Aim To explore the effect of meloxicam on the CUMS-induced depressive-like behaviors in rats and its preliminary mechanism. Methods The rats were exposed to CUMS procedure for 6 weeks to estab-lish the model of depression. Meloxicam(1,3 mg· kg-1 ) and sertraline(5 mg·kg-1 ) were administered to rats from 22d of the stress procedure(once a day,for 21 days,p. o. ) . Depressive-like behaviors were evalu-ated by the open-field test and force swimming test. The levels of PGE2 and TNF-αin cortex were measured by ELISA. Moreover, the concentrations of NE, DA, DOPAC and 5-HIAA were also measured by HPLC, and the protein expression of 5-HT1 AR in cortex was analyzed by the immunohistochemistry. Results Com-pared with the rats of normal control group,the vertical and horizontal movement scores of rats in the open-field test were decreased and the immobility time in the forced swimming test was increased in model group. The levels of PGE2 and TNF-α were both increased signifi-cantly,whereas the concentrations of NE, DA, DOPAC and 5-HIAA were decreased and the expression of 5-HT1AR was reduced in cortex. Compared with the rats of model group, meloxicam significantly improved the depressive behaviors of rats in experimental groups and reversed the content of PGE2 ,TNF-α,NE,DA,DOPAC and 5-HIAA, as well as the expression of 5-HT1AR. Conclusion Meloxicam has a significant protective effect on CUMS-induced depressive-like behaviors, and the protective mechanism might be related to atten-uating inflammation response and reconstructing the balance of the monoamine neurotransmitter system in rat cortex.

Aim To investigate the protective effects of beraprost sodium on cerebral cortical neuron injury in chronic aluminum-overload rats and its effects on PGIS-IP signaling pathway. Methods 75 SD rats were randomized into five groups: normal control group, chronic aluminum-overload group ( model group) and beraprost sodium groups-low dose (6 μg· kg-1 ), medium dose ( 12 μg · kg-1 ) and high dose (24 μg·kg-1). Aluminum gluconate (Al3+ 200 mg ·kg-1 d-1, once a day, 5d a week, for 20 weeks, p. o. ) was administered to rats of cerebral damage model. The rats of experimental groups were concomi-tantly treated with beraprost sodium ( p. o. ) daily for 20 weeks. After the model was built successfully, the spatial learning and memory( SLM) function was done by Morris water maze. The cortical neurons damage was detected by HE staining, SOD activities and MDA contents. The 6-k-PGF1α levels in cortex were meas-ured by ELISA. The expressions of PGIS, IP mRNA and IP protein were also studied. Results Compared with the rats of normal control group, the SLM function was significantly impaired ( P<0. 01 ) and considera-ble karyopycnosis was observed in model group rats. The SOD activities were weakened ( P <0. 01 ), the MDA contents increased ( P<0. 05 ) and the levels of 6-k-PGF1α raised significantly ( P <0. 01). The ex-pressions of PGIS and IP mRNA in the rats cortex obvi-ously increased ( P<0. 01 ), so did the expression of IP protein(P<0. 05). Compared with the rats of mod-el group, the SLM function of rats in experimental groups decreased significantly ( P<0. 01 ) and damage of cortical neurons reduced remarkably. The SOD ac-tivities increased ( P <0. 01 ) and the MDA contents decreased ( P <0. 01). Besides, the content of 6-k-PGF1α, the expressions of PGIS mRNA and IP protein in the rats cortex decreased significantly ( P<0. 05 ) as well as IP mRNA ( P<0. 01). Conclusion Our re-sults demonstrate that in cerebral cortical neuron of chronic aluminum-overload rats, beraprost sodium has notably protective effects and the mechanism might be related to PGIS-IP signaling pathway.