β-基酸盐可以缓解败血症引起的急性损伤
Min Jeong Kim1,2, Young Suk Kim2, Seo Rin Kim1,2
1Department of Internal Medicine, Pusan National University School of Medicine, Yangsan, Republic of Korea.
Molecular biology reports
|September 13, 2023
概括
在小鼠中,β-hydroxybutyrate (β-HB) 的预治疗可以预防败血症引起的急性损伤 (AKI). 这种干预减少了损伤,炎症和细胞死亡,这表明了与败血症相关的脏问题潜在的预防策略.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 免疫学 免疫学 免疫学
- 代谢医学是一种代谢医学.
背景情况:
- 败血症是急性损伤 (AKI) 的主要原因之一.
- 之前的研究表明β-基酸盐 (β-HB) 能保护脏免受缺血-再输血和西斯的损伤.
- 在症诱导的AKI (SIAKI) 中β-HB的疗效仍然未被探索.
研究的目的:
- 调查β-基酸盐 (β-HB) 对败血症诱导的急性损伤 (SIAKI) 的保护作用.
- 在SIAKI的小鼠模型中评估β-HB对损伤,炎症和亡的影响.
主要方法:
- 败血症诱导的AKI (SIAKI) 在C57BL/6雄性小鼠中使用腹膜内脂多糖 (LPS) 注射确立.
- 在暴露于LPS之前,小鼠接受了腹腔内β-基酸盐 (β-HB) 给药.
- 这些组包括假,β-HB,LPS和β-HB + LPS;评估涉及组织学损伤,血清肌素,炎症标志物,巨细胞透和亡标志物.
主要成果:
- 脂聚糖 (LPS) 显著增加了组织学损伤和血清肌水平,这些水平被β-基酸盐 (β-HB) 治疗前减弱.
- 接受β-HB预治疗后,减少了关键炎症标志物的表达 (酸化核因子-κB,瘤缩因子-α,介质素-6) 和F4/80阳性巨细胞.
- 在β-HB + LPS组中,亡显著降低,由TdT介导的dUTP尾标记 (TUNEL) 阳性细胞的较低水平,切割的caspase-3表达和改变的Bax/Bcl-2比率证明.
结论:
- 在小鼠模型中,β-hydroxybutyrate (β-HB) 的预治疗显示出对毒引起的急性损伤 (SIAKI) 的保护作用.
- 保护机制涉及抑制管状亡和炎症反应.
- β-HB具有作为预防策略的潜力,可以预防或减轻与败血症相关的损伤.
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