Physical activity is an effective component of depression management. However, the mechanisms by which exercise affects behavioral disorders remain unclear. The present study was conducted to investigate mechanisms by which voluntary exercise ameliorates depression. Plasma cortisol levels and hippocampal monoamine neurotransmitters were measured. Chronic mild stress (CMS) was used to induce depression in a rat model. The rats were allowed to swim for 10 weeks as part of their exercise treatment. Depressive behavior was analyzed using an open-field test and a sucrose consumption test before and after exercise. Serum cortisol levels were measured by radioimmunoassay. The concentrations of monoamine neurotransmitters in the hippocampus were determined using high-performance liquid chromatography with electrochemical detection. The CMS rats showed behavioral improvement after exercise. Compared with the control, serum cortisol levels were significantly increased by CMS. The serotonin, dopamine, and norepinephrine levels in the hippocampi were significantly increased by exercise. These findings indicate that exercise reverses and prevents the decrease in serotonin and noradrenaline, and restores dopamine in the CMS model.

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-NO plays an important role in cartilage destruction by inducing apoptosis of chondrocytes. Here we investigated the role of c-Jun N-terminal kinase (JNK) signal transduction pathways in the apoptosis induced by NO donor sodium nitroprusside (SNP) in rabbit articular chondrocytes. We used Annexin V-FITC/PI flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) assay to detect apoptosis rate. The expressions of p38, NF-κB p65, caspase-3 and p53 genes at protein levels were measured by Western blotting assay. RT-PCR was performed to show the mRNA expression of caspase-3, and the activity of caspase-3 was also detected. To investigate the effect of JNK-specific inhibitor SP600125, chondrocytes were pretreated with SP600125 ahead of SNP treatment. Treatment with SNP accelerated apoptosis in a concentration dependent manner, while such acceleration was reduced by SP600125 pretreatment. Moreover, we found that SP600125 significantly decreased NO-induced NF-κB, p53, caspase-3 protein expressions and caspase-3 mRNA expression, as well as intracellular caspase-3 activity (P < 0.05). Collectively, these data suggest that JNK plays an important role through stimulating NF-κB, p53 and caspase-3 activation.

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