Abstract A microporous metal-organic framework containing Co(II) as nodes with a polar pore surface, {[Co(SDB)(bpdh)0.5]}n (1), was formed via reaction of a –SO2 functionalized organic connector (H2SDB = 4,4′-sulfonyldibenzoic acid) combined with (bpdh = 2,5-bis(3-pyridyl)-3,4-diaza-2,4-hexadiene), N-rich spacer under the solvothermal conditions. The diamond channels of the framework for 1 have a size of 6.1 Å along the b axis of the crystal, and the surface area of BET is 541 m2·g−1. FT-IR spectra demonstrated 5-Fu loading and ultraviolet–visible spectra showed the loading capacity of 5-Fu of 27.36%. Compared with normal tissue of pH = 7.4, the drug release in simulated cancer tissue of pH = 5.7 was gradual, showing a rational pH-responsive drug release. Clone formation experiments and CCK-8 assay confirmed the antitumor activity of 5-Fu@1a against EOMA hemangioma cells. Detection of apoptotic protein level and Annexin V-FITC/PI analysis showed that 5-Fu@1a could induce the apoptosis in caspase-dependent manner. Antitumor ability of the 5-Fu was verified by experimental data in vivo, which is consistent with the experimental data in vitro. Graphical Abstract

中文翻译：

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微孔 Co(II)-MOF 作为 pH 响应性 5-Fu 递送系统诱导人血管瘤细胞凋亡并阻止其生长

摘要 含有 Co(II) 作为节点的微孔金属有机骨架，具有极性孔表面 {[Co(SDB)(bpdh)0.5]}n (1)，是通过 -SO2 功能化有机连接器 (H2SDB) 的反应形成的。 = 4,4'-磺酰二苯甲酸）与（bpdh = 2,5-双（3-吡啶基）-3,4-二氮杂-2,4-己二烯），在溶剂热条件下富氮间隔物。框架的金刚石通道沿晶体 b 轴的尺寸为 6.1 Å，BET 的表面积为 541 m2·g-1。FT-IR 光谱显示了 5-Fu 的负载量，紫外-可见光谱显示 5-Fu 的负载量为 27.36%。与pH = 7.4的正常组织相比，pH = 5.7的模拟癌组织中的药物释放是渐进的，表现出合理的pH响应性药物释放。克隆形成实验和 CCK-8 测定证实了 5-Fu@1a 对 EOMA 血管瘤细胞的抗肿瘤活性。凋亡蛋白水平检测和Annexin V-FITC/PI分析表明5-Fu@1a可诱导caspase依赖性凋亡。体内实验数据验证了5-Fu的抗肿瘤能力，与体外实验数据一致。图形概要