柏柏林通过对Nrf2/HO-1轴的调节,缓解了大鼠中pyrifos诱导的毒性
Lenah S Binmahfouz1, Emad H M Hassanein2, Amina M Bagher1
1Department of Pharmacology and Toxicology, Faculty of Pharmacy, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Heliyon
|February 8, 2024
概括
柏柏林 (BBR) 通过恢复抗氧化剂平衡,减少炎症和亡,保护甲酸 (CPS) 损伤脏. 这项研究突出了BBR的重点.
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.
- 腎臟病學 (nephrology) 是一種醫學專業.
背景情况:
- pyrifos (CPS) 是一种有机类杀虫剂,与不良健康结果有关.
- 柏柏林 (BBR) 是一种植物化学物质,具有抗炎和抗氧化特性.
- 损伤是与CPS暴露相关的重大健康问题.
研究的目的:
- 调查柏柏林 (BBR) 对大鼠中pyrifos (CPS) 诱导的毒性的保护作用.
- 阐明BBR脏保护作用的基本机制.
主要方法:
- 鼠被分为四组:对照组,单独使用BBR,单独使用CPS和CPS+BBR.
- 治疗每天通过胃输液进行28天.
- 评估了功能,组织学,氧化应激标志物,炎症标志物和与亡相关的蛋白质.
主要成果:
- 与仅服用CPS的组相比,BBR治疗显著改善了功能标志物 (血清尿素,肌素,尿酸).
- 组织学检查证实了BBR的保护作用.
- 通过Keap1/Nrf2/HO-1通路,BBR恢复了氧化剂-抗氧化剂平衡,降低了氧化 (NO) 和髓氧化酶 (MPO) 活性,并抑制了NF-κB.
- BBR通过上调 Bcl-2 和降低 Bax 和 caspase-3 的调节来表现出抗亡作用.
结论:
- 在大鼠模型中,柏柏林 (BBR) 有效地减轻了pyrifos (CPS) 诱导的毒性.
- BBR的保护机制包括恢复氧化剂-抗氧化剂平衡,抑制炎症和减少组织中的亡.
- 对Nrf2/HO-1轴的调节是BBR对CPS毒性的保护作用的关键途径.
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