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通过抑制由于与肝脏NF-kβ相关的氧化应激减小而导致的库普弗细胞增生,皮里多克萨尔酸盐对中毒的肝脏保护作用

Arshia Mahdavi¹, Sina Mahdavifard^2,3, Mohammad Mazani¹

¹Department of Clinical Biochemistry, Faculty of Medicine, Ardabil University of Medical Sciences, P.O. Box, 56189-85991, Ardabil, Iran.

Naunyn-Schmiedeberg's archives of pharmacology

|September 22, 2025

概括

酸 (PLP) 通过减少炎症和氧化应激,保护肝脏免受 (Pb) 毒害. PLP治疗抑制了库普弗细胞增生,增强了肝脏的抗氧化能力,提供了一个有前途的治疗策略.

科学领域:

毒理学毒理学毒理学
肝病学肝病学是一种肝病学.
生物化学生物化学

背景情况:

(Pb) 暴露会导致显著的组织损伤,主要是通过氧化应激和核因子-κB (NF-κB) 信号通路的激活.
肝损伤是与中毒相关的一个主要问题,影响肝功能和细胞完整性.

研究的目的:

调查氧化 (PLP) 对引起的肝毒性的保护作用.
评估PLP对肝脏NF-κB表达,氧化应激标志物和内源抗氧化能力的影响.

主要方法:

44只大鼠被分为四组:对照组,中毒组 (Pb) 和两组,在饮用水中服用不同剂量的PLP (90 mg/L和180 mg/L) 一个月.
乙酸被用于诱导毒性. 血清和肝脏同质物被分析用于氧化应激和炎症标志物.
评估了肝脏的生物化学参数,组织学特征和NF-κB表达.

主要成果:

PLP证明了剂量依赖于中毒的保护作用,减轻了肝损伤.
PLP治疗抑制了库普弗细胞增生,降低了NF-κB/BACT比率,并增强了抗氧化能力 (增加了GSH/GSSG比率).
较高的PLP剂量预防了Pb诱导的组织病理变化和改善肝功能,还降低了髓氧化酶 (MPO) 活性.

结论:

氧酸盐 (PLP) 为缓解中毒提供了一个有前途的治疗策略.
通过降低NF-κB信号的调节,减少库弗弗细胞的增殖,并增强内源抗氧化剂防御系统,PLP保护肝脏.

关键词:

葡萄糖氨酸 (Glutathione) 是一种炎症炎症是一种炎症.中毒是因为中毒.氧化应激是一种氧化应激.皮里多克萨尔酸盐是一种酸盐.

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