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纳灵宁通过调节抗氧化防御,炎症和亡途径来减轻达沙替尼诱导的损伤
Khalid Alhazzani1, Naif N Alqarni1, Khaldoon Aljerian2
1Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
International journal of medical sciences
|January 2, 2025
概括
纳灵宁 (NGN) 通过减少氧化应激,炎症和亡来保护大沙丁尼 (DASA) 诱导的损伤. 这项研究突出了NGNN.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 像达沙替尼 (DASA) 这样的氨酸激酶抑制剂可以引起显著的毒性.
- 纳灵宁 (NGN) 具有已知的抗氧化和抗炎性质.
- 了解预防药物诱导损伤的保护机制至关重要.
研究的目的:
- 为了研究宁素 (NGN) 对达沙替尼 (DASA) 诱导的急性损伤的性保护作用.
- 在小鼠模型中评估NGN对氧化应激,炎症和亡标记物的影响.
主要方法:
- 在一周的时间里,小鼠接受了不同剂量的NGN (50,100毫克/公斤) 的预治疗.
- 在第8天,DASA (25 mg/kg) 单剂量诱导了急性损伤.
- 血清标记物 (BUN,肌素,LDH,尿酸),脏组织MDA,GSH,CAT和基因表达 (TNF-α,NF-κB,IL-6,BAX,BCL-2,Caspase-3) 进行了分析.
主要成果:
- NGN预治疗显著减弱了DASA诱导的血清BUN,肌素,尿酸和LDH的增加.
- 在脏组织中,NGN可以降低高水平的氨酸 (MDA),并恢复氨酸 (GSH) 和酶 (CAT) 水平.
- NGN减轻了DASA诱导的促炎性细胞因子 (TNF-α,NF-κB,IL-6) 的上调和调节的亡基因表达 (BAX,BCL-2,Caspase-3).
结论:
- 纳灵宁 (NGN) 在小鼠中显示出显著的脏保护潜力,防止达沙替尼 (DASA) 诱导的急性损伤.
- NGN通过抗氧化,抗炎和抗亡机制发挥其保护作用.
- 需要进一步的研究,以充分阐明NGN脏保护作用所涉及的分子途径.
关键词:
细胞灭亡 (apoptosis) 是一种死亡的过程.达沙替尼布 (Dasatinib) 是一种炎症 炎症是一种炎症.在Naringenin,我们可以看到.毒性 毒性 毒性氧化应激是一种氧化应激.更多相关视频
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