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Updated: Jan 20, 2026
06:25
Kidney Regeneration in Adult Zebrafish by Gentamicin Induced Injury
Published on: August 3, 2015
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黑素通过Keap1/Nrf2/HO-1信号通路缓解 gentamicin 诱导的急性损伤
Ningning Li1, Xianghua Liu2, Wei Liu3
1Department of Pathology, Henan Medical College, Zhengzhou, 451191, China.
Biochemistry and biophysics reports
|January 19, 2026
概括
根他米辛 (GM) 通过增加氧化应激和抑制KEAP1/NRF2通路,导致剂量依赖的损伤. 黑色素通过恢复抗氧化剂平衡和重新激活这一关键途径,防止转基因诱导的急性损伤.
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:
- 药物诱导的毒性是一个重要的临床问题.
- 甘他素 (GM) 是一种重要的抗生素,但经常导致急性损伤 (AKI).
- 作为一种天然抗氧化剂的黑氨酸显示出减轻药物诱导的损伤的潜力.
研究的目的:
- 调查转基因对功能和损伤的剂量依赖性影响.
- 阐明基因转基因诱导毒性背后的机制.
- 评估黑激素对转基因诱导的AKI的脏保护作用和机制.
主要方法:
- 给大鼠服用不同剂量的转基因药物,以评估剂量依赖性毒性.
- 测量了损伤和功能障碍的尿液和血清生物标志物 (KIM-1,NGAL,BUN,SCr).
- 进行了组织病理学分析,以评估脏组织损伤.
- 评估了氧化应激标志物 (SOD,GSH,MDA) 和KEAP1/NRF2通路组件 (Keap1,NRF2,GPX1,NQO1,HO-1). 这些标志物包括:
- 用黑色素治疗的老鼠,以评估其保护作用.
主要成果:
- 转基因诱导的剂量依赖性毒性,在剂量≥50 mg/kg时显著增加损伤生物标志物 (KIM-1,NGAL) 和功能障碍标志物 (BUN,SCr).
- 组织病理学显示,随着转基因剂量的增加,损伤和炎症等损伤逐渐恶化.
- 转基因通过耗尽SOD和GSH而增加MDA,增加了氧化应激.
- 转基因降低了KEAP1/NRF2通路的调节,抑制了抗氧化基因表达.
- 黑色素治疗显著改善了转基因诱导的AKI,使生物标志物正常化,减少组织病理损伤,恢复抗氧化能力,并重新激活KEAP1/NRF2通路.
结论:
- 转基因生物通过氧化应激和KEAP1/NRF2路径失调引起剂量依赖性毒性和AKI.
- 黑色素显示出显著的脏保护作用,防止转基因诱导的AKI.
- 黑色素的保护机制涉及恢复抗氧化剂平衡和重新激活KEAP1/NRF2通路,突出其治疗潜力.
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