Objective To discuss the change of the expression level of microtubule associated protein-2 (MAP-2) in hippocampus and the effect of fluoxetine combine with enrich environment in chronic unpredictable stress (CUS) rat.Methods Divided 30 male Sprague-Dawle (SD) rats into CUS group,normal group,CUS + fluoxetine group,CUS + enrich environment group,and CUS + fluoxetine + enrich environment group averagely and randomly according to random number table (n=6 each).Rats in CUS group were all fed lonely and received CUS for 6 weeks.Rats in normal group were fed in groups (3 rats in every cage) in standard environment for 6 weeks.Rats in CUS+fluoxetine group,CUS+enrich environment group,and CUS + fluoxetine + enrich environment group received CUS for 6 weeks and had a lavage with fluoxetine,an intervention of enrich environment,a lavage with fluoxetine + an intervention of enrich environment respectively during the last 3 weeks every day.Every rat went a behavioral assessment before and after CUS and after intervention.Behavioral assessment included sucrose water consumption test,weight measurement,and open field test (horizontal moving distance,number of vertical,number of faece).Measured the level of MAP-2 expressed in hippocampus with immunohistochemistry at last.Results (1) Behavioral assessment before CUS:there was no significant difference between CUS group,normal group,CUS + fluoxetine group,CUS + enrich environment group and CUS + fluoxetine + enrich environment group in sucrose water consumption test,weight measurement,horizontal moving distance,number of vertical and number of faece.(2) Behavioral assessment after CUS:consumption of sucrose water,gain of body weight,distance of horizontal moving of rats in CUS group,CUS + fluoxetine group,CUS + enrich environment group,and CUS+fluoxetine+enrich environment group were all less than rats in normal group (all P＜0.05).(3)Behavioral assessment after intervention:consumption of sucrose water,gain of body weight,and distance of horizontal moving of rats in normal group,CUS + fluoxetine group,CUS + enrich environment group,and CUS+fluoxetine+enrich environment group were all more than rats in CUS group (all P＜0.05).Gain of body weight (P=0.005,0.029),and distance of horizontal moving (P=0.028,0.031) of rats in normal group ((84±+3) g,(6 687±664) cm)were more than rats in CUS+fluoxetine group ((75±4) g,(5 859±624) cm) and CUS±enrich environment group ((77±8) g,(5 876±784) cm).Horizontal moving distance of rats in CUS+fluoxetine+enrich environment group ((6 657±430) cm) were longer than rats in CUS+fluoxetine group and CUS+enrich environment group (P=0.033,0.037).(4)Results of immunohistochemistry:the levels of MAP-2 expressed in CA1,CA3,dentate gyrus in hippocampus ofrats in normal group (0.408±0.014,0.405±0.011,0.406 ± 0.012),CUS + fluoxetine group (0.403 ± 0.011,0.403 ± 0.011,0.403 ± 0.012),CUS + enrich environment group (0.406±0.015,0.399±0.013,0.406±0.017),and CUS+fluoxetine+enrich environment group (0.407±0.015,0.401±0.010,0.407 ±0.013) were all higher than rats in CUS group (0.379±0.020,0.390 ± 0.014,0.394± 0.013;all P＜0.05).Conclusions Fluoxetine,enrich environment and fluoxetine combine with enrich environment all could reverse the depressive behaviors of CUS rats,the effect of fluoxetine combine with enrich environment may be superior to fluoxetine or enrich environment alone.The expression level of MAP-2 in CA1,CA3,dentate gyrus of hippocampus in CUS rats may be decreased,fluoxetine,enrich environment and fluoxetine combine with enrich environment all could reverse the decrease.

Objective To discuss the change of the expression level of microtubule associated protein-2 (MAP-2) in hippocampus and the effect of fluoxetine combine with enrich environment in chronic unpredictable stress (CUS) rat.Methods Divided 30 male Sprague-Dawle (SD) rats into CUS group,normal group,CUS + fluoxetine group,CUS + enrich environment group,and CUS + fluoxetine + enrich environment group averagely and randomly according to random number table (n=6 each).Rats in CUS group were all fed lonely and received CUS for 6 weeks.Rats in normal group were fed in groups (3 rats in every cage) in standard environment for 6 weeks.Rats in CUS+fluoxetine group,CUS+enrich environment group,and CUS + fluoxetine + enrich environment group received CUS for 6 weeks and had a lavage with fluoxetine,an intervention of enrich environment,a lavage with fluoxetine + an intervention of enrich environment respectively during the last 3 weeks every day.Every rat went a behavioral assessment before and after CUS and after intervention.Behavioral assessment included sucrose water consumption test,weight measurement,and open field test (horizontal moving distance,number of vertical,number of faece).Measured the level of MAP-2 expressed in hippocampus with immunohistochemistry at last.Results (1) Behavioral assessment before CUS:there was no significant difference between CUS group,normal group,CUS + fluoxetine group,CUS + enrich environment group and CUS + fluoxetine + enrich environment group in sucrose water consumption test,weight measurement,horizontal moving distance,number of vertical and number of faece.(2) Behavioral assessment after CUS:consumption of sucrose water,gain of body weight,distance of horizontal moving of rats in CUS group,CUS + fluoxetine group,CUS + enrich environment group,and CUS+fluoxetine+enrich environment group were all less than rats in normal group (all P＜0.05).(3)Behavioral assessment after intervention:consumption of sucrose water,gain of body weight,and distance of horizontal moving of rats in normal group,CUS + fluoxetine group,CUS + enrich environment group,and CUS+fluoxetine+enrich environment group were all more than rats in CUS group (all P＜0.05).Gain of body weight (P=0.005,0.029),and distance of horizontal moving (P=0.028,0.031) of rats in normal group ((84±+3) g,(6 687±664) cm)were more than rats in CUS+fluoxetine group ((75±4) g,(5 859±624) cm) and CUS±enrich environment group ((77±8) g,(5 876±784) cm).Horizontal moving distance of rats in CUS+fluoxetine+enrich environment group ((6 657±430) cm) were longer than rats in CUS+fluoxetine group and CUS+enrich environment group (P=0.033,0.037).(4)Results of immunohistochemistry:the levels of MAP-2 expressed in CA1,CA3,dentate gyrus in hippocampus ofrats in normal group (0.408±0.014,0.405±0.011,0.406 ± 0.012),CUS + fluoxetine group (0.403 ± 0.011,0.403 ± 0.011,0.403 ± 0.012),CUS + enrich environment group (0.406±0.015,0.399±0.013,0.406±0.017),and CUS+fluoxetine+enrich environment group (0.407±0.015,0.401±0.010,0.407 ±0.013) were all higher than rats in CUS group (0.379±0.020,0.390 ± 0.014,0.394± 0.013;all P＜0.05).Conclusions Fluoxetine,enrich environment and fluoxetine combine with enrich environment all could reverse the depressive behaviors of CUS rats,the effect of fluoxetine combine with enrich environment may be superior to fluoxetine or enrich environment alone.The expression level of MAP-2 in CA1,CA3,dentate gyrus of hippocampus in CUS rats may be decreased,fluoxetine,enrich environment and fluoxetine combine with enrich environment all could reverse the decrease.

Aim To explore the role of a peroxisome proliferators-activated receptor gamma ligand,Rosiglitazone,in angiogenesis in human lung adenocarcinoma cells with reference to the regulation of vascular endothelial growth factor(VEGF).Methods Human lung adenocarcinoma A549 cell line was cultured in vitro.Expression of PPAR? and VEGF in A549 lung adenocarcinoma cells treated with different concentrations of Rosiglitazone was examined by semi-quantitative RT-PCR and immunohistochemical staining.Results PPAR? protein levels were higher in cultured A549 cells.RT-PCR and immunohistochemical staining showed that PPAR? mRNA and protein were enhanced in cells treated with Rosiglitazone in a dose-dependent manner,compared with those of untreated cells.Rosiglitazone had a potent inhibitory effect on the expression of VEGF in A549 cells dose-dependently in a range of concentrations.The effect was maximal with 10 ?mol?L~(-1) RSG and weaken over 20 ?mol?L~(-1) RSG,whereas 100 ?mol?L~(-1) RSG didnot have this down-regulation.GW9662,a PPAR? antagonist,partially blocked this effect of Rosiglitazone.Conclusions Activation of PPAR? suppresses angiogenesis in human lung adenocarcinoma.This action is probably associated with the down-regulation of angiogenic factor,VEGF,which may be modulated by PPAR?.These results suggest that PPAR? might be a novel molecular target for angiogenesis lung adenocarcinoma.