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丁酸在老鼠中减轻了丁素诱导的毒性
Morteza Saeedavi1, Mehdi Goudarzi2, Iman Fatemi3
1Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Tissue & cell
|August 9, 2023
概括
丁酸 (GA) 通过减少氧化应激和炎症来保护 gentamicin (GEN) 诱导的损伤. 这项研究表明GAGA.
科学领域:
- 药理学 药理学是指药理学的学科.
- 毒理学 毒理学 毒理学
- 腎臟病學 (nephrology) 是一種醫學專業.
背景情况:
- 甘他素 (GEN) 是一种已知会引起毒性的抗生素.
- 氧化应激和炎症是GEN诱导损伤的关键机制.
- 甘酸 (GA) 正在研究其潜在的保护性质.
研究的目的:
- 为了评估 gentisic 酸 (GA) 对大鼠 gentamicin (GEN) 诱导的毒性的保护作用.
- 评估GA对氧化应激,炎症标志物和GEN暴露后功能的影响.
主要方法:
- 在14天的时间里,老鼠口服了不同剂量的GA (25,50,100毫克/公斤).
- 从第8天到第14天,Gentamicin (100 mg/kg) 通过腹膜内注射.
- 分析了损伤,氧化应激 (MDA,GSH),炎症 (TNF-α,IL-1β) 和抗氧化酶活动 (CAT,SOD,GPx) 的血清和组织标志物.
主要成果:
- 基因基因的使用显著增加了损伤 (NGAL,KIM-1,BUN,Cr) 和氧化应激 (MDA,NO) 的标志物.
- 在组织中,GEN暴露增加了炎症性细胞因子 (TNF-α,IL-1β) 和降低了抗氧化酶活性 (CAT,SOD,GPx).
- 抗氧化酶治疗显著缓解了GEN诱导的损伤标志物,氧化应激和炎症的增加,同时恢复了抗氧化酶活性.
结论:
- 甘酸 (GA) 显示出显著的脏保护作用,防止甘胺 (GEN) 诱导的脏损伤.
- 通过减轻氧化应激和抑制炎症反应,GA改善了GEN诱导的毒性.
- GA具有作为预防或治疗抗生素诱导损伤的治疗剂的潜力.
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