摘要
目的检测抑郁模型大鼠脑和心肌组织中一氧化氮(NO)和一氧化氮合酶(NOS)水平,探讨抑郁模型大鼠脑和心肌组织损伤的可能机制。方法采用慢性轻度不可预见性的应激结合孤养制备抑郁模型,采用敞箱实验和糖水消耗实验观察大鼠行为改变,以分光光度法检测大鼠脑和心肌组织中NO和NOS的水平。结果抑郁模型大鼠与正常对照组相比较,脑和心肌组织中NO[脑(8.97±2.22)μmol/g prot,(1.86±1.28)μmol/g prot;心肌(9.67±1.53)μmol/g prot,(2.67±1.08)μmol/g prot]和NOS[脑(9.50±1.89)U/mg prot,(2.3l±0.97)U/mg prot;心肌(11.20±1.47)U/mg prot,(2.53±0.97)U/mg prot]水平均显著增加,差异具有显著性(均P〈0.01)。结论抑郁模型大鼠脑和心肌组织中NO和NOS水平显著增加,并可能参与了抑郁模型大鼠脑和心肌组织的损伤。
Objective To study nitric oxide (NO) and nitric oxide synthase (NOS) in brain and myocardium of depression model rats and to explore the mechanism of brain and myocardium injuryed. Methods The depression model rats were produced by chronic mild unpredictable stress and separation. The behavior of rats were detected by open field test and sucrose consumption test. The contents of NO and NOS were determined with spectrophotometric method. Results Compared with the normal control, the contents of NO [ Brain ( 8.97 ± 2.22 ) μmol/g prot vs ( 1. 86 ± 1. 28 ) μmol/g prot ; Myocardium ( 9. 67 ± 1. 53 ) μmol/g prot vs ( 2. 67 ± 1.08 ) μmol/g prot ] and NOS [ Brain ( 9.50 ± 1.89 ) U/mg prot vs ( 2.31 ± 0.97 ) U/mg prot ; Myocardium ( 11.20 ± 1.47 )U/mg prot vs( 2.53 ± 0.97 )U/mg prot ] in brain and myocardium were significantly increased ( P 〈 0.01 ) of depression model rats. Conclusion The contents of NO and NOS increase significantly in brain and myocardium of depression model rats and it may induce the injury on brain and myocardium of them.
出处
《中华行为医学与脑科学杂志》
CAS
CSCD
北大核心
2009年第7期589-590,共2页
Chinese Journal of Behavioral Medicine and Brain Science
关键词
抑郁
脑
心肌
一氧化氮
一氧化氮合酶
Depression
Brain
Myocardium
Nitric oxide
Nitric oxide synthase