Role of JNK signaling pathway in chondrocyte apoptosis induced by nitric oxide / 中华劳动卫生职业病杂志
Chinese Journal of Industrial Hygiene and Occupational Diseases
;
(12): 271-275, 2013.
Artigo
em Chinês
| WPRIM
| ID: wpr-343677
ABSTRACT
<p><b>OBJECTIVE</b>To study the role of c-jun N-terminal kinase (JNK) signaling pathway in chondrocyte apoptosis induced by nitric oxide (NO) using NO donor sodium nitroprusside (SNP) and JNK inhibitor SP600125.</p><p><b>METHODS</b>Articular chondrocytes were separated from New Zealand rabbits aged 3 weeks by mechanical digestion and enzyme digestion and identified by toluidine blue staining, and then the chondrocytes were treated with SNP and SP600125 for 24 h. The cell apoptosis was evaluated by Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL), and the expression levels of nuclear factor-kappa B (NF-κB) p65 and p53 were measured by western blot.</p><p><b>RESULTS</b>Compared with those in control group, the early apoptotic rate of SNP-treated chondrocytes increased as the concentration of SNProse, exhibiting a concentration dependency (P < 0.05), and the expression levels of NF-κB p65 and p53 also increased (P < 0.05); JNK inhibitor SP600125 inhibited these increases (P < 0.05).</p><p><b>CONCLUSION</b>JNK signaling pathway plays an important role in NO-induced chondrocyte apoptosis. JNK inhibitor SP600125 can reduce NO-induced apoptosis and expression of NF-κB p65 and p53 in articular chondrocytes of rabbits in a concentration-dependent manner.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Farmacologia
/
Células Cultivadas
/
NF-kappa B
/
Proteína Supressora de Tumor p53
/
Apoptose
/
Condrócitos
/
Sistema de Sinalização das MAP Quinases
/
Fator de Transcrição RelA
/
Metabolismo
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Industrial Hygiene and Occupational Diseases
Ano de publicação:
2013
Tipo de documento:
Artigo
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