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nM。",{"key":241,"value":242},"相关类别","信号通路\n>>\n细胞周期\u002FDNA损伤\n>>\nHDAC\n信号通路\n>>\n表观遗传学\n>>\nHDAC\n研究领域\n>>\n癌症",{"key":244,"value":245},"靶点","HDAC1:36 nM (IC50)\nHDAC2:47 nM (IC50)\nHDAC4:510 nM (IC50)\nHDAC6:14000 nM (IC50)",{"key":247,"value":248},"体外研究","罗米地辛有效抑制HDAC1和HDAC2(IC50 = 36,47 nM,分别)。罗米地辛对HDAC4和HDAC6具有轻微抑制作用(IC50 = 510,14000nM)。罗米地辛诱导组蛋白乙酰化和p21表达,EC50为3.0 nM。由于redFK在HeLa细胞中的不稳定性,Romidepsin比redFK更强,EC50为11 nM [1]。 Romidepsin的效力是TSA的100倍,在抑制A549细胞增殖方面比丁酸盐强1,000,000倍。 Romidepsin导致有丝分裂停滞,HDIs治疗导致有丝分裂染色体分离缺陷[2]。罗米地辛抑制U-937,K562和CCRF-CEM细胞的生长,IC50值分别为5.92 nM,8.36 nM和6.95 nM [3]。",{"key":250,"value":251},"体内研究","在scid小鼠淋巴瘤模型中,罗米地辛治疗小鼠每周一次或两次比对照小鼠存活时间更长,中位生存时间分别为30.5(0.56 mg\u002Fkg)和33天(0.32 mg\u002Fkg)(相对于20天)控制小鼠)。值得注意的是,用罗米地辛治疗的12只小鼠中有2只(0.56mg\u002Fkg,每周一次或两次)在60天的观察期后存活。在用罗米地辛处理48小时后,U-937细胞的凋亡群体以时间依赖性方式增加至37.7％。此外,罗米地辛诱导G1和G2\u002FM阻滞以及U-937细胞分化为CD11b(+)\u002F CD14(+)表型。在用罗米地辛处理24小时后,p21(WAF1\u002FCip1)和凝溶胶蛋白mRNA的表达分别增加至654倍和152倍。 Romidepsin在p21(WAF1\u002FCip1)启动子区域引起组蛋白乙酰化,包括Sp1结合位点[3]。",{"key":253,"value":254},"激酶实验","对于酶测定，将10μL[3H]乙酰基标记的组蛋白（25,000cpm \u002F10μg）加入到90μL从过量表达HDAC1或HDAC2的293T细胞中提取的HDAC酶级分中，在增加浓度的罗米地辛存在下，和将混合物在37℃下温育15分钟。酶反应是线性的至少1小时。加入10μL浓HCl终止反应。用1mL乙酸乙酯萃取释放的[3H]乙酸，并将0.9mL溶剂层加入5mL含水计数闪烁液II水溶液中以测定放射性。 IC50值由至少三个独立的剂量 - 反应曲线确定。",{"key":256,"value":257},"细胞实验","将细胞在96孔板中暴露于各种浓度的罗米地辛72小时。向每个孔中加入20μL5mg\u002F mL MTT的PBS溶液4小时。除去培养基后，向各孔中加入170μLDMSO以溶解甲crystals晶体。测定540nm处的吸光度。另外，将细胞与台盼蓝一起孵育，并在血细胞计数器中计数蓝色（死亡）细胞和透明（活）细胞的数量。对于细胞周期分析，将细胞在含有0.05mg \u002F mL碘化丙啶，1mM EDTA，0.1％Triton X-100和PBS中1mg \u002F mL RNase A的碘化丙锭染色溶液中孵育30分钟。然后使悬浮液通过尼龙筛网过滤器并在Becton Dickinson FACScan上分析。",{"key":259,"value":260},"动物实验","简而言之，腹膜内注射150mg \u002F kg环磷酰胺的雄性scidmice。所有注射环磷酰胺的小鼠仅在观察期内存活。环磷酰胺注射后24小时，用500μLPBS中的1×107U-937细胞腹膜内接种小鼠。在肿瘤细胞接种后24小时，用或不用FK228腹膜内处理小鼠，剂量范围为0.1至1mg \u002F kg，每周一次或两次。对照小鼠每周两次用10％HCO60盐水处理。 6只和12只小鼠分别用于FK228处理组和对照组。观察期为细胞接种后60天，通过存活时间评估抗肿瘤效果，通过Peto检验分析其统计学显着性。",{"key":262,"value":263},"参考文献","[1].\nFurumai R, et al. FK228 (depsipeptide) as a natural prodrug that inhibits class I histone deacetylases. Cancer Res. 2002 Sep 1;62(17):4916-21.\n[2].\nBlagosklonny MV, et al. Histone deacetylase inhibitors all induce p21 but differentially cause tubulin acetylation, mitotic arrest, and cytotoxicity. Mol Cancer Ther. 2002 Sep;1(11):937-41.\n[3].\nSasakawa Y, et al. Effects of FK228, a novel histone deacetylase inhibitor, on human lymphoma U-937 cells in vitro and in vivo. 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