ABSTRACT
Objective To explore the effects of aripiprazole on clinical symptoms and neurotrophic factor levels in patients with schizophrenia. Methods Forty patients with schizophrenia and 40 normal controls were included in the study. The clinical symptoms of patients receiving aripiprazole only for 12 weeks were evaluated by using the Positive and Negative Syndrome Scale (PANSS). Stroop Color-Word Test (SCWT), Continuous Performance Test, Digit-Symbol Coding Test and Trail Making Test-A were used to evaluate the cognitive function both in patients and controls. Serum levels of Nerve Growth Factor (NGF), Brain Derived Neurotrophic Factor (BDNF) and Neurotrophin 3 (NT-3) were measured using enzyme linked immunosorbent assay. Results The clinical scores, cognitive function and levels of neurotrophic factors were different before and after treatment (P<0.01). And those were significantly lower in patients than in control group (P<0.05). Before treatment, BDNF was negatively correlated with PANSS negative symptom score (r=-0.362, P=0.022);NGF was related to the total score of PANSS (r=0.332, P=0.037) and positive symptoms (r=0.401, P=0.010); NT-3 was associated with negative symptom scores (r=-0.376, P=0.017) and SCWT-color words (r=0.332, P=0.037) in patient group. After treatment, the increase in BDNF was correlated with the reduction in PANSS total score (r=0.371, P=0.018), negative symptom score (r=0.345, P=0.029) and general pathology score (r=0.342, P=0.031). There was a correlation of the increase of NGF with the decrease of PANSS total scores (r=0.437, P=0.005) and with positive symptom scores (r=0.357, P=0.024). Conclusion Treatment with Aripiprazole can improve the clinical symptoms and cognitive functiona impairments in patients with schizophrenia, which may be related to the increase in serum levels of BDNF, NGF and NT-3.
ABSTRACT
Objective To investigate the expression of miR-16 in spinal cord and the effects of miR-16 mimics on the pain behavior and the expression of its target gene BDNF during the development and maintenance of bone cancer pain.Methods The bone cancer pain model rats were developed by intra-tibia inoculation of Walker 256 mammary gland cells.Before inoculation and 3,5,7,10,14 d after inoculation,the samples of spinal cord L4～6 lumbar enlargement were collected to detect the expression of miR-16 using real-time PCR.Mice in group BM and group BN were intrathcal injected of miR-16 mimics and its negative control products on 10 d,11 d,12 d after inoculation.Paw withdrawal mechanical threshold (PWMT) was measured using von Frey hair mechanical stimulation.The expression of BDNF was detected using western-blot on 14 d after behavior tests.Results Compared with the base level and the level in group S,the significant decrease of miR-16 expression was observed at 5 d～14dingroupT (5d (0.91±0.04),7 d (0.77±0.01),10 d (0.73±0.03),14d (0.42±0.08)) (all P＜ 0.05).Compared with SH group,PWMT was significantly decreased in BC and BP groups at 5 d～ 14 d (P＜0.05),and in group BM at 5 d～ 10 d(P＜0.05).Compared with BP group,PWMT was significantly higher in BM group at 10～12 d(P＜0.05).Compared with SH group,the expression of BDNF was significantly increased in BN and BP groups((2.78±0.31),(2.34±0.23)) (all P＜0.01).Compared with BP group,the expression of BDNF was significantly decreased in BM group (1.42±0.16) (P＜0.01).Conclusion miR-16 is downregulated in spinal cord of bone cancer pain rats,while intrathcal injection of miR-16 mimics can attenuate the pain behaviors in a rat model of bone cancer pain and decrease the expression of BDNF.miR-16 may modulate bone cancer pain through BDNF.