阿戈美拉汀对阿霉素肝毒性的改善作用。

IF 2.7 3区 医学 Q2 PHARMACOLOGY & PHARMACY
Hasan Basri Savas, Mehmet Enes Sozen, Gokhan Cuce, Tuba Batur
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引用次数: 0

摘要

药物引起的肝毒性是阿霉素使用的一个重大障碍,阿霉素是一种常用的化疗药物,在癌症治疗中已确立疗效。本研究旨在确定阿戈美拉汀在大鼠毒性模型中对阿霉素肝毒性的潜在保护作用。将32只大鼠分为4组:对照组(生理盐水给药)、Doxo组(阿霉素40mg /kg给药)、Doxo + Ago20组和Doxo + Ago40组(阿戈美拉汀20、40mg /kg给药和阿霉素40mg /kg给药)。处死14只大鼠,取标本进行免疫组化、血液学、生化分析比较。在免疫组织化学、血液学和生化参数方面,研究组之间存在统计学差异。阿戈美拉汀降低了阿霉素增加的tnf - α和caspase-3,并逆转了阿霉素改变的氧化应激标志物水平(p
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ameliorative effects of agomelatine against doxorubicin-induced hepatotoxicity.

Drug-induced hepatotoxicity is a significant impediment to the use of doxorubicin, a commonly employed chemotherapeutic agent with established efficacy in cancer treatment. The present study aimed to determine the potential protective effects of agomelatine against doxorubicin hepatotoxicity in rat toxicity models. Thirty-two rats were divided into four groups: control (with saline administration), Doxo (with 40 mg/kg doxorubicin administration), Doxo + Ago20, and Doxo + Ago40 (with 20 and 40 mg/kg agomelatine administration and 40 mg/kg doxorubicin administration). On the day of 14 rats were sacrificed, samples were collected for comparison of immunohistochemical, hematological, and biochemical analysis. There were statistically significant differences between the study groups in terms of immunohistochemical, hematological, and biochemical parameters. Agomelatine administration reduced the TNF-alpha, and caspase-3, which increased by doxorubicin, and reversed levels of oxidative stress markers altered by doxorubicin (p < 0.05). Doxorubicin induces oxidative stress, apoptosis, and hepatotoxicity. Agomelatine may be favored as a primary antidepressant to mitigate hepatic damage induced by doxorubicin.

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来源期刊
BMC Pharmacology & Toxicology
BMC Pharmacology & Toxicology PHARMACOLOGY & PHARMACYTOXICOLOGY&nb-TOXICOLOGY
CiteScore
4.80
自引率
0.00%
发文量
87
审稿时长
12 weeks
期刊介绍: BMC Pharmacology and Toxicology is an open access, peer-reviewed journal that considers articles on all aspects of chemically defined therapeutic and toxic agents. The journal welcomes submissions from all fields of experimental and clinical pharmacology including clinical trials and toxicology.
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