甘酸通过抑制内质网膜应激和上调Nrf2通路来改善西斯胺诱导的复发毒性
Ahmet Mentese1, Selim Demir2, Sevdegul Aydin Mungan3
1Department of Medical Biochemistry, Faculty of Medicine, Karadeniz Technical University, 61080 Trabzon, Turkey.
Tissue & cell
|November 2, 2023
概括
甘酸 (GTA) 在老鼠中显示出对西斯 (CP) 诱导的丸毒性有治疗潜力. 通过激活Nrf2通路,GTA治疗改善了氧化应激,炎症和亡.
科学领域:
- 毒理学 毒理学 毒理学
- 生殖生物学 生殖生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 西斯普拉丁 (CP) 化疗与显著的生殖毒性有关.
- 丁酸 (GTA) 是一种酸,具有强大的抗氧化特性.
- 对于CP诱导的丸损伤,GTA的保护作用仍然未被探索.
研究的目的:
- 在大鼠模型中调查Gentisic acid (GTA) 对西斯 (CP) 诱导的丸毒性治疗效果.
- 阐明潜在的机制,包括氧化应激,炎症,内质网膜应激,亡和Nrf2通路.
主要方法:
- 雄性斯普拉格-道利大鼠被给予单剂量CP (5毫克/公斤).
- 随后,大鼠用GTA (1.5和3毫克/公斤) 连续三天接受治疗.
- 对丸组织进行了氧化应激,炎症,内分泌网膜应激,亡生物标志物和Nrf2通路激活的分析.
主要成果:
- 施用CP诱导了显著的丸组织病理损伤.
- 脑膜炎治疗导致氧化应激增加,炎症,内质网膜应激和亡生物标志物.
- CP降低了抗氧化能力和Nrf2表达,而GTA的使用改善了这些效应,并提高了Nrf2的调节.
结论:
- 甘酸 (GTA) 在大鼠中显示出对西斯 (CP) 诱导的丸毒性有保护作用.
- GTA的治疗作用与减轻氧化应激,炎症,内质网膜应激和亡有关.
- 激活Nrf2通路是GTA保护作用的关键机制.
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