 20 min of reperfusion of the anterior descending branch of left coronary artery; IR + SMT group (SMT), given the selective iNOS inhibitor S-methylisothiourea sulfate (SMT, 5 mg/kg, i.v.) before reperfusion; control group (C), didn't occlude coronary artery after exposing heart and observed 80 min. Electrocardiogram (ECG) was recorded. Nitrite and nitrate content were measured in myocardium and blood serum. The changes of myocardial ultrastructure were observed with electron microscope. RESULTS: Ischemia reperfusion induced ST segment elevation and T waves inversion or tallness in ECG, damaged myocardial ultrastructure, increased nitrite and nitrate content in myocardium and blood serum after IR compared with before IR(P < 0.01). Administration of SMT improved the changes of ECG and the injury of myocardial ultrastructure. Nitrite and nitrate content of myocardium were lower than IR group (P < 0.05). The change of nitrite and nitrate level of blood serum in SMT group was nearly in C group. CONCLUSION: SMT can prevent myocardium injury from reperfusion following ischemia.


Assuntos
Isotiurônio/farmacologia , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica/patologia , Miocárdio/ultraestrutura , Animais , Feminino , Isotiurônio/análogos & derivados , Masculino , Óxido Nítrico Sintase/antagonistas & inibidores , Ratos , Ratos Sprague-Dawley
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA