1. 细胞的基础信息

2. 细胞常见的研究有哪些？

a) 癌变机理研究

b) 抗癌药筛选检测

c) 有关该癌症细胞耐药机制的研究

d) 建立细胞模型

3. 细胞相关的文献有哪些？

[1] 李建芬,刘嘉欣,黄凤蕊,等.依达拉奉对小鼠单核巨噬细胞白血病细胞RAW264.7炎性反应的抑制作用[J].中国药业,2024,33(14):57-60.

（目的：探讨依达拉奉（EDA）对小鼠单核巨噬细胞白血病细胞RAW264.7炎性反应的抑制作用。方法：以脂多糖诱导RAW264.7细胞，复制炎性细胞模型。采用CCK-8法检测EDA的细胞毒性作用。实验分为空白组（等体积培养基）、模型组（等体积培养基）、给药组（40μg/mL EDA）。采用Griess法检测细胞中一氧化氮（NO）水平，采用酶联免疫吸附（ELISA）法测定细胞中前列腺素E2（PGE2）、白细胞介素1β（IL-1β）、白细胞介素18（IL-18）、肿瘤坏死因子-α（TNF-α）、活性氧（ROS）水平；采用实时荧光定量聚合酶链反应（qPCR）法测定细胞中IL-1β和IL-18 mRNA表达水平；采用Western blot法检测细胞中JAK2/信号转导和转录激活因子3(STAT3)通路相关蛋白JAK2, p-JAK2, STAT3, p-STAT3, IL-1β, IL-18的蛋白表达水平。结果：与0μg/mL比较，20,40,80,160μg/mL EDA处理下细胞存活率无显著变化（P <0.05）。与模型组比较，给药组细胞中NO,PGE2,IL-1β,IL-18,TNF-α,ROS水平均显著降低（P <0.05）；IL-1β与IL-18 mRNA及蛋白表达水平和p-JAK2/JAK2与p-STAT3/STAT3均显著降低（P <0.05）。结论：EDA可能通过抑制JAK2/STAT3通路的激活而抑制RAW264.7细胞的炎性反应。）

[2] Scerba MT, Tweedie D, Greig NH. 2-(Piperidin-3-yl) phthalimides reduce classical markers of cellular inflammation in LPS-challenged RAW 264.7 cells and also demonstrate potentially relevant sigma and serotonin receptor affinity in membrane preparations. Bioorg Med Chem Lett. 2024 Sep 15;110:129885.

（Herein, we report the synthesis of new 4-amino-2-(piperidin-3-yl) isoindoline-1,3-diones and their biological evaluation in a series of in vitro experiments. The synthetic production of these materials was initiated upon the condensation of appropriate nitrophthalic acid derivatives with various 3-aminopiperidines; subsequent reduction provided the final products in moderate to good yields. Readily available chiral pool reagents facilitated entry into optically enriched samples, while the piperidine scaffold furnished a variety of amide and alkylated entries. In total, 16 candidates were produced, and their ensuing treatment in LPS-challenged RAW cells effected slight reductions in secreted TNF-α but provided more robust and dose-dependent declines in nitrite and IL-6 levels relative to basal amounts, all concurrent with maintenance of cellular viability across the concentration ranges screened. The secondary amine cohort including rac-6, (R)-7, and (S)-8 rendered the most pronounced dose-dependent reductions in nitrite and IL-6. When dosed at 30 μM, (R)-7 demonstrated the most compelling effects, with decreases of 32 % and 40 % for nitrite and IL-6, respectively. Notable reductions in the inflammatory markers were also observed for 19 which effected declines in TNF-α (14 %), nitrite (19 %), and IL-6 (11 %) when treated at 30 μM. Additionally, four representative compounds were further evaluated against numerous CNS receptors, channels, and transporters, with 6, 9, and 19 demonstrating varying degrees of nanomolar-to-low-micromolar binding to the σ-1 and σ-2 receptors and also to serotonin receptors 5HT2A, 5HT2B and 5HT3. In this regard, 6 displayed perhaps the most noteworthy affinities, with binding at σ-2 (Ki = 2.2uM), 5HT2B (Ki = 561 nM) and 5HT3 (Ki = 536 nM). Furthermore, no pronounced or dose-dependent Cereblon/DDB1 binding was observed for the screened representative compounds 6, 9, 18 and 19.）