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
2010年
7期
621-623
,共3页
陈江瑛%闫振文%张付生%张素平
陳江瑛%閆振文%張付生%張素平
진강영%염진문%장부생%장소평
瘦素%血管性痴呆%认知功能%细胞凋亡
瘦素%血管性癡呆%認知功能%細胞凋亡
수소%혈관성치태%인지공능%세포조망
Leptin%Vascular dementia%Cognitive function%Apoptosis
目的 研究瘦素脑内注射对双侧颈总动脉永久性结扎(2VO)所致血管性痴呆(VaD)大鼠认知功能的改善作用.方法 在缺糖缺氧培养条件下,观察瘦素对体外培养的海马神经元的保护作用,以及Western Blotting检测海马神经元瘦素受体的表达.在大鼠海马区预注射瘦素的基础上,用2VO法制作VaD大鼠模型,Morris水迷宫测试瘦素治疗后认知功能的改善情况,Tunel染色测定各组大鼠海马脑组织内细胞凋亡的变化.结果 体外培养海马神经元上存在着瘦素受体的表达,在缺糖缺氧培养12h后,海马神经元出现大量的细胞凋亡,凋亡率为(72.96±6.25)%,而在瘦素预处理1μg和5μg组,细胞凋亡率分别为(46.33 ±7.85)%和(23.58±5.08)%,与对照组相比,差异有统计学意义(P<0.01).瘦素脑内注射的VaD大鼠,与未予治疗的VaD大鼠组相比,VaD瘦素治疗组大鼠找到平台的潜伏期缩短(P<0.01),找到平台的平均速度加快(P<0.01),与痴呆组相比,瘦素治疗组大鼠脑组织海马区凋亡细胞数明显减少,差异具有统计学意义(P<0.01).结论 瘦索对大鼠体外培养和脑组织内海马神经元具有神经保护作用,脑内注射瘦素可以明显改善VaD大鼠的认知功能.
目的 研究瘦素腦內註射對雙側頸總動脈永久性結扎(2VO)所緻血管性癡呆(VaD)大鼠認知功能的改善作用.方法 在缺糖缺氧培養條件下,觀察瘦素對體外培養的海馬神經元的保護作用,以及Western Blotting檢測海馬神經元瘦素受體的錶達.在大鼠海馬區預註射瘦素的基礎上,用2VO法製作VaD大鼠模型,Morris水迷宮測試瘦素治療後認知功能的改善情況,Tunel染色測定各組大鼠海馬腦組織內細胞凋亡的變化.結果 體外培養海馬神經元上存在著瘦素受體的錶達,在缺糖缺氧培養12h後,海馬神經元齣現大量的細胞凋亡,凋亡率為(72.96±6.25)%,而在瘦素預處理1μg和5μg組,細胞凋亡率分彆為(46.33 ±7.85)%和(23.58±5.08)%,與對照組相比,差異有統計學意義(P<0.01).瘦素腦內註射的VaD大鼠,與未予治療的VaD大鼠組相比,VaD瘦素治療組大鼠找到平檯的潛伏期縮短(P<0.01),找到平檯的平均速度加快(P<0.01),與癡呆組相比,瘦素治療組大鼠腦組織海馬區凋亡細胞數明顯減少,差異具有統計學意義(P<0.01).結論 瘦索對大鼠體外培養和腦組織內海馬神經元具有神經保護作用,腦內註射瘦素可以明顯改善VaD大鼠的認知功能.
목적 연구수소뇌내주사대쌍측경총동맥영구성결찰(2VO)소치혈관성치태(VaD)대서인지공능적개선작용.방법 재결당결양배양조건하,관찰수소대체외배양적해마신경원적보호작용,이급Western Blotting검측해마신경원수소수체적표체.재대서해마구예주사수소적기출상,용2VO법제작VaD대서모형,Morris수미궁측시수소치료후인지공능적개선정황,Tunel염색측정각조대서해마뇌조직내세포조망적변화.결과 체외배양해마신경원상존재착수소수체적표체,재결당결양배양12h후,해마신경원출현대량적세포조망,조망솔위(72.96±6.25)%,이재수소예처리1μg화5μg조,세포조망솔분별위(46.33 ±7.85)%화(23.58±5.08)%,여대조조상비,차이유통계학의의(P<0.01).수소뇌내주사적VaD대서,여미여치료적VaD대서조상비,VaD수소치료조대서조도평태적잠복기축단(P<0.01),조도평태적평균속도가쾌(P<0.01),여치태조상비,수소치료조대서뇌조직해마구조망세포수명현감소,차이구유통계학의의(P<0.01).결론 수색대대서체외배양화뇌조직내해마신경원구유신경보호작용,뇌내주사수소가이명현개선VaD대서적인지공능.
Objective To study improvement of cognitive function impairment of vascular dementia rats induced by a permanent bilateral ligation of common carotid arteries (2VO) after administration of leptin in brain. Methods Hippocampal neurons was isolated and cultured from SD rats. At oxygen-glucose deprivation condition, protection role of leptin on hippocampal neurons was observed and expression of leptin receptor was detected. Animal model of rats was established by 2VO. Pre-treatment VaD model of leptin was established by administration leptin into hippocampus region. The Morris water test was performed to detect difference in the cognitive function between VaD group and control group. Neuron apoptosis in hippocampus tissue were determined with TUNEL. Results Leptin receptor expression could be seen in hippocampal neurons. After oxygen-glucose deprivation cultured for 12 h , plenty of apoptotic cells were seen in hippocampal neurons, apoptosis rat was up to (72.96 ± 6.25) % , while apoptosis rate was (46.33 ±7.85)% and (23.58 ±5.08)% in 1 ( μg and 5μg leptin treatment group,respectively. Compared leptin treatment group with control group,difference had a statistical significance(P<0.01). Compared with untreated VaD group, latency time was shorter and average velocity was increased in leptin-treat-ment VaD group. Neuron apoptosis in hippocampus tissue of leptin-treated group were different significantly from those of untreated group (P < 0.01). Conclusion Leptin could protect hippocampal neurons from apoptosis in vitro. Cognitive function impairment could be improved by administration of leptin into brain in VaD rats.
