体重(g)、血糖(mmol/L)和HbA1c(%):成模10周时,DM组和DT组大鼠体重分别为266 77±55 47和279 5

体重(g)、血糖(mmol/L)和HbA1c(%):成模10周时,DM组和DT组大鼠体重分别为266.77±55.47和279.50±43.56,增长幅度小于NC组的356.22±50.73(P<0.001);NC组大鼠血糖(5.72±1.22)、HbA1c(3.30±0.10)保持在正常范围内,DM组和DT组血糖分别为25.37±3.56和23.54±8.70,HbA1c分别为5.92±0.72和6.12±0.07,均显著高于NC组(P0.05)。 {Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|selleck Anti-infection Compound Library|selleck Antiinfection Compound Library|selleck Anti-infection Compound Library|selleck Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|buy Anti-infection Compound Library|Anti-infection Compound Library半抑制浓度|Anti-infection Compound Library价格|Anti-infection Compound Library花费|Anti-infection Compound Library溶解度|Anti-infection Compound Library购买|Anti-infection Compound Library制造商|Anti-infection Compound Library查找购买|Anti-infection Compound Library订单|Anti-infection Compound Library mouse|Anti-infection Compound Library chemical structure|Anti-infection Compound Library分子量|Anti-infection Compound Library molecular weight|Anti-infection Compound Library数据表|Anti-infection Compound Library supplier|Anti-infection Compound Library体外|Anti-infection Compound Library细胞系|Anti-infection Compound Library concentration|Anti-infection Compound Library nmr|Anti-infection Compound Library体内|Anti-infection Compound Library clinical trial|Anti-infection Compound Library cell assay|Anti-infection Compound Library screening|Anti-infection Compound Library high throughput|buy Antiinfection Compound Library|Antiinfection Compound Library半抑制浓度|Antiinfection Compound Library价格|Antiinfection Compound Library花费|Antiinfection Compound Library溶解度|Antiinfection Compound Library购买|Antiinfection Compound Library制造商|Antiinfection Compound Library查找购买|Antiinfection Compound Library订单|Antiinfection Compound Library chemical structure|Antiinfection Compound Library数据表|Antiinfection Compound Library supplier|Antiinfection Compound Library体外|Antiinfection Compound Library细胞系|Antiinfection Compound Library concentration|Antiinfection Compound Library clinical trial|Antiinfection Compound Library cell assay|Antiinfection Compound Library screening|Antiinfection Compound Library high throughput|Anti-infection Compound high throughput screening| 2.肾功能及肾重/体重比:糖尿病大鼠的肾功能受累,成模10周时,DM组与DT组大鼠尿MA/Cre(mg/mmol)分别为17.35±3.51和15.54±3.57,较NC组(3.79±1.02)明显升高(P<0.05);DM组与DT组相对肾重(%)分别为6.09±0.91和5.93±0.69,较NC组(4.03±0.50)明显升高(P0.05)。各组血肌酐、肌酐清除率值无明显的统计学意义(P>0.05)。

3.肾组织病理变化:PAS及PASM染色显示,DM组大鼠肾小球系膜基质明显增多,系膜细胞增生,基底膜增厚,少数表现为结节性肾小球硬化改变,符合糖尿病肾病病变特征。而治疗组上述病理改变均有不同程度减轻。 4. RT-PCR:DM组IGF-1 mRNA表达量(0.52±0.17)较NC组(0.38±0.11)明显上调(P0.05)。DM和DT组的Akt1 mRNA表达量分别为1.02±0.58和0.89±0.34,较NC组(0.56±0.19)明显增多(P<0.05),DT组的表达量低于DM组(P<0.001),DT组大鼠p-Akt水平(0.65±0.06)较DM组降低(P<0.001);DM组及DT组Akt1的表达量分别为15.49±2.33和9.20±1.27,与NC组(3.01±1.13)比较显著增加(P<0.001),DT组较DM组显著减少(P
目的

也许 探讨糖原合成酶激酶-3β(glycogen synthase kinase-3β,GSK-3β)在曲古抑菌素A (trichostatin A ,TSA)诱导的肺腺癌A549细胞生长抑制、周期阻滞和抑制肿瘤细胞浸润转移中的作用及其可能机制。 方法 常规传代培养A549细胞,分组予以不同浓度的TSA干预和GSK-3β酶抑制剂预处理后进行相关实验;MTT比色法检测TSA对A549细胞增殖的影响,并用GSK-3β特异性小分子抑制剂SB216763抑制GSK-3β活性后,观察上述浓度的TSA对A549细胞生长的作用效果;流式细胞仪分析用酶抑制剂干预前后TSA作用A549细胞的周期变化;Transwell小室法检测抑制GSK-3β活性前后TSA对A549细胞的侵袭力的影响;Western Blot法检测不同浓度的TSA对A549细胞中GSK-3β、磷酸化的GSK-3β(pGSK-3β)蛋白和粘附分子E-cadherin蛋白表达水平及用酶抑制剂预处理后TSA作用A549细胞24h上述蛋白水平的变化;免疫细胞化学法检测予酶抑制剂前后各组细胞中细胞周期素依赖性激酶抑制剂p27的蛋白水平。

结果 1、MTT法结果显示TSA抑制A549细胞的增殖,此作用呈剂量依赖性(P<0.05);用酶抑制剂SB216763预处理后明显减弱了TSA对A549细胞的生长抑制作用和细胞周期阻滞(P<0.05);用酶抑制剂SB216763预处理后A549细胞侵袭力较单用TSA组增加(P0.05);12.5ug/L的TSA并不影响A549细胞中pGSK-3β和p27蛋白表达情况(P>0.05),从25ug/L组起,pGSK-3β蛋白水平降低,E-cadherin蛋白和p27蛋白表达增加(P<0.05);酶抑制剂SB216763使活性受抑制形式的GSK-3β(pGSK-3β)表达增加,而下调E-cadherin和p27的蛋白水平(P
蛋白磷酸酯酶-2A(PP2A)是多功能的蛋白质丝氨酸/苏氨酸磷酸酯酶。PP2A由一个催化亚基C和结构亚基A组成的核心酶,和另一个调节亚基B所组成。PP2A翻译后催化亚基的修饰调节影响PP2A活性的调节。PP2A催化亚基Tyr307位点经蛋白酪氨酸激酶(如src)磷酸化后活性下降;催化亚基Leu309位点可以被PP2A特异性甲基转移酶(PPMT1)/甲酯酶(PME-1)甲基化/去甲基化修饰调节,甲基化后可增强PP2A活性。PP2A与糖原合酶激酶-3(GSK-3)是微管相关蛋白Tau磷酸化修饰调节最为重要的蛋白磷酸酯酶和磷酸激酶,它们的调节失衡可造成Tau过度磷酸化,导致AD样改变。在阿尔茨海默病患者脑中PP2A活性下降,其具体机制还不明确。我们课题组已经发现,GSK-3可上调蛋白磷酸酯酶抑制因子-2 没有 (I2PP2A)的表达水平而下调PP2A活性,GSK-3与I2PP2A相关系数R=0.9158,GSK-3活性与PP2A活性成负相关系数R=0.9166,而I2PP2A与PP2A负相关系数R=0.

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