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荣基醇通过向巴克斯蛋白来对抗诱导的超结构性核变异和肝细胞的线粒体功能障碍

Aftab Shaukat¹, Irfan Shaukat², Mohammed Al-Rasheed³

¹College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.

Poultry science

|February 8, 2026

概括

红 (HNK) 通过减少氧化应激和预防亡,有效地减轻 (Cd) 诱导的肝损伤. 这项研究强调了HNK.

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.
动物营养动物营养

背景情况:

(Cd) 暴露会导致动物显著的氧化应激,炎症和肝毒性.
红醇 (HNK),以其抗氧化和抗炎作用而闻名,可以防止肝损伤.
需要进一步研究HNK对Cd诱导的肝毒性的保护机制,特别是在超结构和功能层面.

研究的目的:

调查霍诺基 (HNK) 的潜力,以改善 (Cd) 诱导的肝毒性在肉.
为了评估HNK对Cd诱导的超结构变化,氧化应激,脂质积累和肝细胞的亡的影响.
使用in silico和in vivo方法探索HNK对Cd毒性的保护作用背后的分子机制.

主要方法:

肉被暴露在 (Cd) 和/或 (HNK) 中42天.
在基分析中进行了预测HNK与亡相关蛋白质 (Bax和Bcl-2) 的相互作用.
评估了肝细胞超结构,氧化应激标志物 (SOD,GSH-Px,MDA),脂质积累以及与亡相关的基因/蛋白质表达 (Caspase-3,Bcl-2).

主要成果:

暴露于Cd显著损害了肝细胞的超结构和功能,增加了氧化应激和脂质积累.
HNK治疗恢复了肝细胞的完整性,减少了氧化应激标志物,并防止了Cd诱导的脂质积累.
在HNK下调的亲细胞亡蛋白 (Caspase-3) 和上调的抗细胞亡蛋白 (Bcl-2) 表达,减轻细胞亡.

结论:

红醇 (HNK) 在缓解 (Cd) 诱导的肝毒性方面显示出显著的潜力.
HNK通过保持超结构完整性,减少氧化应激,防止脂质积累和抑制亡来保护肝细胞.
在动物中,HNK是一种有前途的治疗剂,用于治疗中毒和相关的肝损伤.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.是的组成部分.霍诺基奥尔 (Honokiol) 是一个线粒体功能障碍线粒体功能障碍氧化应激是一种氧化应激.

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