解剖学报
解剖學報
해부학보
ACTA ANATOMICA SINICA
2009年
4期
533-538
,共6页
柯荔宁%王玮%徐剑文%林建银
柯荔寧%王瑋%徐劍文%林建銀
가려저%왕위%서검문%림건은
人参皂苷Rb1%小胶质细胞N9%缺氧%应激活化%免疫荧光法%小鼠
人參皂苷Rb1%小膠質細胞N9%缺氧%應激活化%免疫熒光法%小鼠
인삼조감Rb1%소효질세포N9%결양%응격활화%면역형광법%소서
Ginsenoside Rb1%Microglia N9%Hypoxic%Activation%Immunofluorescence
目的 探讨人参皂苷Rb1对缺氧诱导的小胶质细胞活化的的影响. 方法 通过人参皂苷Rb1对缺氧状态下N9细胞的干预,检测细胞形态、增殖活力改变.采用ELISA法、荧光探针DAF-FM DA、Griess Reagent法检测细胞TNF-α、O-2产量以及NO含量改变的影响.借助化学发光法、免疫荧光法分别检测各组细胞线粒体膜电位、细胞色素C含量. 结果 无论是预防性给药还是治疗性给药,人参皂苷Rb1能明显降低缺氧诱导活化的N9细胞NO、O-2以及TNF-α产量,抑制线粒体膜电位的降低,缓解细胞内细胞色素C含量的改变程度. 结论 人参皂苷Rb1均能在一定程度上下调由于缺氧活化导致神经毒性因子的高表达,稳定细胞线粒体的结构和功能,抑制缺氧诱导的N9细胞活化.
目的 探討人參皂苷Rb1對缺氧誘導的小膠質細胞活化的的影響. 方法 通過人參皂苷Rb1對缺氧狀態下N9細胞的榦預,檢測細胞形態、增殖活力改變.採用ELISA法、熒光探針DAF-FM DA、Griess Reagent法檢測細胞TNF-α、O-2產量以及NO含量改變的影響.藉助化學髮光法、免疫熒光法分彆檢測各組細胞線粒體膜電位、細胞色素C含量. 結果 無論是預防性給藥還是治療性給藥,人參皂苷Rb1能明顯降低缺氧誘導活化的N9細胞NO、O-2以及TNF-α產量,抑製線粒體膜電位的降低,緩解細胞內細胞色素C含量的改變程度. 結論 人參皂苷Rb1均能在一定程度上下調由于缺氧活化導緻神經毒性因子的高錶達,穩定細胞線粒體的結構和功能,抑製缺氧誘導的N9細胞活化.
목적 탐토인삼조감Rb1대결양유도적소효질세포활화적적영향. 방법 통과인삼조감Rb1대결양상태하N9세포적간예,검측세포형태、증식활력개변.채용ELISA법、형광탐침DAF-FM DA、Griess Reagent법검측세포TNF-α、O-2산량이급NO함량개변적영향.차조화학발광법、면역형광법분별검측각조세포선립체막전위、세포색소C함량. 결과 무론시예방성급약환시치료성급약,인삼조감Rb1능명현강저결양유도활화적N9세포NO、O-2이급TNF-α산량,억제선립체막전위적강저,완해세포내세포색소C함량적개변정도. 결론 인삼조감Rb1균능재일정정도상하조유우결양활화도치신경독성인자적고표체,은정세포선립체적결구화공능,억제결양유도적N9세포활화.
Objective To activate microglia N9 cell through the oxygen deficit, and to discuss the influence to the N9 cell by ginsenoside Rb1, laying the foundation for the basic study and the clinical medicine development. Methods Through ginsenoside Rb1 intervention, the cell morphology the proliferation ability were observed, ELISA, fluorescent probe DAF-FM DA, Griess the reagent examination, were used to measure TNF-α, the O-2 output, the NO content change, chemiluminescence, the immunofluorescence method, and plastochondria membrane potential, were carried out to detect the cytochrome C content. Results Regardless of being preventive or medical gives, ginsenoside Rb1 can decline the NO,O-2,TNF-α high expression; and reduce the plastochondria membrane potential changing, the cytochrome C redistribution. Conclusion Ginsenoside Rb1 can decline N9 cell activation to a certain extent, reduce expression of the nerve toxic factor, and to stabilize mitochondrial membrane potential and distribution of cytochrome C.