柏柏林通过调节抗氧化剂防御系统,减轻了大鼠中乙胺暴露诱导的线粒体功能障碍和亡
Annu Phogat1, Jagjeet Singh1,2, Reena Sheoran1
1Department of Zoology, Maharshi Dayanand University, Rohtak 124001, India.
Journal of xenobiotics
|August 27, 2024
概括
柏柏林 (BBR) 通过维护肝脏线粒体功能和减少亡来防止乙胺 (ACMP) 杀虫剂的毒性. 这种天然类化合物提供了一种潜在的治疗策略,可以对抗农药诱导的细胞损伤.
科学领域:
- 毒理学 毒理学 毒理学
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
背景情况:
- 乙胺普里德 (ACMP) 是一种新烟类杀虫剂,通过氧化应激和线粒体功能障碍诱导毒性.
- 柏柏林 (BBR) 是一种天然的化物,具有治疗性质.
- 了解BBR对ACMP诱导的肝损伤的保护作用至关重要.
研究的目的:
- 为了研究BBR对ACMP诱导的线粒体功能障碍和老鼠肝脏的亡的保护作用.
- 阐明BBR肝脏保护作用背后的分子机制.
主要方法:
- 雄性Wistar大鼠被分为对照组,BBR治疗组,ACMP暴露组和BBR+ACMP联合治疗组.
- 动物每天接受BBR (150毫克/公斤) 和ACMP (21.7毫克/公斤) 的胃内剂量,持续21天.
- 在肝脏组织中分析了线粒体功能,抗氧化剂状况,亡标记物和相关的基因/蛋白质表达.
主要成果:
- 暴露于ACMP损害了线粒体复合物的活性,降低了关键线粒体基因表达 (ND1,ND2,COX1,COX4),减少了抗氧化剂,并诱导了亡.
- BBR预处理显著恢复了线粒体复合物的活性,并使线粒体基因的表达正常化.
- 通过调节Bax,Bcl-2和caspase-3水平,BBR减弱了ACMP诱导的亡,并通过PGC-1α,MnSOD和UCP-2上调增强了抗氧化剂防御系统.
结论:
- 柏柏林显示出显著的肝脏保护潜力,防止乙胺诱导的毒性.
- BBR保留了线粒体功能,增强了抗氧化能力,并抑制了亡.
- 这项研究强调BBR是减轻农药引起的肝损伤的有希望的药物.
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