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大花红天素对脑微血管内皮细胞凋亡的双相调节作用及机制(英文)
引用本文:钱睿哲,张国平,金惠铭,王文健,乐飞,史连国,曲晓义.大花红天素对脑微血管内皮细胞凋亡的双相调节作用及机制(英文)[J].中国病理生理杂志,2005,21(11):2086-2090.
作者姓名:钱睿哲  张国平  金惠铭  王文健  乐飞  史连国  曲晓义
作者单位:1. 复旦大学上海医学院生理与病理生理学系,上海,200032
2. 复旦大学附属华山医院中西医结合研究所,上海,200040
基金项目:SupportedpartiallybythekeysubjectofdevelopmentfoundationfromtheNational10thfiveyearplan,211project,Shanghaiscienceandtechnologyfoundation(No.014319321)andUnileverResearchandDevelopmentfoundation.
摘    要:目的:研究中药红景天的有效成分-大花红天素对小鼠脑微血管内皮细胞凋亡的作用及机制。 方法: 观察不同剂量的大花红天素(25 mg/L, 100 mg/L)对体外培养的小鼠脑微血管内皮细胞(bEnd.3株)凋亡的影响。细胞凋亡分别用流式细胞术、免疫细胞化学ABC法(Fas/Bcl-2)及Western blotting(caspase-3)测定。 结果: 与对照组比,在bEnd.3细胞中含药浓度25 mg/L组凋亡明显抑制(P<0.05),而100 mg/L组凋亡明显加剧(P<0.05)。凋亡抑制组Fas免疫细胞化学染色比对照组弱,阳性细胞明显减少(P<0.05);而Bcl-2染色比对照组强,阳性细胞明显增加(P<0.05),caspase-3表达明显抑制(P<0.05)。凋亡加剧组中(100 mg/L)变化相反。 结论: 大花红天素对bEnd.3细胞凋亡有双相调节作用,其机制与Fas/Bcl-2蛋白表达及caspase-3激活的变化有关。

关 键 词:细胞凋亡  大花红天素  bEnd.3细胞
文章编号:1000-4718(2005)11-2086-05
收稿时间:2004-12-31
修稿时间:2004-12-312005-04-13

Dual-direction effect of crenulatin on apoptosis of cerebral microvascular endothelial cells and it's mechanism
QIAN Rui-zhe,ZHANG Guo-ping,JIN Hui-ming,WANG Wen-jian,YUE Fei,SHI Lian-guo,QU Xiao-yi.Dual-direction effect of crenulatin on apoptosis of cerebral microvascular endothelial cells and it''s mechanism[J].Chinese Journal of Pathophysiology,2005,21(11):2086-2090.
Authors:QIAN Rui-zhe  ZHANG Guo-ping  JIN Hui-ming  WANG Wen-jian  YUE Fei  SHI Lian-guo  QU Xiao-yi
Institution:1DepartmentofPhysiology&Pathophysiology,ShanghaiMedicalCollege,FudanUniversity,Shanghai200032,China;2InstituteofCombinationofChineseTraditionalandWesternMedicine,HuasangHospital,Shanghai200040,China
Abstract:] AIM: To study the effect and the mechanism of crenulatin, an effective constituent of Chinese traditional medicine, on apoptosis of cerebral microvascular endothelial cells. METHODS: The following terminal concentrations of crenulatin were used in the study: 25 mg/L and 100 mg/L. Apoptosis of mouse cerebral microvascular endothelial cells (bEnd.3 cell line) was evaluated by flow cytometer, immunocytochemical assay (Fas, Bcl-2) and Western blotting (caspase-3) after culture for 24 h. RESULTS: Compared with control group, apoptosis of bEnd.3 cells in 25 mg/L group was significantly inhibited (P<0.05), but apoptosis in the 100 mg/L group was significantly increased (P<0.05). In apoptosis inhibited group, the Fas immunocytochemical staining was weaker, the positive cells were significantly decreased (P<0.05) and caspase-3 expression was decreased compared with control group; however, the Bcl-2 staining was stronger and the positive cells were significantly increased (P<0.05). On the other hand, in apoptosis increased group (100 mg/L group), the changes were just opposite. CONCLUSIONS: The effect of crenulatin on apoptosis of mouse cerebral microvascular endothelial cells possesses a dual-direction change, inhibitive effect in 25 mg/L and stimulative effect in 100 mg/L group, respectively. The mechanism is related to the alterations of Fas/Bcl-2 expression and caspase-3 activity.
Keywords:Apoptosis  Crenulation  bEnd 3 cells
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