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Cisplatin
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Cisplatin图片
包装与价格:
包装价格(元)
10mM (in 1mL DMF)电议
100mg电议
500mg电议
1g电议

产品介绍
顺铂 (CDDP) 是一种抗肿瘤化疗药物,通过与 DNA 交联并在癌细胞中造成 DNA 损伤。顺铂激活铁死亡并诱导自噬。

Cell lines

H69 SCLC cells

Reaction Conditions

H69 SCLC cells were treated with100 ng/ml cisplatin, to produce the H69-CP or 200 ng/ml cisplatin to obtain the H69CIS200 cells. These doses are below an IC50 for cisplatin and are within the range achieved in the clinical use of cisplatin.

Applications

The cells were 2- to 4-fold resistant to cisplatin, which could be used to further study the resistance mechanism.

Animal models

Adult male Wistar rats, weighing 160-200 g

Preparation Method

The rats were kept at 25 ℃ on a 12/12 h light/dark cycle, in single plastic cages with bedding, with access to standard rat food and water ad libitum. Rats were randomly assigned to one of three groups: 1) Control group, who received no intervention and maintained a regular diet; 2) Gentamicin group, who were administered 100 mg/kg BW IP gentamicin daily for 7 days; 3) Cisplatin group, who were administered 1.5 mg/kg BW IP cisplatin twice a week for 3 weeks.

Dosage form

1.5 mg/kg

Applications

Cisplatin and gentamicin could significantly elevate serum levels of creatinine, uric acid, and urea, with cisplatin showing higher elevation. Cisplatin could also significantly decrease the GSH and GPx levels.

文献引用
产品描述

Cisplatin is one of the best and first metal-based chemotherapeutic drugs, which is used for wide range of solid cancers such as testicular, ovarian, bladder, lung, cervical, head and neck cancer, gastric cancer and some other cancers. Studies confirmed that cisplatin exerts its anticancer activity by attacking more than one place. Cisplatin generally binds with genomic DNA (gDNA) or mitochondrial DNA (mtDNA) to create DNA lesions, block the production of DNA, mRNA and proteins, arrest DNA replication, activate several transduction pathways which finally led to necrosis or apoptosis.[1]

In vitro and in vivo experiments indicated that cisplatin induced cell resistance and cisplatin administrated rats exhibited increased creatinine, urea, and uric acid and this effect was more pronounced than in rats treated with gentamicin.[1][2]

References:
[1]. Stordal B, et al. Understanding cisplatin resistance using cellular models. IUBMB Life. 2007 Nov;59(11):696-9.
[2]. Abouzed TK, et al. Assessment of gentamicin and cisplatin-induced kidney damage mediated via necrotic and apoptosis genes in albino rats. BMC Vet Res. 2021 Nov 16;17(1):350.