Methods:Immunohistochemical

staining with SP method was c

Methods:Immunohistochemical

staining with SP method was conducted to determine the expressions of GSK-3beta,Beta-catenin and PPAR-gamma in 48 cases of medulloblastoma and 10 normal cerebellar tissues. Results:The rate of abnormal expressions of beta-catenin and PPAR-gamma in MB was higher than that in normal. Conversely,GSK-3beta in MB was lower than that in the normal 那个 (P

目的研究糖原合酶激酶3β(glycogen synthase kinase-3β,GSK-3β)抑制剂抗前列腺癌细胞裸鼠移植瘤生长的效用。方法建立前列腺癌PC-3和LNCaP/Bcl-xL细胞株裸鼠移植瘤模型,观测GSK-3β抑制剂氯化锂(LiCl)及SB216763腹腔内给药后移植瘤重量及体积的变化。同时通过BrdU掺入的免疫组化染色探讨移植瘤的增殖状态,TUNEL染色比较对移植瘤细胞凋亡的影响。结果LiCl及SB216763均可明显抑制移植瘤生长(P<0.05)。与对照组相比,LiCl给药组细胞BrdU标记明显降低(P<0.05),TUNEL染色差异无统计学意义。结论抑制GSK-3β活性可抑制前列腺癌裸鼠移植瘤细胞在体内的生长,其中LiCl可能通过干扰癌细胞DNA复制发挥作用。
BACKGROUND: Previous studies have demonstrated that mutant amyloid precursor protein

(APP)or presenilin-1 (PS1) genes increase susceptibility to ischemic brain damage induced by middlecerebral artery occlusion. Possible mechanisms include over-production of beta-amyloid peptide(Aβ).OBJECTIVE: Because Aβ is over-produced FDA-approved Drug Library chemical structure in the APP/PS1 double-transgenic mouse, the presentstudy focused on mechanisms of increased ischemic damage due to mutant APP and PS1 genes bymeasuring oxidative stress, mitochondrial function, and calcium homeostasis.DESIGN, TIME AND SETTING: The non-randomized, controlled, in vivo and in vitro

这个 experimentswere performed at the Medical Research Center, Second Clinical College, Jinan University betweenMay and October 2008.MATERIALS: Male APP transgenic mice carrying the mutant 695swe gene and female PS1transgenic mice carrying the mutant Leu235Pro gene were donated from the University of HongKong. SHSY5Y human neuroblastoma cells were purchased from ATCC (Manassas, VA, USA), andAβ_(1-42) was obtained from Sigma-Aldrich (St. Louis, MO, USA).METHODS: APP transgenic mice were mated with PS1 transgenic mice to produce APP/PS1double-transgenic mice and wildtype littermates mice. The photothrombotic stroke model wasinduced in six APP/PS1 double-transgenic and 6 wildtype littermates mice.

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