中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
5期
828-833
,共6页
皮质酮%抑郁症%糖原%海马
皮質酮%抑鬱癥%糖原%海馬
피질동%억욱증%당원%해마
Corticosterone%Depression%Glycogen%Hippocampus
目的：探讨慢性皮质酮注射对小鼠抑郁样行为以及脑糖原水平的影响。方法：将40只雄性C57 BL／6 N小鼠随机分为正常对照组与模型组，模型组小鼠连续4周给予皮质酮皮下注射，构建慢性应激抑郁障碍小鼠模型。采用强迫游泳实验和旷场实验验证慢性应激模型的建立；放免法测定小鼠血清中皮质酮（ CORT）水平；采用蛋白免疫印迹法检测海马突触素（ SYP）和脑源性神经营养因子（ BDNF）的蛋白表达水平；采用荧光间接测定法检测海马组织的糖原以及糖原合酶和糖原磷酸化酶的水平。结果：与正常对照组相比，模型组强迫游泳静止不动时间延长（P＜0.01）、自主活动能力降低（P＜0.01），表明慢性皮质酮注射诱导小鼠产生抑郁样行为。抑郁小鼠的皮质酮明显升高（P＜0.01）。皮质酮注射降低海马SYP和BDNF的蛋白表达（P＜0.01），同时海马组织糖原含量减少（P＜0.05），糖原合酶的活性降低（P＜0.05），而糖原磷酸化酶活性增加（P＜0.05）。结论：慢性皮质酮注射引起的海马神经元损伤和诱导小鼠抑郁样行为，可能与皮质酮降低海马糖原水平有关。
目的：探討慢性皮質酮註射對小鼠抑鬱樣行為以及腦糖原水平的影響。方法：將40隻雄性C57 BL／6 N小鼠隨機分為正常對照組與模型組，模型組小鼠連續4週給予皮質酮皮下註射，構建慢性應激抑鬱障礙小鼠模型。採用彊迫遊泳實驗和曠場實驗驗證慢性應激模型的建立；放免法測定小鼠血清中皮質酮（ CORT）水平；採用蛋白免疫印跡法檢測海馬突觸素（ SYP）和腦源性神經營養因子（ BDNF）的蛋白錶達水平；採用熒光間接測定法檢測海馬組織的糖原以及糖原閤酶和糖原燐痠化酶的水平。結果：與正常對照組相比，模型組彊迫遊泳靜止不動時間延長（P＜0.01）、自主活動能力降低（P＜0.01），錶明慢性皮質酮註射誘導小鼠產生抑鬱樣行為。抑鬱小鼠的皮質酮明顯升高（P＜0.01）。皮質酮註射降低海馬SYP和BDNF的蛋白錶達（P＜0.01），同時海馬組織糖原含量減少（P＜0.05），糖原閤酶的活性降低（P＜0.05），而糖原燐痠化酶活性增加（P＜0.05）。結論：慢性皮質酮註射引起的海馬神經元損傷和誘導小鼠抑鬱樣行為，可能與皮質酮降低海馬糖原水平有關。
목적：탐토만성피질동주사대소서억욱양행위이급뇌당원수평적영향。방법：장40지웅성C57 BL／6 N소서수궤분위정상대조조여모형조，모형조소서련속4주급여피질동피하주사，구건만성응격억욱장애소서모형。채용강박유영실험화광장실험험증만성응격모형적건립；방면법측정소서혈청중피질동（ CORT）수평；채용단백면역인적법검측해마돌촉소（ SYP）화뇌원성신경영양인자（ BDNF）적단백표체수평；채용형광간접측정법검측해마조직적당원이급당원합매화당원린산화매적수평。결과：여정상대조조상비，모형조강박유영정지불동시간연장（P＜0.01）、자주활동능력강저（P＜0.01），표명만성피질동주사유도소서산생억욱양행위。억욱소서적피질동명현승고（P＜0.01）。피질동주사강저해마SYP화BDNF적단백표체（P＜0.01），동시해마조직당원함량감소（P＜0.05），당원합매적활성강저（P＜0.05），이당원린산화매활성증가（P＜0.05）。결론：만성피질동주사인기적해마신경원손상화유도소서억욱양행위，가능여피질동강저해마당원수평유관。
AIM:To study the effect of chronic corticosterone ( CORT) injection on the depression-like behav-iors and the brain glycogen level in mice.METHODS:Male C57BL/6N mice (n=40) were randomly divided into nor-mal control group and model group.The mice in model group were subcutaneously consecutively injected with CORT for 4 weeks.The mouse model of chronic stress depression was constructed.The forced swim test and open field experiment were conducted to prove chronic stress model.The serum level of CORT in the mice was measured by radioimmunoassay.The protein levels of hippocampal synaptophysin ( SYP) and brain-derived neurotrophic factor ( BDNF) were detected by West-ern blot.Hippocampus glycogen, glycogen synthase and glycogen phosphorylase were determined by indirect fluorescence measurement.RESULTS:Compared with normal control group, the immobility time of the forced swim test in model group was significantly lengthened (P<0.01), and the ability of spontaneous activity was reduced (P<0.01), indicating that chronic CORT injection induced depression-like behaviors in mice.The CORT level increased significantly (P<0.01) in model group.CORT injection decreased the protein expression of hippocampal SYP and BDNF (P<0.01), reduced hipp-ocampal glycogen level (P<0.05) and glycogen synthase activity (P<0.05), and increased glycogen phosphorylase ac-tivity (P<0.05).CONCLUSION:Chronic CORT injection causes hippocampal neuron damage and induces the depres-sion-like behaviors of mice, which may be associated with decreasing hippocampal glycogen level by CORT.
