| 名称 | Cisplatin |
| 描述 | Cisplatin (CDDP) is a chemotherapeutic agent with antitumor activity and is a classic DNA crosslinker. It inhibits DNA synthesis and induces DNA damage in cancer cells by forming DNA adducts, ultimately leading to cell death. In addition, Cisplatin can activate ferroptosis and induce autophagy. In animal studies, it is commonly used to establish models of chronic kidney injury and acute renal failure. |
| 细胞实验 | Rabbit renal proximal tubules were isolated using the iron oxide perfusion method and grown in 35-mm tissue culture dishes under improved conditions as described previously. The cell culture medium was a 1:1 mixture of Dulbecco's modified Eagle's medium/Ham's F-12 (without D-glucose, phenol red, or sodium pyruvate) supplemented with 15 mM HEPES buffer, 2.5 mM L-glutamine, 1 μM pyridoxine HCl, 15 mM sodium bicarbonate, and 6 mM lactate. Hydrocortisone (50 nM), selenium (5 ng/ml), human transferrin (5 μg/ml), bovine insulin (10 nM), and L-ascorbic acid-2-phosphate (50 μM) were added to fresh culture medium immediately before daily media change. In general, confluent RPTCs were treated with inhibitors or diluent control [typically DMSO at 0.1% (v/v)] for 30 min before treatment with cisplatin. Aliquots of RPTCs were used for various assays as detailed below [1]. |
| 动物实验 | Mice were divided randomly into three groups (Control, Cisplatin and Cisplatin+HemoHIM), and each group consisted of twenty mice. B16F0 melanoma (5 × 10^5 cells/mouse) was inoculated into subcutaneous femoral left region of mice at 3 days before an initial injection of cisplatin. Cisplatin was injected intraperitoneally at 4 mg/kg body weight (B.W.) on day 0, 7 and 14 (total three injections). Experimental group was intubated with HemoHIM at a final concentration of 100 mg/kgB.W. by everyday from day -1 to day 16, while the control group received only water. On day 17 after initial injection of cisplatin, all mice of each group were experimented, respectively, to evaluate tumor weight or tumor size. The tumor size was calculated as follows: tumor size = ab^2/2, where a and b are the larger and smaller diameters, respectively [3]. |
| 体外活性 | 方法：人非小细胞肺癌细胞 A549、SKMES-1、MOR 和 H460 用 Cisplatin (0.001-100 μM) 处理 72 h，使用 MTT 方法检测细胞生长抑制情况。
结果：Cisplatin 剂量依赖性地抑制 A549、SKMES-1、MOR 和 H460 细胞生长，IC50 分别为 1.58 µM、4.09 µM、6.39 µM 和 5.72 µM。[1]
方法：人乳腺癌 MCF-7 和 MDA-MB-231 用 Cisplatin (2-10 μg/mL) 处理 48 h，使用 Western Blot 方法检测靶点蛋白表达水平。
结果：Cisplatin 剂量依赖性诱导 MCF-7 和 MDA-MB-231 细胞中凋亡相关蛋白 cleaved-caspase 3 和 cleaved-PARP 的水平增加。[2]
方法：间皮瘤细胞 JU77、LO68 和 ONE58 用 Cisplatin (5-100 μg/mL) 处理 24 h，使用 JC-1 染料检测线粒体膜电位 (MMP)。
结果：Cisplatin 剂量依赖性降低 JU77、LO68 和 ONE58 细胞的 MMP，抑制线粒体功能。[3] |
| 体内活性 | 方法：为检测体内抗肿瘤活性，将 Cisplatin (5 mg/kg/6 天) 和 Chloroquine (13 mg/kg/天) 腹腔注射给携带咽下鳞状细胞癌肿瘤 (HSCC) FaDu 的 BALB/c nude 小鼠，持续十八天。
结果：Cisplatin 治疗显著抑制 HSCC 肿瘤生长，Chloroquine 抑制自噬并增加 Cisplatin 诱导的细胞凋亡，从而增强了 Cisplatin 的疗效，导致小鼠的肿瘤生长减少和生存期延长。[4]
方法：为减轻 Cisplatin 治疗引起的肾毒性，将 Cisplatin (3-6 mg/kg/3天) 腹腔注射和 Cilastatin (100 mg/kg/天) 皮下注射给人肺腺癌肿瘤 A549 的 BALB/c 小鼠，持续七天。
结果：Cilastatin 可以在不影响 Cisplatin 抗肿瘤作用的情况下减少其诱导的肾毒性。[5] |
| 存储条件 | keep away from direct sunlight | Powder: -20°C for 3 years | Shipping with blue ice/Shipping at ambient temperature. |
| 溶解度 | H2O : 1 mg/mL (3.3 mM), Heating to 50℃ is recommended.（DMSO can inactivate Cisplatin's activity.)
DMF : 20 mg/mL (66.66 mM), Sonication is recommended.
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| 关键字 | RNASynthesis | RNA Synthesis | Inhibitor | inhibit | Ferroptosis | drug | DNASynthesis | DNAAlkylator | DNA Synthesis | DNA synthesis | DNA Alkylator/Crosslinker | DNA Alkylator | DNA | damage | cross-linking | Crosslinker | cis-Platinum | Cisplatin | chemotherapy | Autophagy | antineoplastic |
| 相关产品 | Naringin | Guanidine hydrochloride | L-Glutamic acid | Gefitinib | Cysteamine hydrochloride | Alginic acid | Aceglutamide | Hydroxychloroquine | Stavudine | Thymidine | Paeonol | Sodium 4-phenylbutyrate |