间歇性禁食对阿德里亚素诱导的脏病的影响:可能的潜在机制
Fathy H Elsaid1, Abdelaziz M Hussein2, Elsayed A Eid3
1Department of Medical Physiology, Faculty of Medicine, Al-Azhar University, Assuit, Egypt.
Tissue & cell
|March 15, 2024
概括
间歇性禁食 (IF) 通过增强抗氧化剂防御和减少损伤,改善了大鼠的阿德里亚米辛诱导的病. 这种禁食方法可能会激活Sirt1和Nrf2/HO-1等保护通路.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 细胞生物学 细胞生物学
- 代谢研究研究 代谢研究
背景情况:
- 间歇性禁食 (IF) 触发细胞自适应性防御机制,促进抗氧化剂的产生,DNA修复,线粒体生物发生和抗炎基因表达.
- 阿德里亚米 (ADR) 是一种已知的诱导病的化疗剂,其特点是损伤和功能受损.
研究的目的:
- 为了研究间歇性禁食 (IF) 对大胺素 (ADR) 诱导的脏病的保护作用,在老鼠模型中.
- 探索潜在的分子机制,包括抗氧化剂和亡相关途径的作用.
主要方法:
- 成年雄性Sprague-Dawley大鼠被分为四组:对照组,禁食组,ADR诱导的病组和具有IF的ADR组.
- 在8周后评估了功能 (血清肌素,BUN,尿蛋白),氧化应激标记 (MDA,GSH,CAT),亡 (caspase-3) 和基因表达 (Sirt1,Nrf2,HO-1,AQP2).
主要成果:
- 在ADR治疗的老鼠中,IF显著改善了损伤标志物 (肌素,BUN,尿蛋白).
- IF通过降低氨酸 (MDA) 和增加酶 (CAT) 和氨酸 (GSH) 水平来降低氧化应激.
- IF治疗导致caspase-3的表达减少,这表明细胞亡减少,并增加了Sirt1,Nrf2/HO-1和aquaporin2 (AQP2) 的表达.
结论:
- 间歇性禁食 (IF) 在大鼠中显示出对阿德里亚米辛诱导的脏病的保护作用.
- 似乎IF的保护作用是通过激活Sirt1,Nrf2/HO-1信号传递和aquaporin2 (AQP2) 来实现的.
- IF增强了内源性抗氧化能力,减少了亡,减轻了管间损伤,并有助于保持淋巴细胞完整性.
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