ABSTRACT
Objective@#To establish a novel stress-induced depression model by changing the lighting conditions and continuously damping cushion (L-D).@*Methods@#The L-D stress depression animal model was established in C57BL / 6 mice with body weight of 18-22 g. Seventy-five mice with the horizontal and vertical scores higher than 30 and less than 120 in open field test were employed.In the research of model construction, mice were randomly divided into three groups: control group (n=9), chronic unpredictable mild stress(CUMS) model group (n=10) and L-D model group (n=9). In the drug intervention experiments, mice were randomly divided into five groups: control group (n=9), chronic unpredictable mild stress(CUMS) model group (n=10), L-D model group (n=9), CUMS+ fluoxetine group (n=10) and L-D model+ fluoxetine group (n=9). Open field test, forced swimming test and sucrose preference test were used to evaluate the degree of depression in animals.@*Results@#(1) In the open field test, the horizontal score of CUMS model group (67.20±5.81) and the L-D model group (52.56±19.05) were significantly lower than that of the control group (76.44±9.22) (t=2.645, t=3.387, both P<0.05). And horizontal score of the L-D model was significantly lower than that of the CUMS model (t=2.321, both P<0.05). In forced swimming experiment, compared with the control group ((39.67±21.12)s), the immobility time of the CUMS model group ((60.90±10.34)s) and the L-D model group ((74.89±16.10)s) were significantly prolonged (t=2.831, 3.979, both P<0.05). The immobility time of the L-D model group was also significantly higher than that of the CUMS model group (t=2.278, P<0.05). In the sucrose preference experiment, the percentage of sucrose preference in CUMS model group ((72±7)%) and L-D model group ((65±5)%) was lower than that in the control group ((81±12)%) (t=2.195, 3.875, both P<0.05). The percentage of sucrose preference of L-D model group was significantly higher than that of CUMS model group (t=2.286, P<0.05). (2) After intervention with antidepressants, the horizontal scores of the CUMS model group (65.60±6.43) and the L-D model group (54.33±14.67) were significantly lower than that of the control group (75.78±8.27) in open field test (t=3.011, t=3.861, both P<0.05), and the score of L-D group was lower than that of CUMS group(t=2.235, P<0.05). The vertical score of the L-D model group (33.44±4.54) was significantly lower than that of the control group (39.22±5.56) (t=2.553, P<0.05). There was significant increase in the level score and vertical score of CUMS model and L-D model after fluoxetine intervention (t=3.090, t=2.692, both P<0.05), and significant twist in the vertical score of CUMS model and L-D model (t=2.681, t=2.354; both P<0.05). In the forced swimming experiment, the immobility time of the L-D model((64.11±13.06)s) was significantly longer than that of the control group ((42.00±13.77)s) (t=3.494, P<0.05). The immobility time of CUMS model and L-D model mice was significantly longer than that of non-intervention group (t=2.137, 2.940, both P<0.05). After the intervention of fluoxetine, there was no significant difference between the CUMS group, L-D group, the control group(all P>0.05).@*Conclusion@#Changing the lighting conditions and continuously damping cushion is a new method to establish mice model with depression behavior.Shorter modeling duration and simple operation are the main advantages of this model.
ABSTRACT
Objective To screen altered proteins of hippocampus in the stress-induced depression (STRID) rat model, and explore the potential molecular mechanism. Methods Twenty Sprague-Dawley rats were randomly divided into the control group and STRID group, 10 rats in each group. Chronic unpredictable mild stress (CUMS) methods including fasting for solids and liquids, electric foot-shock, reversing day and night, cold water swimming, cage tilt, scare stimulation and tail pinch were conducted on STRID rats with no repeats for 28 days to make up the depression animal model. The control group was normally fed during this period. After the stress stimulation, the hippocampus protein samples were used for two dimensional electrophoresis to screen the differentially expressed protein, and then mass spectrum identification and function analyze were conducted. Results Compared with the control group, 34 proteins were altered in STRID group. Among which, 18 were up-regulated, and 16 were down-regulated. The differentially expressed proteins mainly located in cytoplasm, mitochondrion, extracellular exosome and myelin sheath. The involved signaling pathways included metabolic pathway, oxidative phosphorylation pathway, and Alzheimer's disease, Parkinson's disease and Huntington's disease pathways. Conclusion The altered proteins and dysfunction of nerve signaling, and the excess of oxidative phosphorylation in hippocampus of STRID rats may be one of the pathogenesises.
ABSTRACT
Objective To explore the effects of mangiterin on behaviors and brain-derived neurotrophic factor(BDNF) of hippocampus in chronic stress depression mice.Methods 60 male mice were randomly divided into normol control group,model group,fluoxetin control group and mangiterin groups (low,medium and high dose),10 mice in each group.All mice except normal control group were singly housed and subjected to chronic stress-induced depression model for 21 consecutive days.The behaviors of mice were detected by open-field test and tail-suspension test.The expression of BDNF in the hippocampus were assessed using western blot.Results Compared with the normal group,mice exposed chronic stress showed decreased body weight((5.33 ±1.20) g),crossing lines (102 ± 18) and distances ((3425 ± 112) mm) notably decreased in open-field behavior test.The duration of immobility during tail-suspension was increased significantly.BDNF expression in the hippocampus(0.45 ± 0.03) was downregulated significantly(P＜ 0.01),while it was upregulated in the groups of mangiterin(P ＜ 0.01).Mangiterin group in high dose had the similar effects to fluoxetin group(P ＞ 0.05).Conclusion Mangiterin can ameliorate behavior impairment of chronic stress induced-depression mice and it may be related to the upregulation of BDNF expression in the hippocampus.