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奥布图西福林通过Nrf2/HO-1信号通路改善了西斯普拉丁诱导的肝脏毒性

Selcan Cesur¹, Berrin Yalinbas-Kaya², Ali Tureyen²

¹Department of Gastroenterology, Ministry of Health Eskisehir City Hospital, 26080, Eskisehir, Turkey. drselcancesur@gmail.com.

Naunyn-Schmiedeberg's archives of pharmacology

|February 20, 2025

概括

奥布图西福林 (OBS) 通过减少氧化应激和亡,保护免受西斯 (CIS) 诱导的肝脏和脏毒性. 这项研究表明,OBS是减轻化疗副作用的潜在治疗剂.

科学领域:

药理学药理学是指药理学的学科.
毒理学毒理学毒理学
生物化学生物化学

背景情况:

西斯 (CIS) 是一种强大的化疗剂,具有显著的肝脏毒性.
奥布图西福林 (OBS) 具有已知的抗氧化和抗糖尿病特性.
需要研究OBS对CIS引起的器官损伤的保护作用.

研究的目的:

在雄性小鼠中研究奥布图西福林 (OBS) 对西斯 (CIS) 诱导的肝脏毒性保护作用.
阐明OBS保护作用的潜在机制,重点关注氧化应激,炎症和亡.

主要方法:

雄性小鼠接受了OBS (0.5和1毫克/公斤) 10天,CIS (20毫克/公斤) 于第7天.
分析了生物化学标记物 (AST,ALT,ALP,BUN,肌),氧化应激标记物 (MDA,GSH,SOD,CAT) 和基因/蛋白质表达 (Nrf2,HO-1,Bcl-2,NF-κB,TNF-α,Bax,Cas-3).这些标记物包括:
对肝脏和脏组织进行了组织病理学检查.

主要成果:

OBS显著降低了CIS诱导的肝脏和损伤标志物 (AST,ALT,ALP,BUN,肌) 的升高.
在肝脏和脏组织中,OBS降低了脂质过氧化 (MDA) 和增强了抗氧化防御 (GSH,SOD,CAT).
OBS调节了参与氧化应激,炎症和亡的关键基因和蛋白质的表达,包括Nrf2/HO-1通路,并减少了他的病理损伤.

结论:

奥布图西福林 (OBS) 显示出显著的保护作用,防止西斯 (CIS) 诱导的肝脏毒性.
通过减少氧化应激,炎症和亡,OBS可减轻CIS引起的器官损伤.
OBS的机制涉及Nrf2/HO-1通路的调节,这表明它有可能作为化疗相关副作用的治疗剂.

关键词:

西斯普拉丁诱导的肝脏毒性炎症炎症是一种炎症.Nrf2 / HO-1 的一个.获得了folin 的优势.氧化应激是一种氧化应激.

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