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在大鼠模型中,1,8-基能保护于由Aroclor-1254诱导的肝毒性

Hadiqa Arshad¹, Muhammed Fatih Doğan¹, Münevver Nazlıcan Zengin¹

¹Department of Pharmacology, Faculty of Medicine, Pamukkale University, Kinikli, Denizli, Turkey.

Journal of biochemical and molecular toxicology

|July 28, 2025

概括

1,8-烯通过减少氧化应激和炎症来保护雄性大鼠免受Aroclor 1254诱导的肝毒性. 这项研究证明了1,8-烯作为治疗剂的潜力,可以对抗持续有机污染物引起的肝损伤.

科学领域:

毒理学毒理学毒理学
药理学药理学是指药理学的学科.
肝病学肝病学是一种肝病学.

背景情况:

亚洛克1254 (A1254) 是一种持久性有机污染物,已知可诱导肝脏毒性.
1,8-烯醇是一种单烯,具有已证明的抗氧化和抗炎特性.

研究的目的:

为了研究1,8-cineole对雄性大鼠A1254-诱导的肝毒性的保护作用.
阐明这种保护作用的基本机制.

主要方法:

雄性威斯塔尔白色老鼠被分为四组:对照组,阿洛克,Cineole和Aroclor+Cineole.
动物接受了A1254 (腹膜内) 和/或1,8-cineole (口服) 30天的治疗.
使用ELISA,RT-PCR,组织病理学和免疫组织化学分析了肝脏组织和血清.

主要成果:

A1254增加了氧化应激 (TOS升高,TAS降低) 和亲细胞亡/炎症标志物 (Bax,TNF-α,IL-1β,iNOS,INF-γ).
1,8-烯治疗显著扭转了这些变化,减少了TOS,增加了TAS.
1,8-cineole降低了亲细胞亡的基因表达,并抑制了亲炎性细胞因子的基因表达.

结论:

1,8-烯醇对A1254引起的毒性具有显著的肝脏保护作用.
保护机制包括减少氧化损伤,抑制亡和减轻炎症.
1,8-烯显示出作为治疗性剂的潜力,用于由持久性有机污染物引起的肝损伤.

关键词:

1,8-cineoleole 的使用.灭症 (apoptosis) 是一种死亡的过程.亚洛克 1254 的使用.肝毒性肝毒性肝毒性这是一种炎症炎症炎症炎症.氧化损伤是因为氧化损伤.

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