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1.
Chinese Journal of Applied Physiology ; (6): 273-278, 2019.
Artigo em Chinês | WPRIM | ID: wpr-776516

RESUMO

OBJECTIVE@#To investigate the effects of myeloid differentiation-2 (MD2) gene silencing on high glucose-induced proliferation inhibition, apoptosis and inflammation in rat cardiomyocytes.@*METHODS@#The immortalized rat cardiomyocyte cell line H9C2 were transfected with MD2 small interfering RNA (si-MD2) and negative control for 24 h, then stimulated with high glucose (HG) for 48 h. RT-qPCR was performed to detect the mRNA levels of MD2 and inflammatory factors TNF-α, IL-1β and IL-6. MTS and flow cytometry were used to evaluate cell proliferation, cell cycle and apoptosis rate. Western blot was used to detect protein expression levels and phosphorylation levels.@*RESULTS@#The mRNA and protein levels of MD2 in H9C2 cells were dramatically decreased after transfected with si-MD2 (P<0.01). After stimulation of high glucose, the mRNA levels of inflammatory factors, the cells in G0/G1 phase , the cell apoptosis rate and the protein level of cleaved Caspase-3 were significantly increased, while the cell proliferation ability was decreased (P<0.01). MD2 gene silencing antagonized the effects of high glucose on cell proliferation, cell cycle, cell apoptosis and the mRNA levels of TNF-α, IL-1β , IL-6(P<0.05). Western blot analysis showed that the phosphorylation levels of extracellular signal-regulated kinase(ERK1/2), P38 mitogen-activated protein kinase(P38 MAPK) and C-Jun N-terminal kinase(JNK) protein were increased significantly in H9C2 cells treated with high glucose, which could be reversed by silencing of MD2 (P<0.01).@*CONCLUSION@#This study demonstrates that MD2 gene silencing reverses high glucose-induced myocardial inflammation, apoptosis and proliferation inhibition via the mechanisms involving suppression of ERK, P38 MAPK, JNK signaling pathway.


Assuntos
Animais , Ratos , Apoptose , Proliferação de Células , Células Cultivadas , Citocinas , Metabolismo , Inativação Gênica , Glucose , Inflamação , Proteínas Quinases JNK Ativadas por Mitógeno , Metabolismo , Antígeno 96 de Linfócito , Genética , Miócitos Cardíacos , Biologia Celular , Proteínas Quinases p38 Ativadas por Mitógeno , Metabolismo
2.
Chinese Journal of Applied Physiology ; (6): 72-75, 2015.
Artigo em Chinês | WPRIM | ID: wpr-243429

RESUMO

<p><b>OBJECTIVE</b>To explore the relationship between the expression of Survivin and Ki67 with prognosis of pancreatic endocrine tumors (PETs).</p><p><b>METHODS</b>Immunohistochemistry for Survivin and Ki67 was performed in 25 cases of normal pancreatic tissues and 81 cases of PETs by tissue microarrays and to observe the expression and evaluate the relationship with prognosis.</p><p><b>RESULTS</b>(1)The expression of Survivin and Ki67 in PETs was significantly higher than that in normal pancreatic tissues (P <0.01); (2)The expression of Survivin and Ki67 in PETs was correlated with tissue grading and the TNM-staging (P < 0.05), but not related with tumor size, location and functional status. In addition, the expression of nuclear Survivin was association with lymph node metastasis (P < 0.05). (3)The high expression of Ki67 was related with the expression of nuclear Survivin, but not related with the expression of cytoplasmic Survivin.</p><p><b>CONCLUSION</b>Survivin and Ki67 were both expressed in PETs, which were closely related to the clinical pathological characteristics. They could be used as new indicators in the evaluation of prognosis of PETs. The expression of Survivin in nucleus had more diagnostic significance than that in cytoplasm, and that could be highly correlated with lymph node metastasis, which would be used as a new marker of poor prognosis.</p>


Assuntos
Humanos , Biomarcadores Tumorais , Metabolismo , Núcleo Celular , Metabolismo , Citoplasma , Metabolismo , Imuno-Histoquímica , Proteínas Inibidoras de Apoptose , Metabolismo , Antígeno Ki-67 , Metabolismo , Metástase Linfática , Estadiamento de Neoplasias , Neoplasias Pancreáticas , Diagnóstico , Prognóstico
3.
Chinese Journal of Applied Physiology ; (6): 38-42, 2014.
Artigo em Chinês | WPRIM | ID: wpr-236391

RESUMO

<p><b>OBJECTIVE</b>To investigate the protective effect and mechanism of curcumin derivatives B06 on myocardium from type 2 diabetic rats.</p><p><b>METHODS</b>Thirty-five male SD rats were randomly divided into 5 groups, normal control group (NC group), high fat group (HF group), high fat treatment group (FT group), diabetes mellitus group (DM group) and diabetes treatment group (DT group) (n = 7). The late four groups were fed with high fat food, after four weeks of high fat feeding, the rats from DM group and DT group were injected with low dosage of streptozocin intraperitoneally to induce diabetes mellitus, FT group and DT group were gavaged with curcumin derivatives B06 at the dosage of 0.2 mg/kg x d. The blood glucose and lipid were detected biochemically, blood insulin was assayed by ELISA and the insulin resistance index was calculated, the morphology of myocardium was observed by light and transmission electron microscopy, the protein expression of AMP-activated protein kinase alpha (AMPKalpha) and phosphorylated AMP-activated protein kinase alpha (p-AMPKalpha) in myocardium were tested by Western blot.</p><p><b>RESULTS</b>The level of blood glucose, lipid, insulin and the insulin resistance index were increased in HF group and DM group, but they were decreased after the treatment with B06. The expression of AMPKalpha and p-AMPKalpha were decreased, but they became increased after the treatment of B06. There were increased collagen fibers in interstitium and expansion of mitochondria in cytoplasm of myocardium from DM group, but they were ameliorated in B06 treatment group.</p><p><b>CONCLUSION</b>It is suggested that B06 may relieve the damage of myocardium from type 2 diabetic rats and the increased expression of AMPKalpha and p-AMPKalpha may be involved in it.</p>


Assuntos
Animais , Masculino , Ratos , Proteínas Quinases Ativadas por AMP , Metabolismo , Glicemia , Curcumina , Farmacologia , Diabetes Mellitus Experimental , Coração , Resistência à Insulina , Miocárdio , Patologia , Ratos Sprague-Dawley , Estreptozocina
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