中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
4期
659-663
,共5页
周子懿%高俊鹏%向军%陈依萍%蔡业峰%罗恩丽%蔡定芳
週子懿%高俊鵬%嚮軍%陳依萍%蔡業峰%囉恩麗%蔡定芳
주자의%고준붕%향군%진의평%채업봉%라은려%채정방
帕金森病%小胶质细胞%雷公藤内酯%多巴胺能神经元
帕金森病%小膠質細胞%雷公籐內酯%多巴胺能神經元
파금삼병%소효질세포%뢰공등내지%다파알능신경원
Parkinson’ s disease%Microglia%Triptolide%Dopaminergic neuron
目的：探讨雷公藤内酯对1-甲基-4-苯基吡啶（ MPP＋）帕金森病模型大鼠的保护作用及其可能机制。方法：采用MPP＋黑质内注射建立帕金森病大鼠模型。实验分为假手术组、模型组、雷公藤内酯组及其溶剂对照组，利用酪氨酸羟化酶（ TH）免疫荧光强度测定多巴胺神经元存活率、小胶质细胞标记物OX-42免疫荧光强度测定小胶质细胞激活程度、Western blotting测定趋化因子受体CX3CR1表达量。结果：免疫组化结果表明，MPP＋黑质内注射可使模型组OX-42免疫荧光强度增高，DA神经元进行性变性死亡。雷公藤内酯组OX-42免疫荧光强度较模型组低（ P＜0.01）， TH阳性神经元数量较模型组多（ P＜0.01）。 Western blotting结果提示雷公藤内酯组CX3CR1表达量较模型组低（ P＜0.05）。结论：雷公藤内酯对MPP＋帕金森病大鼠模型具有神经保护作用，其机制可能与抑制小胶质细胞激活有关，抑制CX3 CR1可能是其抑制小胶质细胞的途径之一。
目的：探討雷公籐內酯對1-甲基-4-苯基吡啶（ MPP＋）帕金森病模型大鼠的保護作用及其可能機製。方法：採用MPP＋黑質內註射建立帕金森病大鼠模型。實驗分為假手術組、模型組、雷公籐內酯組及其溶劑對照組，利用酪氨痠羥化酶（ TH）免疫熒光彊度測定多巴胺神經元存活率、小膠質細胞標記物OX-42免疫熒光彊度測定小膠質細胞激活程度、Western blotting測定趨化因子受體CX3CR1錶達量。結果：免疫組化結果錶明，MPP＋黑質內註射可使模型組OX-42免疫熒光彊度增高，DA神經元進行性變性死亡。雷公籐內酯組OX-42免疫熒光彊度較模型組低（ P＜0.01）， TH暘性神經元數量較模型組多（ P＜0.01）。 Western blotting結果提示雷公籐內酯組CX3CR1錶達量較模型組低（ P＜0.05）。結論：雷公籐內酯對MPP＋帕金森病大鼠模型具有神經保護作用，其機製可能與抑製小膠質細胞激活有關，抑製CX3 CR1可能是其抑製小膠質細胞的途徑之一。
목적：탐토뢰공등내지대1-갑기-4-분기필정（ MPP＋）파금삼병모형대서적보호작용급기가능궤제。방법：채용MPP＋흑질내주사건립파금삼병대서모형。실험분위가수술조、모형조、뢰공등내지조급기용제대조조，이용락안산간화매（ TH）면역형광강도측정다파알신경원존활솔、소효질세포표기물OX-42면역형광강도측정소효질세포격활정도、Western blotting측정추화인자수체CX3CR1표체량。결과：면역조화결과표명，MPP＋흑질내주사가사모형조OX-42면역형광강도증고，DA신경원진행성변성사망。뢰공등내지조OX-42면역형광강도교모형조저（ P＜0.01）， TH양성신경원수량교모형조다（ P＜0.01）。 Western blotting결과제시뢰공등내지조CX3CR1표체량교모형조저（ P＜0.05）。결론：뢰공등내지대MPP＋파금삼병대서모형구유신경보호작용，기궤제가능여억제소효질세포격활유관，억제CX3 CR1가능시기억제소효질세포적도경지일。
[ ABSTRACT] AIM:To investigate the effect of triptolide on the inhibition of microglial activation in 1-methyl-4-phenyl pyridinium ( MPP+)-induced hemiparkinson disease rats.METHODS:The rat model of Parkinson disease was es-tablished by intranigral injection of MPP +.The rats were randomly divided into sham group, MPP+group, triptolide group and vehicle group.The survival of dopaminergic neurons was detected by the immunofluorescence of tyrosine hydroxylase ( TH) in the substantia nigra ( SN) .The activation of microglia was determined by immunofluorescence of OX-42 ( micro-glia marker) in the SN.The expression of chemokine receptor CX3CR1 in SN was measured by Western blotting.RE-SULTS:Intranigral injection of MPP+increased the fluorescence intensity of the microglial marker, and promoted DA neu-ron degenerative death.Immunohistological analysis showed that the OX-42 density was decreased (P<0.01) and tyrosine hydroxylase (TH) positive neurons were increased in the triptolide group (P<0.01).The expression of CX3CR1 was lower in triptolide group than that in model group (P<0.05).CONCLUSION:Triptolide may improve PA neurons func-tion in MPP+-induced rats through inhibiting CX3CR1 expression and microglial activation.
