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methyl已被证明可诱导癌细胞分化,抑制增殖并诱导细胞凋亡[2]。",{"key":242,"value":243},"体内研究","来自Bardoxolone甲基处理的猴子的肾切片显示出降低的巨蛋白蛋白表达,尽管各组中mRNA表达相似。通过光密度测定分析证实了巨蛋白蛋白质表达的可视化降低,其证明Bardoxolone甲基施用显着降低猴肾中巨蛋白蛋白质的表达。 Bardoxolone甲基给药不影响肾脏中cubilin的蛋白质表达或肾脏中cubilin的mRNA表达。给予Bardoxolone methyl的猴子肌酐清除率与基线和载体治疗的动物在第28天显着不同.Bardoxolone甲基给药28天后,从24小时尿液中测定尿白蛋白与肌酐比值(UACRs)与接受载体的动物相比,收集量显着增加。值得注意的是,载体处理动物的UACR降低了53.3％,而巴多索隆甲基处理的猴子降低了27.9％[3]。在HFD喂养(HFD\u002FBARD)期间给雄性C57BL\u002F6J小鼠口服BARD,仅喂食高脂肪饮食(HFD),或喂食低脂饮食(LFD)21周。与LFD小鼠相比,HFD小鼠F4\u002F80冠状结构的数量显着增加(+ 95％; p \u003C0.001),这被BARD有效预防(-50％; p \u003C0.01)。类似地,与LFD小鼠相比,HFD小鼠中F4\u002F80间质巨噬细胞的数量显着高98％(p \u003C0.001),与HFD\u002FBARD小鼠相比,显着高出32％(p \u003C0.01)[4]。",{"key":245,"value":246},"动物实验","猴子[3]在食蟹猴（Cynomolgus Monkeys）中进行了两项独立的研究。其中一例，食蟹猴（每性别\u002F剂量组n = 9）以5,30和300 mg \u002F kg口服给予Bardoxolone甲基，每日一次，持续12个月，中期分析为6个月，后给药后恢复分析为4周在最终剂量后，在GLP环境中。在第二项研究中，如上所述，给予Bardoxolone methyl（30mg \u002F kg每天）雌性食蟹猴（n = 6用于载体，n = 12用于治疗），每天一次，持续28天。小鼠[4]使用雄性C57BL \u002F 6J小鼠。在适应机构动物设施1周后（温度22℃，12小时光照\u002F黑暗循环），将动物分成三组（n = 7）:( 1）喂食正常饮食的小鼠（LFD组）; （2）小鼠喂食高脂饮食（HFD组）（40％脂肪）; （3）小鼠喂食相同的HFD并在饮用水（10mg \u002F kg体重）（HFD \u002F BARD组）中补充BARD。选择BARD的剂量和口服给药。 21周后，使用CO 2窒息使所有小鼠安乐死。收集每只动物的部分肠系膜脂肪量并在-80℃下储存用于Western印迹分析。另一部分肠系膜脂肪库在4％多聚甲醛中固定并包埋在石蜡中以测定形态和免疫组织化学。",{"key":248,"value":249},"参考文献","[1].\nMcCullough PA, et al. Cardiac and renal function in patients with type 2 diabetes who have chronic kidney disease: potential effectsof bardoxolone methyl. Drug Des Devel Ther. 2012;6:141-9.\n[2].\nHong DS, et al. A phase I first-in-human trial of bardoxolone methyl in patients with advanced solid tumors and lymphomas. Clin Cancer Res. 2012 Jun 15;18(12):3396-406.\n[3].\nReisman SA, et al. Bardoxolone Methyl Decreases Megalin and Activates Nrf2 in the Kidney. J Am Soc Nephrol. 2012 Oct;23(10):1663-73.\n[4].\nDinh CH, et al. Bardoxolone Methyl Prevents Mesenteric Fat Deposition and Inflammation in High-Fat Diet Mice. 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