Cisplatin  (Synonyms: 顺铂; cis-Platinum; CDDP; cis-Diaminodichloroplatinum)

HeLa and A549 cells are maintained in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum, 100 units of Penicillin, and 100 μg of Streptomycin/mL. They are cultured at 37°C in a humidified chamber containing 5% CO₂. For the induction of apoptosis, cells are plated in 60-mm dishes 1 day prior to Cisplatin (0-30 μM) treatment^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Mice^[3]
Mice are divided randomly into three groups (Control, Cisplatin and Cisplatin+HemoHIM), and each group consists of twenty mice. B16F0 melanoma (5×10⁵ cells/mouse) is inoculated into subcutaneous femoral left region of mice at 3 days before an initial injection of Cisplatin. Cisplatin is injected intraperitoneally at 4 mg/kg body weight (B.W.) on day 0, 7 and 14 (total three injections). Experimental group is 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 are experimented, respectively, to evaluate tumor weight or tumor size. The tumor size is calculated as follows: tumor size=ab²/2, where a and b are the larger and smaller diameters, respectively.
Rats^[4]
Male Sprague-Dawley rats weighing 200 to 250 g are divided at random into 4 groups of 4 or 5 animals each. The first group (control) received a vehicle (5% carboxymethyl cellulose sodium solution (CMC-Na), 5 mL/kg body wt., p.o.) used for Capsaicin (Cap). The second group received Cap (10 mg/kg/d, p.o.) in 5% CMC-Na (5 mL/kg), and the third received 5% CMC-Na for 6 consecutive days injected with Cisplatin (5 mg/kg in physiological saline solution, i.p.). The fourth group received Cap (10 mg/kg/d, p.o.) in 5% CMC-Na for 6 consecutive days after Cisplatin injection (5 mg/kg, i.p.). For all groups, Cap or vehicle is given twice daily. The selected Cap concentration and the dose administration schedule without inducing any rat intestinal damage are chosen using data from our preliminary experiments.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Wang X, et al. Requirement for ERK activation in cisplatin-induced apoptosis. J Biol Chem. 2000 Dec 15;275(50):39435-43.  [Content Brief]

  [2]. Cummings BS, et al. Cisplatin-induced renal cell apoptosis: caspase 3-dependent and -independent pathways. J Pharmacol Exp Ther. 2002 Jul;302(1):8-17.  [Content Brief]

  [3]. Park HR, et al. Enhanced antitumor efficacy of cisplatin in combination with HemoHIM in tumor-bearing mice. BMC Cancer. 2009 Mar 17;9:85.  [Content Brief]

  [4]. Shimeda Y, et al. Protective effects of capsaicin against cisplatin-induced nephrotoxicity in rats. Biol Pharm Bull. 2005 Sep;28(9):1635-8.  [Content Brief]

  [5]. Hall MD, et al. Say no to DMSO: dimethylsulfoxide inactivates cisplatin, NSC 241240, and other platinum complexes. Cancer Res. 2014 Jul 15;74(14):3913-22.  [Content Brief]

  [6]. Wu K, et al. Cisplatin inhibits the progression of bladder cancer by selectively depleting G-MDSCs: A novel chemoimmunomodulating strategy. Clin Immunol. 2018 Aug;193:60-69.  [Content Brief]

  [7]. Noha Alassaf, et al. Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential. Front Pharmacol. 2023 Jan 30:14:1103062.  [Content Brief]

  [8]. Ryan M Williams, et al. Kidney-Targeted Redox Scavenger Therapy Prevents Cisplatin-Induced Acute Kidney Injury. Front Pharmacol. 2022 Jan 3:12:790913.  [Content Brief]