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nM)。伊马替尼还有效抑制Kit(体外IC50,410 nM)和PDGFR(体外IC50,380 nM)[2]。伊马替尼(STI571)是v-Abl,c-Kit的多靶点抑制剂,可抑制Bcr\u002FAbl,v-Abl,Tel\u002FAbl,天然PDGFβ受体和c-Kit,但不抑制Src家族激酶,c-Fms,Flt3,EGFR或多种其他酪氨酸激酶。伊马替尼抑制表达Bcr\u002FAbl,Tel\u002FAbl,Tel \u002FPDGFβR和Tel\u002FArg的Ba\u002FF3细胞的酪氨酸磷酸化和细胞生长,每种情况下IC50约为0.5μM,但对未转化的Ba\u002FF3没有影响。细胞在IL-3或通过Tel\u002FJAK2转化的Ba\u002FF3细胞中生长[3]。伊马替尼(STI571)的IC50s是v-Abl,c-Kit和BON-1和H727细胞的多靶点抑制剂,暴露48小时后分别为32.4和32.8μM[4]。",{"key":266,"value":267},"体内研究","在硫代磷酸酯反义寡脱氧核苷酸(PS-ASODN)组中,肿瘤生长被抑制了59.437％,这显着高于伊马替尼(STI571)是v-Abl,c-Kit和组的多靶点抑制剂(11.071％) )和脂质体阴性对照组(2.759％)。与伊马替尼组(1.838±0.241),脂质体阴性对照组(2.013±0.273)和生理盐水组(2.004±0.163)相比,PS-ASODN组端粒酶活性显着降低(P \u003C0.01)(0.689±0.158) [5]。伊马替尼(25mg\u002Fkg \u002F天,口服)抑制子宫内膜异位组织的生长并减少大鼠模型中卵巢卵泡的数量。伊马替尼通过其对血管生成和细胞增殖的抑制作用有效地治疗实验性子宫内膜异位症[6]。",{"key":269,"value":270},"细胞实验","将BON-1细胞（每孔7,500个）和NCI-H727细胞（每孔5,000个）接种到平底96孔板中，一式三份，并使其在10％胎牛血清补充的DMEM或RPMI 1640完全培养基中粘附过夜。 ， 分别;然后将培养基更换为含有连续稀释的伊马替尼的无血清培养基（阴性对照）或无血清培养基。 48小时后（对照培养物未达到汇合），通过溴化3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑鎓测定法测定代谢活性细胞的数量，并测量吸光度。 Packard Spectra酶标仪，540 nm。计算生长抑制。实验一式三份进行[4]。",{"key":272,"value":273},"动物实验","小鼠[5]将40只携带肿瘤的SCID小鼠随机分成4组（每组10只小鼠）：PS-ASODN组（5μM，每只小鼠通过肿瘤内注射每天一次接受0.2mL）;伊马替尼组（0.1 mg \u002F g体重）;脂质体阴性对照组（0.01 mL \u002F g）;和生理盐水组（0.01mL \u002F g）。每组中的小鼠在植入后第7天至第28天每天一次通过肿瘤内注射接受相关治疗。 28天后，处死小鼠，分别用电子秤和游标卡尺测量肿瘤重量，最长和最短直径。计算肿瘤生长的抑制。大鼠[6]使用成年雌性Wistar-Albino大鼠（220-240g）。在第一次外科手术后21天，对大鼠进行第二次剖腹手术以评估子宫内膜异位症的发生。 24只大鼠视力确诊子宫内膜异位症植入物，随机分为3组，接受伊马替尼（25 mg \u002F kg \u002F天，口服），阿那曲唑（0.004 mg \u002F天，口服）或生理盐水（0.1 mL，ip）14天。",{"key":275,"value":276},"参考文献","[1].\nHeinrich MC, et al. Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood. 2000 Aug 1;96(3):925-32.\n[2].\nGuida T, et al. Sorafenib inhibits imatinib-resistant KIT and platelet-derived growth factor receptor beta gatekeeper mutants. Clin Cancer Res. 2007 Jun 1;13(11):3363-9.\n[3].\nOkuda K, et al. ARG tyrosine kinase activity is inhibited by STI571.Blood. 2001 Apr 15;97(8):2440-8\n[4].\nYao JC, et al. Clinical and in vitro studies of imatinib in advanced carcinoid tumors. Clin Cancer Res. 2007 Jan 1;13(1):234-40.\n[5].\nSun XC, et al. Depletion of telomerase RNA inhibits growth of gastrointestinal tumors transplanted in mice. World J Gastroenterol. 2013 Apr 21;19(15):2340-7.\n[6].\nYildiz C, et al. Effect of imatinib on growth of experimental endometriosis in rats. 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