中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
Chinese Journal of Behavioral Medicine and Brain Science
2015年
8期
680-683
,共4页
侯菊花%刘圆月%李灿%邓叔华%刘柏炎
侯菊花%劉圓月%李燦%鄧叔華%劉柏炎
후국화%류원월%리찬%산숙화%류백염
卒中后抑郁%补阳还五汤%细胞周期蛋白D1%细胞周期蛋白依赖性激酶2%大鼠
卒中後抑鬱%補暘還五湯%細胞週期蛋白D1%細胞週期蛋白依賴性激酶2%大鼠
졸중후억욱%보양환오탕%세포주기단백D1%세포주기단백의뢰성격매2%대서
Post stroke depression%Buyang Huanwu decoction%Cyclin D1%Cdk2%Rats
目的 探讨补阳还五汤对卒中后抑郁大鼠海马区细胞周期蛋白1(Cyclin D1)、细胞周期蛋白依赖性激酶2(Cdk2)的影响.方法 运用大脑中动脉局灶性永久性线栓法结合慢性不可预见温和应激及孤养法制备大鼠卒中后抑郁模型,将实验动物随机分为五组:假手术组、缺血性脑卒中组、卒中后抑郁组、卒中后抑郁±氟西汀组(以下简称氟西汀组)和卒中后抑郁±补阳还五汤组(以下简称补阳还五汤组),分别给予不同的处理,在7d,14d,21d不同时间点处死动物,观察海马区神经细胞的形态改变,并运用免疫组织化学方法检测Cyclin D1、Cdk2的表达.结果 缺血性脑卒中组和模型组大鼠与假手术组相比,海马区神经细胞出现退化、变性、坏死等病理改变,细胞凋亡数量增加;在正常大鼠海马区神经细胞内,处理后7、14、21 d Cyclin D1的表达阳性率分别为(1.16±0.34)％、(1.62±0.29)％和(1.60±0.24)％,Cdk2在各时间点的表达阳性率分别为(1.52±0.26)％、(1.85±0.23)％和(1.97±0.10)％;卒中后抑郁组海马区Cyclin D1和Cdk2表达均上调,Cyclin D1在各时间点分别是(49.69±5.68)％、(58.17±2.89)％和(50.87±2.48)％,Cdk 2在各时间点分别是(50.63±2.93)％、(70.34±1.47)％和(61.35±3.04)％;而与模型组比较,氟西汀组、补阳还五汤组表达则下调,氟西汀组Cyclin D1在各时间点分别是(16.62±4.27)％、(29.66±5.24)％和(26.71±1.32)％,氟西汀组Cdk2在各时间点分别是(18.05±2.26)％、(33.84±3.12)％和(24.51±2.66)％,补阳还五汤组Cyclin D1在各时间点分别是(14.62±2.06)％、(26.89±3.41)％和(23.68±2.01)％,补阳还五汤组Cdk2在各时间点分别是(16.60±2.42)％、(20.09±3.45)％和(22.19±1.70)％.结论 脑缺血性卒中后抑郁Cyclin D1和Cdk2的异常表达可能诱发了神经细胞的死亡,补阳还五汤可能是通过抑制Cyclin D1、Cdk2的表达来减少缺血后神经细胞的损伤.
目的 探討補暘還五湯對卒中後抑鬱大鼠海馬區細胞週期蛋白1(Cyclin D1)、細胞週期蛋白依賴性激酶2(Cdk2)的影響.方法 運用大腦中動脈跼竈性永久性線栓法結閤慢性不可預見溫和應激及孤養法製備大鼠卒中後抑鬱模型,將實驗動物隨機分為五組:假手術組、缺血性腦卒中組、卒中後抑鬱組、卒中後抑鬱±氟西汀組(以下簡稱氟西汀組)和卒中後抑鬱±補暘還五湯組(以下簡稱補暘還五湯組),分彆給予不同的處理,在7d,14d,21d不同時間點處死動物,觀察海馬區神經細胞的形態改變,併運用免疫組織化學方法檢測Cyclin D1、Cdk2的錶達.結果 缺血性腦卒中組和模型組大鼠與假手術組相比,海馬區神經細胞齣現退化、變性、壞死等病理改變,細胞凋亡數量增加;在正常大鼠海馬區神經細胞內,處理後7、14、21 d Cyclin D1的錶達暘性率分彆為(1.16±0.34)％、(1.62±0.29)％和(1.60±0.24)％,Cdk2在各時間點的錶達暘性率分彆為(1.52±0.26)％、(1.85±0.23)％和(1.97±0.10)％;卒中後抑鬱組海馬區Cyclin D1和Cdk2錶達均上調,Cyclin D1在各時間點分彆是(49.69±5.68)％、(58.17±2.89)％和(50.87±2.48)％,Cdk 2在各時間點分彆是(50.63±2.93)％、(70.34±1.47)％和(61.35±3.04)％;而與模型組比較,氟西汀組、補暘還五湯組錶達則下調,氟西汀組Cyclin D1在各時間點分彆是(16.62±4.27)％、(29.66±5.24)％和(26.71±1.32)％,氟西汀組Cdk2在各時間點分彆是(18.05±2.26)％、(33.84±3.12)％和(24.51±2.66)％,補暘還五湯組Cyclin D1在各時間點分彆是(14.62±2.06)％、(26.89±3.41)％和(23.68±2.01)％,補暘還五湯組Cdk2在各時間點分彆是(16.60±2.42)％、(20.09±3.45)％和(22.19±1.70)％.結論 腦缺血性卒中後抑鬱Cyclin D1和Cdk2的異常錶達可能誘髮瞭神經細胞的死亡,補暘還五湯可能是通過抑製Cyclin D1、Cdk2的錶達來減少缺血後神經細胞的損傷.
목적 탐토보양환오탕대졸중후억욱대서해마구세포주기단백1(Cyclin D1)、세포주기단백의뢰성격매2(Cdk2)적영향.방법 운용대뇌중동맥국조성영구성선전법결합만성불가예견온화응격급고양법제비대서졸중후억욱모형,장실험동물수궤분위오조:가수술조、결혈성뇌졸중조、졸중후억욱조、졸중후억욱±불서정조(이하간칭불서정조)화졸중후억욱±보양환오탕조(이하간칭보양환오탕조),분별급여불동적처리,재7d,14d,21d불동시간점처사동물,관찰해마구신경세포적형태개변,병운용면역조직화학방법검측Cyclin D1、Cdk2적표체.결과 결혈성뇌졸중조화모형조대서여가수술조상비,해마구신경세포출현퇴화、변성、배사등병리개변,세포조망수량증가;재정상대서해마구신경세포내,처리후7、14、21 d Cyclin D1적표체양성솔분별위(1.16±0.34)％、(1.62±0.29)％화(1.60±0.24)％,Cdk2재각시간점적표체양성솔분별위(1.52±0.26)％、(1.85±0.23)％화(1.97±0.10)％;졸중후억욱조해마구Cyclin D1화Cdk2표체균상조,Cyclin D1재각시간점분별시(49.69±5.68)％、(58.17±2.89)％화(50.87±2.48)％,Cdk 2재각시간점분별시(50.63±2.93)％、(70.34±1.47)％화(61.35±3.04)％;이여모형조비교,불서정조、보양환오탕조표체칙하조,불서정조Cyclin D1재각시간점분별시(16.62±4.27)％、(29.66±5.24)％화(26.71±1.32)％,불서정조Cdk2재각시간점분별시(18.05±2.26)％、(33.84±3.12)％화(24.51±2.66)％,보양환오탕조Cyclin D1재각시간점분별시(14.62±2.06)％、(26.89±3.41)％화(23.68±2.01)％,보양환오탕조Cdk2재각시간점분별시(16.60±2.42)％、(20.09±3.45)％화(22.19±1.70)％.결론 뇌결혈성졸중후억욱Cyclin D1화Cdk2적이상표체가능유발료신경세포적사망,보양환오탕가능시통과억제Cyclin D1、Cdk2적표체래감소결혈후신경세포적손상.
Objective To observe the effects of Buyang Huanwu decoction(BYHW) on the expression of Cyclin D1 and Cdk2 in rats with post-stroke depression(PSD).Methods The rats model of focal cerebral ischemia was established by means of middle cerebral artery occlusion(MCAO).Then three weeks of salute-living and chronic unpredictable mild stress(CUMS) was given to the animal after cerebral stroke to induce the post-stoke depression animal model.The rats were divided into 5 groups:the sham operated group,the midge cerebral artery occlusion(MCAO) group,the PSD group,the fluoxetine group and the BYHWD group.The rats were subjected to left MCAO rebuilding in consistent focal cerebral ischemia,followed by an 21-day exposure to chronic mild stress (CMS)and single housing to induce PSD animal model.All rats were killed in 7,14 and 21 day after operation.The expressions of Cyclin D1 and Cdk2 were measured by immunohistochemical staining.Results Pathological changes such as hippocampal nerve cell regression,degeneration and necrosis were observed in the model rats compare with the sham operated group.The expression of Cyclin D1 in normal hippocampus in 7,14 or 21 day after operation was (1.16±0.34)％,(1.62±0.29)％ and (1.60±0.24)％ respectively,and Cdk2 was (1.52±0.26)％,(1.85±0.23)％ and (1.97±0.10)％.After PSD the expression of Cyclin D1 was (49.69±5.68)％,(58.17± 2.89) ％ and (50.87 ± 2.48) ％ respectively,and Cdk2 was (50.63 ± 2.93) ％,(70.34± 1.47) ％ and (61.35 ± 3.04) ％.Compared with model group,Fluoxetine and BYHW significantly reduced the numbers of Cyclin D1 and Cdk2 positive cells,the expression of Cyclin D1 was (16.62±4.27)％,(29.66±5.24)％ and (26.71±1.32)％ at fluoxetine group,and Cdk2 was (18.05±2.26) ％,(33.84±3.12) ％ and (24.51±2.66) ％.The expression of Cvclin D1 was (14.62±2.06)％,(26.89±3.41)％ and (23.68±2.01)％ at BYHWD group,and Cdk2 was (16.60± 2.42) ％,(20.09±3.45) ％ and (22.19± 1.70) ％.Conclusion The abnormal expression of Cyclin D1 and Cdk2 at the PSD rats indicate that they may be involved in the mechanism of neuronal death.Buyang Huanwu decoction may reduce the neuronal apoptosis through down-regulating the expression of Cyclin D1 and Cdk2.
