细胞与分子免疫学杂志
細胞與分子免疫學雜誌
세포여분자면역학잡지
2009年
11期
994-997
,共4页
雷志年%曾水林%王磊%朱建宝%李涛
雷誌年%曾水林%王磊%硃建寶%李濤
뢰지년%증수림%왕뢰%주건보%리도
脑中风%神经炎症%Parthenolide%神经发生%TNF-α
腦中風%神經炎癥%Parthenolide%神經髮生%TNF-α
뇌중풍%신경염증%Parthenolide%신경발생%TNF-α
stroke%neuroinflammation%parthenolide%neurogenesis%TNF-α
目的:检测Parthenolide是否抑制脑缺血诱发的神经炎症及其分子机制.方法:MCAO大鼠腹腔注射parthenolide (500 μg/kg), 行BrdU、 BrdU-DCX、 BrdU-Tuj-1、 BrdU-MAP-2、 BrdU-GFAP免疫组化和Western blot检测缺血侧纹状体组织TNF-α表达水平.结果:脑缺血增加缺血侧纹状体内TNF-α表达水平, Parthenolide抑制TNF-α的表达并促进缺血侧纹状体内新生细胞的增殖.给予Parthenolide在脑缺血后3 d、 7 d 或28 d增加BrdU~+-DCX~+, BrdU~+-Tuj-1~+, and BrdU~+-MAP-2~+阳性细胞数, 同时减少BrdU~+-GFAP~+阳性细胞数.结论:Parthenolide抑制脑缺血诱发的神经炎症, 促进非神经发生区-纹状体内神经发生.尚需在此模型上进一步阐明其分子作用机制.
目的:檢測Parthenolide是否抑製腦缺血誘髮的神經炎癥及其分子機製.方法:MCAO大鼠腹腔註射parthenolide (500 μg/kg), 行BrdU、 BrdU-DCX、 BrdU-Tuj-1、 BrdU-MAP-2、 BrdU-GFAP免疫組化和Western blot檢測缺血側紋狀體組織TNF-α錶達水平.結果:腦缺血增加缺血側紋狀體內TNF-α錶達水平, Parthenolide抑製TNF-α的錶達併促進缺血側紋狀體內新生細胞的增殖.給予Parthenolide在腦缺血後3 d、 7 d 或28 d增加BrdU~+-DCX~+, BrdU~+-Tuj-1~+, and BrdU~+-MAP-2~+暘性細胞數, 同時減少BrdU~+-GFAP~+暘性細胞數.結論:Parthenolide抑製腦缺血誘髮的神經炎癥, 促進非神經髮生區-紋狀體內神經髮生.尚需在此模型上進一步闡明其分子作用機製.
목적:검측Parthenolide시부억제뇌결혈유발적신경염증급기분자궤제.방법:MCAO대서복강주사parthenolide (500 μg/kg), 행BrdU、 BrdU-DCX、 BrdU-Tuj-1、 BrdU-MAP-2、 BrdU-GFAP면역조화화Western blot검측결혈측문상체조직TNF-α표체수평.결과:뇌결혈증가결혈측문상체내TNF-α표체수평, Parthenolide억제TNF-α적표체병촉진결혈측문상체내신생세포적증식.급여Parthenolide재뇌결혈후3 d、 7 d 혹28 d증가BrdU~+-DCX~+, BrdU~+-Tuj-1~+, and BrdU~+-MAP-2~+양성세포수, 동시감소BrdU~+-GFAP~+양성세포수.결론:Parthenolide억제뇌결혈유발적신경염증, 촉진비신경발생구-문상체내신경발생.상수재차모형상진일보천명기분자작용궤제.
AIM: The objective of this study was to test the hypothesis that parthenolide suppresses ischemia-induced neuroinflammation in the MCAO model of adult rat. METHODS: MCAO rats were treated i.p. with parthenolide (500 μg/kg). Brain sections were analyzed for BrdU, BrdU-DCX, BrdU-Tuj-1, BrdU-MAP-2 and BrdU-GFAP staining. Total protein was extracted from ischemic striatum, and Western blot was used to determine TNF-α expression. RESULTS: Cerebral ischemia increases expression of TNF-α in the ischemic striatum. Parthenolide suppressed the expression of TNF-α and enhances the proliferation of newborn cells in the ischemic striatum. The cell number of BrdU~+-DCX~+, BrdU~+-Tuj-1~+, and BrdU~+-MAP-2~+ is increased in the ischemic striatum after parthenolide treatment at 3 d, 7 d or 28 d after MCAO. Furthermore, parthenolide depressed the cell number of BrdU~+-GFAP~+ in the ischemic striatum at 3 d, 7 d and 28 d after MCAO. CONCLUSION: Parthenolide inhibits neuroinflammation induced by cerebral ischemia and promotes neurogenesis in the ischemic striatum. Further study of the effects of parthenolide on inflammatory gene expression using model animal systems as described here are critical to elucidating their mechanisms of action.
