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临界压力（KPa）：未确定\n16. 油水（辛醇\u002F水）分配系数的对数值：未确定\n17. 爆炸上限（%,V\u002FV）：未确定\n18. 爆炸下限（%,V\u002FV）：未确定\n19. 溶解性：能溶于热水、乙醇、甲醇、戊醇、丙酮、乙酸乙酯、吡啶、冰乙酸等，不溶于醚、氯仿和苯。",null,[],[250,253,256,259,262,265,268,271,274],{"key":251,"value":252},"描述","Phlorizin 是一种非选择性的 SGLT 抑制剂,对于 hSGLT1 和 hSGLT2 的 Ki 值分别为 300 和 39 nM。Phlorizin 也是一个 Na+\u002FK+-ATPase 抑制剂。",{"key":254,"value":255},"相关类别","信号通路\n>>\n跨膜转运\n>>\nNa+\u002FK+ATP酶\n信号通路\n>>\n跨膜转运\n>>\nSGLT\n天然产物\n>>\n黄酮类化合物\n研究领域\n>>\n代谢疾病",{"key":257,"value":258},"靶点","Ki: 300 nM (hSGLT1), 39 nM (hSGLT2)[1] Na+\u002FK+-ATPase[2]",{"key":260,"value":261},"体外研究","Phlorizin是一种非选择性SGLT抑制剂,hSGLT1和hSGLT2的Kis分别为300和39 nM [1]。 Phlorizin也是Na +\u002FK + -ATPase抑制剂[2]。 2×10-4M的Phlorizin抑制人红细胞膜中Na +和Rb +激活的ATP酶活性43％。在1 mM和7 mM RbCl时,rub吸收不会被2×10-4 M Phlorizin改变或略微抑制(小于15％)[2]。 Phlorizin \u003C100μM的剂量不会显着改变细胞活力。用Phlorizin预处理细胞不会显着降低亚硝酸盐或PGE2水平。 Phlorizin不抑制IL-6或TNF-α的产生,尽管100μM的Phlorizin可以显着抑制TNF-α的表达[3]。",{"key":263,"value":264},"体内研究","在Phlorizin治疗之前,SDT肥胖大鼠的血糖水平为370±49mg\u002FdL。给药后6小时,根皮苷治疗组的血糖水平降至几乎正常水平(139±32mg\u002FdL)。在12周后,根皮苷治疗的SDT肥胖大鼠比媒介物处理的SDT肥胖大鼠更重。根皮苷治疗显着降低葡萄糖排泄并延迟胰岛素降低。根据Phlorizin处理,肌酐清除率显着降低。 Phlorizin治疗23周可防止神经纤维减少(23.6±3.2纤维\u002F mm)。 Phlorizin可完全阻止视网膜异常[4]。",{"key":266,"value":267},"激酶实验","当红细胞溶血时，通过添加4×10-3M ATP和5×10-3M MgCl2（有或没有5×10-4M Phlorizin（终浓度））获得重新密封的重影。将对应于0.4-0.45mL原始血细胞的鬼与0.9mL培养基A和86RbCl一起孵育45或90分钟，并测定200μL上清液中的放射性。重新密封的重影中的ATP酶活性是由孵育后无机磷酸盐的增加决定的[1]。",{"key":269,"value":270},"细胞实验","使用RAW264.7鼠巨噬细胞衍生的细胞系。使用3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化物（MTT）测定法测量细胞活力。将细胞（105个细胞\u002F孔）在96孔板中培养，并用不同浓度的Phlorizin处理24小时。接下来，除去上清液，将细胞与MTT（50mg \u002F mL）在37℃下孵育4小时。洗涤板并加入异丙醇以溶解形态区晶体，然后使用酶标仪在570nm处测量吸光度值[3]。",{"key":272,"value":273},"动物实验","在该研究中使用雌性SDT肥胖大鼠。在6周龄时，将SDT肥胖大鼠分成两组（n = 8）; Phlorizin治疗组和媒介物治疗组。年龄匹配的雌性Sprague-Dawley（SD）大鼠用作对照动物（n = 8）。将动物饲养在气候控制室内（温度23±3℃，湿度55±15％，光照周期12小时）并允许自由获取基础饮食和水。将Phlorizin每日一次（100mg \u002F kg \u002F天）皮下注射到Phlorizin治疗组的动物中23周。向载体处理组和对照SD大鼠的动物施用20％丙二醇[4]。",{"key":275,"value":276},"参考文献","[1].\nPajor AM, et al. Inhibitor binding in the human renal low- and high-affinity Na+\u002Fglucose cotransporters. J Pharmacol Exp Ther. 2008 Mar;324(3):985-91.\n[2].\nNakagawa A, et al. Localization of the phlorizin site on Na, K-ATPase in red cell membranes. J Biochem. 1977 May;81(5):1511-5.\n[3].\nChang WT, et al. Evaluation of the anti-inflammatory effects of phloretin and phlorizin in lipopolysaccharide-stimulated mouse macrophages. Food Chem. 2012 Sep 15;134(2):972-9.\n[4].\nKatsuda Y, et al. Contribution of hyperglycemia on diabetic complications in obese type 2 diabetic SDT fatty rats: effects of SGLT inhibitor phlorizin. 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