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1.
Acta Physiologica Sinica ; (6): 209-216, 2022.
Artigo em Chinês | WPRIM | ID: wpr-927596

RESUMO

Mounting evidence has shown that exercise exerts extensive beneficial effects, including preventing and protecting against chronic diseases, through improving metabolism and other mechanisms. Recent studies have shown that exercise preconditioning affords significant cardioprotective effects. However, whether exercise preconditioning improves high fat diet (HFD)-induced obesity and lipid metabolic disorder remains unknown. The study was aimed to explore the effects of exercise preconditioning on HFD-induced obesity and lipid metabolic disorder in mice. 4-week-old C57BL/6 mice were subjected to swimming or sedentary control for 3 months, and then were fed with normal diet (ND) or HFD for 4 more months. The results showed that the blood glucose was decreased, and the glucose tolerance and grip strength were increased in exercised mice after training. Exercise preconditioning failed to improve HFD-induced body weight gain, but improved HFD-induced glucose intolerance. Exercise preconditioning showed no significant effects on both exercise capacity and physical activity in ND- and HFD-fed mice. HFD feeding increased total cholesterol and low density lipoprotein (LDL) levels in circulation, promoted subcutaneous fat and epididymal fat accumulation in mice. Exercise preconditioning increased circulating high density lipoprotein (HDL) and decreased circulating LDL, without affecting the subcutaneous fat and epididymal fat in HFD-fed mice. HFD feeding increased liver weight and hepatic total cholesterol contents, and dysregulated the expressions of several mitochondria function-related proteins in mice. These abnormalities were partially reversed by exercise preconditioning. Together, these results suggest that exercise preconditioning can partially reverse the HFD-induced lipid metabolic disorder and hepatic dysfunction, and these beneficial effects of exercise sustain for a period of time, even after exercise is discontinued.


Assuntos
Animais , Camundongos , Colesterol/metabolismo , Dieta Hiperlipídica/efeitos adversos , Lipídeos , Fígado , Camundongos Endogâmicos C57BL , Obesidade
2.
Journal of Southern Medical University ; (12): 296-300, 2012.
Artigo em Chinês | WPRIM | ID: wpr-267613

RESUMO

<p><b>OBJECTIVE</b>To study the responses of different pancreatic cancer cells to stimulations by nerve growth factor (NGF) and explore the role of Trk-A in such responses.</p><p><b>METHODS</b>Five pancreatic cancer cell lines (MIA-PaCa-2, PANC-1, SW-1990, AsPC-1, and BxPC-3) were exposed to different concentrations of NGF (0, 4, 20, 100, and 500 ng/ml). MTT and Matrigel invasion method were used to observe the changes in the cell proliferation and invasion ability. Trk-A expression in these cells was detected by PCR and Western blotting, and the relations of Trk-A expression to the cell proliferative and invasive abilities following NGF treatment were analyzed.</p><p><b>RESULTS</b>NGF at 100 ng/ml most obviously stimulated the cell proliferation, and PANC-1 cells showed the highest while AsPC-1 cells showed the least sensitivity to 100 ng/ml NGF stimulation. Matrigel invasion test showed that NGF enhanced the invasiveness of PANC-1 and MIA-PaCa-2 cells but produced only limited effect on AsPC-1 cells; the effect of NGF was completely inhibited by the Trk-A inhibitor CEP701. The expression levels of Trk-A mRNA and protein were the highest in PANC-1 cells and the lowest in AsPC-1 cells.</p><p><b>CONCLUSION</b>NGF can enhance the proliferation and invasiveness of pancreatic cancer cells, and this effect is possibly mediated by Trk-A protein.</p>


Assuntos
Humanos , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Invasividade Neoplásica , Fator de Crescimento Neural , Farmacologia , Neoplasias Pancreáticas , Metabolismo , Patologia , Receptor trkA , Genética , Metabolismo
3.
Journal of Southern Medical University ; (12): 1870-1873, 2009.
Artigo em Chinês | WPRIM | ID: wpr-336062

RESUMO

<p><b>OBJECTIVE</b>To construct a plasmid carrying small interfering RNA (siRNA) targeting human C-erbB2 gene (pGenesil- erbB2) and test its effect on Her-2 expression at the post-transcriptional level in human colon cancer cell lines HT-29 cells that highly express erbB2.</p><p><b>METHODS</b>A HT-29 cell line that highly expressed CerbB-2 was selected using immunohistochemical method. The double-stranded siRNA targeting human CerbB-2 cDNA and the negative control fragment were cloned into pGenesil-1 vector, and after identification and sequence analysis, the constructed pGenesil-erbB2 plasmid was transfected into the selected HT-29 cell line.</p><p><b>RESULTS</b>The pGenesil-erbB2 plasmid was successfully constructed and stably transferred into HT-29 cells. The transfection resulted in significant inhibition of Her-2 protein expression in the HT-29 cells, as shown by Western blotting.</p><p><b>CONCLUSION</b>The pGenesil-erbB plasmid we constructed can be stably transfected into HT-29 cells to inhibit the expression of Her-2 protein, and can be useful in further studies of increasing the radiosensitivity of HT-29 cell lines.</p>


Assuntos
Humanos , Sequência de Bases , Genes erbB-2 , Genética , Células HT29 , Dados de Sequência Molecular , Plasmídeos , Genética , Interferência de RNA , RNA Interferente Pequeno , Receptor ErbB-2 , Genética , Transfecção
4.
Journal of Central South University(Medical Sciences) ; (12): 138-143, 2007.
Artigo em Chinês | WPRIM | ID: wpr-813921

RESUMO

OBJECTIVE@#To determine the clinical application of the new classification of adenocarcinoma of esophagogastric junction (AEG).@*METHODS@#The data of cancer of distal esophagus, cancer of cardia, and proximal gastric cancer were reviewed. Clinicopathologic characteristics, surgical modes and survival were analyzed according to Siewert's standards.@*RESULTS@#Among the 203 patients that were up to the standard, 29 had adenocarcinoma of the distal esophagus (Type I), 80 had true carcinoma of cardia (Type II), and 94 had subcardial carcinoma (Type III). The 5-year survival rates of the 3 types of patients after the operation were 34% for Type I, 27.5% for Type II, and 24.5% for Type III (P0.05).@*CONCLUSION@#Difference has been found in the clinicopathologic characteristics of the 3 types of adenocarcinoma of the esophagogastric junction. The exact relation of the 3 types is still unknown. The TNM classification, complete tumor resection and the extent of lymph node metastasis are critical for the prognosis of the patients.


Assuntos
Feminino , Humanos , Masculino , Adenocarcinoma , Classificação , Mortalidade , Cirurgia Geral , China , Neoplasias Esofágicas , Classificação , Mortalidade , Cirurgia Geral , Esofagectomia , Junção Esofagogástrica , Patologia , Cirurgia Geral , Estudos Retrospectivos , Análise de Sobrevida , Taxa de Sobrevida
5.
Journal of Southern Medical University ; (12): 1173-1175, 2006.
Artigo em Chinês | WPRIM | ID: wpr-334965

RESUMO

<p><b>OBJECTIVE</b>To investigate the expression of beta-protein 1 (BP(1)) gene, a novel member of DLX homeobox gene family, in lung cancer tissue and its relationship with clinical features of lung cancer.</p><p><b>METHODS</b>RT-PCR was employed for detecting BP(1) gene expression in the lung cancer tissues, adjacent tissues, non-cancer lung tissues of 46 lung cancer patients.</p><p><b>RESULTS</b>Thirty-six lung cancer tissues and 6 adjacent tissues but none of the normal tissues were found to have BP(1) gene overexpression, showing significant difference in BP(1) expression between the tissues (P<0.01). Significant difference in BP1 gene overexpression was noted between well differentiated cancers (13 of out 21) and poorly differentiated cancers (22 of the 25), but not between cancers of different stages or between squamous carcinoma and adenocarcinoma.</p><p><b>CONCLUSION</b>BP(1) gene expression is up-regulated in human lung cancer in related to the differentiation level of lung cancer but not to the clinical stage.</p>


Assuntos
Feminino , Humanos , Masculino , Adenocarcinoma , Genética , Patologia , Carcinoma de Células Escamosas , Genética , Patologia , Regulação Neoplásica da Expressão Gênica , Proteínas de Homeodomínio , Genética , Neoplasias Pulmonares , Genética , Patologia , RNA Mensageiro , Genética , Metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Transcrição , Genética
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