素诱导的肝细胞染色体P450 2E1的表达和活性在小鼠中通过施用奎尔来减少
Jambour-Shabestary Amir-Ata1, Vardast Mohammad-Reza2, Hassan Malekinejad1,3
1Department of Pharmacology & Toxicology, Experimental and Applied Pharmaceutical Sciences Research Center, Urmia University of Medical Sciences, Urmia, Iran.
Current pharmaceutical design
|February 29, 2024
概括
奎尔 (QCN) 通过降低有害酶活性,保护肝脏免受 (BNZ) 毒性影响. 这项研究表明,QCN降低了P450 2E1细胞染色体的下调,为BNZ诱导的肝损伤提供了潜在的治疗方法.
科学领域:
- 肝脏保护作用 肝脏保护作用
- 毒理学 毒理学 毒理学
- 酶动力学 酶动力学
背景情况:
- (BNZ) 是一种环境毒素,会导致代谢依赖的肝损伤.
- 细胞染色体P450 2E1 (CYP 2E1) 在BNZ代谢和毒性中起着关键作用.
- 调查天然化合物对BNZ的保护作用至关重要.
研究的目的:
- 调查奎尔素 (QCN) 对乙酸诱导的肝脏CYP 2E1.1.的变化的影响.
- 评估QCN对氧化应激标志物和BNZ暴露小鼠肝酶活性的影响.
主要方法:
- 成年雄性小鼠被暴露在BNZ中,并在28天内接受不同剂量的QCN治疗.
- 通过4 - 尼托芬醇氧化分离,将肝脏显微体分离出来,以测量CYP 2E1活性.
- 评估了肝脏髓氧化酶,氧化和抗氧化能力;使用qPCR分析了CYP 2E1mRNA表达.
主要成果:
- QCN显著降低了BNZ诱导的氧化和髓氧化酶水平.
- 在暴露于BNZ的小鼠中,QCN恢复了抗氧化能力.
- 在接受BNZ治疗的动物中,QCN的使用降低了肝CYP 2E1的表达和活性.
结论:
- 奎尔 (QCN) 显示出显著的肝脏保护性质,可以防止 (BNZ) 引起的毒性.
- 保护机制涉及肝脏CYP 2E1表达和活性的下调.
- 作为BNZ诱导的肝损伤的治疗剂,QCN显示出前景.
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