北京中医药大学学报
北京中醫藥大學學報
북경중의약대학학보
Journal of Beijing University of Traditional Chinese Medicine
2015年
9期
611-618
,共8页
邹海艳%杨亦龙%屠蘅菁%姚晓泉%王雅丽%刘思思%欧阳俊%王海征%赵晖%王蕾%张弛%张秋霞
鄒海豔%楊亦龍%屠蘅菁%姚曉泉%王雅麗%劉思思%歐暘俊%王海徵%趙暉%王蕾%張弛%張鞦霞
추해염%양역룡%도형정%요효천%왕아려%류사사%구양준%왕해정%조휘%왕뢰%장이%장추하
解郁安神%慢性不可预见性应激抑郁模型%神经递质%脑源性神经营养因子%大鼠
解鬱安神%慢性不可預見性應激抑鬱模型%神經遞質%腦源性神經營養因子%大鼠
해욱안신%만성불가예견성응격억욱모형%신경체질%뇌원성신경영양인자%대서
relieving stagnation and tranquilizing%chronic unpredictable stress(CUS)%neurotransmit-ters%brain derived neurotrophic factor(BDNF)%rats
目的：观察解郁安神中药对慢性不可预见性应激（ CUS）抑郁大鼠模型神经递质及脑源性神经营养因子（ BDNF）的影响，探讨其抗抑郁的作用机制。方法雄性SD大鼠随机分为正常组，模型组，解郁安神中药小、中、大剂量组（8.2、16.3、32.7 g／kg），盐酸氟西汀组（10 mg／kg）。应激刺激开始的同时连续灌胃药物35 d。通过敞箱实验、新奇抑制摄食实验观察药物对大鼠行为学的影响；采用HPLC法测定药物对大鼠海马、皮层的多巴胺（ DA）、5-羟色胺（5-HT）及其代谢产物5-羟吲哚乙酸（5-HIAA）、去甲肾上腺素（NE）含量的影响；利用Western blot观察药物对大鼠海马BNDF的表达。结果模型组大鼠体重增长缓慢，在行为学测试中表现出自主活动减少；皮层的5-HT和NE的含量明显降低（ P＜0.05），海马5-HT及5-HIAA、NE的水平亦显著降低（ P＜0.05）， BDNF的表达显著下降（P＜0.05）。与模型组比较，解郁安神中药各剂量均可不同程度改善CUS抑郁大鼠自发活动的减少；中药中、大剂量及盐酸氟西汀可显著提高皮层5-HT、NE的含量（ P＜0.05），中药小、大剂量组可显著提高海马NE的含量（ P＜0.05），中药各剂量可显著提高海马5-HT、5-HIAA的含量（P＜0.05）；中药大剂量及盐酸氟西汀可上调海马BDNF的表达（P＜0.05）。结论解郁安神中药抗抑郁的作用机制可能与其对神经递质的影响及上调脑源性神经营养因子有关。
目的：觀察解鬱安神中藥對慢性不可預見性應激（ CUS）抑鬱大鼠模型神經遞質及腦源性神經營養因子（ BDNF）的影響，探討其抗抑鬱的作用機製。方法雄性SD大鼠隨機分為正常組，模型組，解鬱安神中藥小、中、大劑量組（8.2、16.3、32.7 g／kg），鹽痠氟西汀組（10 mg／kg）。應激刺激開始的同時連續灌胃藥物35 d。通過敞箱實驗、新奇抑製攝食實驗觀察藥物對大鼠行為學的影響；採用HPLC法測定藥物對大鼠海馬、皮層的多巴胺（ DA）、5-羥色胺（5-HT）及其代謝產物5-羥吲哚乙痠（5-HIAA）、去甲腎上腺素（NE）含量的影響；利用Western blot觀察藥物對大鼠海馬BNDF的錶達。結果模型組大鼠體重增長緩慢，在行為學測試中錶現齣自主活動減少；皮層的5-HT和NE的含量明顯降低（ P＜0.05），海馬5-HT及5-HIAA、NE的水平亦顯著降低（ P＜0.05）， BDNF的錶達顯著下降（P＜0.05）。與模型組比較，解鬱安神中藥各劑量均可不同程度改善CUS抑鬱大鼠自髮活動的減少；中藥中、大劑量及鹽痠氟西汀可顯著提高皮層5-HT、NE的含量（ P＜0.05），中藥小、大劑量組可顯著提高海馬NE的含量（ P＜0.05），中藥各劑量可顯著提高海馬5-HT、5-HIAA的含量（P＜0.05）；中藥大劑量及鹽痠氟西汀可上調海馬BDNF的錶達（P＜0.05）。結論解鬱安神中藥抗抑鬱的作用機製可能與其對神經遞質的影響及上調腦源性神經營養因子有關。
목적：관찰해욱안신중약대만성불가예견성응격（ CUS）억욱대서모형신경체질급뇌원성신경영양인자（ BDNF）적영향，탐토기항억욱적작용궤제。방법웅성SD대서수궤분위정상조，모형조，해욱안신중약소、중、대제량조（8.2、16.3、32.7 g／kg），염산불서정조（10 mg／kg）。응격자격개시적동시련속관위약물35 d。통과창상실험、신기억제섭식실험관찰약물대대서행위학적영향；채용HPLC법측정약물대대서해마、피층적다파알（ DA）、5-간색알（5-HT）급기대사산물5-간신타을산（5-HIAA）、거갑신상선소（NE）함량적영향；이용Western blot관찰약물대대서해마BNDF적표체。결과모형조대서체중증장완만，재행위학측시중표현출자주활동감소；피층적5-HT화NE적함량명현강저（ P＜0.05），해마5-HT급5-HIAA、NE적수평역현저강저（ P＜0.05）， BDNF적표체현저하강（P＜0.05）。여모형조비교，해욱안신중약각제량균가불동정도개선CUS억욱대서자발활동적감소；중약중、대제량급염산불서정가현저제고피층5-HT、NE적함량（ P＜0.05），중약소、대제량조가현저제고해마NE적함량（ P＜0.05），중약각제량가현저제고해마5-HT、5-HIAA적함량（P＜0.05）；중약대제량급염산불서정가상조해마BDNF적표체（P＜0.05）。결론해욱안신중약항억욱적작용궤제가능여기대신경체질적영향급상조뇌원성신경영양인자유관。
Objective To observe the effect of TCM compound of resolving stagnation for tranquilization ( RST) on neurotransmitters and brain derived neurotrophic factors ( BNDF ) in depression rat model induced by chronic unpredictable stress ( CUS) , and to reveal the mechanism of RST on the treatment of depression.Methods Altogether 60 male SD rats were randomly divided into normal group, model group, high-, mid-and low-dose RST groups at dosage of 8.2, 16.3, 32.7 g/kg, and fluoxetine group with dose of 10 mg/kg.The rats of four therapy groups were administered intragastrically drugs with undergoing CUS for consecutive thirty-five days.The behavioral changes of rats were observed by open field test and novelty-suppressed feeding-test.The content of dopamine ( DA) , 5-hydroxeytryptamine(5-HT) , 5-hydroxyindole acetic acid (5-HIAA) and norepi-nephrine( NE) in hippocampus and cortex were determined by HPLC.And the expression of BDNF in hippocampus was measured by Western blot.Results Compared with the normal group, the rats ’ weight increased slowlier and the spontaneous activity decreased in model group; the contents of 5-HT and NE in cortex and the content of 5-HT, 5-HIAA and NE in hippocampus significantly reduced ( P<0.05 ).Compared with the model group, the spontaneous activity significantly increased in all therapy groups;the contents of 5-HT and NE in cortex dramatically increased in fluoxetine group and mid-, high-dose group ( P<0.05 );the contents of 5-HT and 5-HIAA in hippocampus significantly increased in all three RST groups ( P<0.05 ); the content of NE in hippocampus significantly increased in low-and high-dose group ( P<0.05 ).The expression of BDNF in hippocampus significantly increased in fluoxetine group and high-dose RST group ( P<0.05).Conclusion The anti-depression mechanism of TCM compound formulated by principle of resolving stagnation for tranquilization may be related to the effects of increasing neurotransmitters and up-regulation of BDNF.
