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
2009年
1期
13-15
,共3页
吕风月%赵咏梅%李军泉%徐群渊
呂風月%趙詠梅%李軍泉%徐群淵
려풍월%조영매%리군천%서군연
炎症%脂多糖%黑质%多巴胺能神经元%星形胶质细胞
炎癥%脂多糖%黑質%多巴胺能神經元%星形膠質細胞
염증%지다당%흑질%다파알능신경원%성형효질세포
Inflammation%Lipopolysaccharide (LPS)%Substantia nigra%Dopaminergic neurons%Astrocyte
目的 观察脑室内注射脂多糖(lipopolysaccharide,LPS)引起的脑内炎症对大鼠黑质多巴胺能神经元的慢性毒性作用,探讨星形胶质细胞是否参与脑内炎症致大鼠多巴胺能神经元变性.方法 60只SD大鼠分为LPS实验组和生理盐水(NS)对照组(n=30).大鼠右侧脑室一次性注射LPS 20μl(1.25μg/μl)或同体积的NS.于给药后不同时间检测大鼠行为,免疫组织化学染色法观察黑质内酪氨酸羟化酶(TH)阳性神经元,并用Western blot检测大鼠黑质纹状内胶质纤维酸性蛋白(GFAP)的表达.结果 1)LPS给药后大鼠平均运动速度呈进行性下降,与相应NS对照组相比,在16周[(2.12±0.43) cm/s,(1.67±0.36)cm/s,t=2.537,P<0.05]、20周[(2.03±0.31)cm/s,(1.46±0.33) cm/s,t=3.981,P<0.01]和24周[(2.00±0.36)cm/s,(1.46±0.32)cm/s,t=3.545,P<0.01]均差异有显著性.LPS给药后大鼠黑质TH阳性神经元数量减少,在24周时是相应NS对照组的75.4% (P<0.01).2) LPS实验组大鼠给药后2周时,黑质纹状体部位GFAP蛋白表达量比相应NS对照组明显增高,为NS对照组的258%(P<0.01).到给药后24周时,LPS实验组大鼠黑质纹状体内GFAP蛋白表达量又比NS对照组明显增高,为NS对照组的168%(P<0.05).结论 侧脑室注射LPS引发大鼠黑质部位星形胶质细胞激活,参与了黑质多巴胺能神经元的变性过程.
目的 觀察腦室內註射脂多糖(lipopolysaccharide,LPS)引起的腦內炎癥對大鼠黑質多巴胺能神經元的慢性毒性作用,探討星形膠質細胞是否參與腦內炎癥緻大鼠多巴胺能神經元變性.方法 60隻SD大鼠分為LPS實驗組和生理鹽水(NS)對照組(n=30).大鼠右側腦室一次性註射LPS 20μl(1.25μg/μl)或同體積的NS.于給藥後不同時間檢測大鼠行為,免疫組織化學染色法觀察黑質內酪氨痠羥化酶(TH)暘性神經元,併用Western blot檢測大鼠黑質紋狀內膠質纖維痠性蛋白(GFAP)的錶達.結果 1)LPS給藥後大鼠平均運動速度呈進行性下降,與相應NS對照組相比,在16週[(2.12±0.43) cm/s,(1.67±0.36)cm/s,t=2.537,P<0.05]、20週[(2.03±0.31)cm/s,(1.46±0.33) cm/s,t=3.981,P<0.01]和24週[(2.00±0.36)cm/s,(1.46±0.32)cm/s,t=3.545,P<0.01]均差異有顯著性.LPS給藥後大鼠黑質TH暘性神經元數量減少,在24週時是相應NS對照組的75.4% (P<0.01).2) LPS實驗組大鼠給藥後2週時,黑質紋狀體部位GFAP蛋白錶達量比相應NS對照組明顯增高,為NS對照組的258%(P<0.01).到給藥後24週時,LPS實驗組大鼠黑質紋狀體內GFAP蛋白錶達量又比NS對照組明顯增高,為NS對照組的168%(P<0.05).結論 側腦室註射LPS引髮大鼠黑質部位星形膠質細胞激活,參與瞭黑質多巴胺能神經元的變性過程.
목적 관찰뇌실내주사지다당(lipopolysaccharide,LPS)인기적뇌내염증대대서흑질다파알능신경원적만성독성작용,탐토성형효질세포시부삼여뇌내염증치대서다파알능신경원변성.방법 60지SD대서분위LPS실험조화생리염수(NS)대조조(n=30).대서우측뇌실일차성주사LPS 20μl(1.25μg/μl)혹동체적적NS.우급약후불동시간검측대서행위,면역조직화학염색법관찰흑질내락안산간화매(TH)양성신경원,병용Western blot검측대서흑질문상내효질섬유산성단백(GFAP)적표체.결과 1)LPS급약후대서평균운동속도정진행성하강,여상응NS대조조상비,재16주[(2.12±0.43) cm/s,(1.67±0.36)cm/s,t=2.537,P<0.05]、20주[(2.03±0.31)cm/s,(1.46±0.33) cm/s,t=3.981,P<0.01]화24주[(2.00±0.36)cm/s,(1.46±0.32)cm/s,t=3.545,P<0.01]균차이유현저성.LPS급약후대서흑질TH양성신경원수량감소,재24주시시상응NS대조조적75.4% (P<0.01).2) LPS실험조대서급약후2주시,흑질문상체부위GFAP단백표체량비상응NS대조조명현증고,위NS대조조적258%(P<0.01).도급약후24주시,LPS실험조대서흑질문상체내GFAP단백표체량우비NS대조조명현증고,위NS대조조적168%(P<0.05).결론 측뇌실주사LPS인발대서흑질부위성형효질세포격활,삼여료흑질다파알능신경원적변성과정.
ObjectiveTo investigate the role of astrocytes in the process of long-term degeneration of dopaminergic neurons in inflammation rat model induced by intracerebroventricular injection of lipopolysaccharide (LPS). MethodsAltogether 60 SD rats were assigned into LPS group(n=30) or saline control group(n=30).All injections were made intracerebroventricularly on right side of the rats with LPS 20μl(1.25μg/μl)or saline 20μl. After injection, movement speed of rats was measured,and the changes of substantia nigra dopaminergic neurons were observed by using tyrosine-hydroxylase(TH) immunohistochemical staining. Western blot was performed to detect GFAP expression in rat substantia nigra and corpus striatum. Results1) Intracerebroventricular injection of LPS induced dopaminergic neurons degeneration in rat. Movement mean speed of LPS-treated rats decreased significantly compared with those of saline-treated rats at 16 weeks [(2.12±0.43)cm/s vs (1.67±0.36)cm/s,t=2.537,P<0.05],20 weeks [(2.03±0.31)cm/s vs (1.46±0.33) cm/s,t=3.981,P<0.01] and 24 weeks[(2.00±0.36)cm/s vs (1.46±0.32)cm/s,t=3.545,P<0.01] post injection. The number of TH-positive neurons in the substantia nigra of LPS-injected rats decreased after LPS injection. TH-positive neurons in LPS-injected rats were 75.4% of those of saline-injected group at 24 weeks (P<0.01). 2) The expression of GFAP in substantia nigra and corpus striatum in LPS-injected group was 258% of that of saline control group at 2 weeks(P<0.01),the expression of GFAP in LPS-injected group was 168% of saline control group at 24 weeks(P<0.05).ConclusionA single intracerebroventricular administration of LPS may result in the activation of astrocytes in the substantia nigra in rat, which may involve in the degeneration process of dopaminergic neurons.
