内毒素诱导的死亡率与氧化应激增加和末端器官功能障碍有关,而不是耐火性低血压,在缺乏血氧酶-1的小鼠中
P Wiesel1, A P Patel, N DiFonzo
1Program of Developmental Cardiovascular Biology, the Cardiovascular Division, Brigham and Women's Hospital, Boston, MA 02115, USA.
Circulation
|January 11, 2000
概括
血氧酶-1 (HO-1) 缺乏会增加因氧化应激和器官损伤而引起的内毒性休克的死亡率,而不是低血压. HO-1 在内毒性血症中起着保护作用.
科学领域:
- 生物化学 生物化学
- 身体生理学 身体生理学
- 免疫学 免疫学 免疫学
背景情况:
- 血红素氧化酶 (HO) -1 是一种降解血红素的酶,产生一氧化碳 (CO),铁和白素.
- 内毒性休克涉及血管度下降和氧化应激增加.
- 在各种器官中,HO-1在对内毒素 (脂聚糖 (LPS)) 的反应中被上调.
研究的目的:
- 用转基因小鼠研究HO-1在内毒性病中的作用.
- 为了确定HO-1缺乏对血压,器官功能和内毒性休克期间生存的影响.
主要方法:
- 将LPS给野生型,异合体和HO-1同合体无菌小鼠.
- 监测系统血压 (SBP),HO-1表达 (mRNA和蛋白质) 和内甲蛋白-1水平.
- 评估肝脏和功能,氧化应激标志物和死亡率.
主要成果:
- 在野生类型和异合体小鼠中,LPS诱导了HO-1,但在HO-1零小鼠中没有.
- 与对照小鼠相比,HO-1无小鼠在LPS后24小时表现出较高的SBP,与增加的内甲蛋白-1相关.
- 尽管SBP较高,但HO-1无值小鼠的死亡率增加,肝/功能障碍,氧化应激增加.
结论:
- 在内毒性病期间,HO-1无细胞小鼠的死亡率增加是由于氧化应激增加和末端器官损伤.
- HO-1在减轻内毒性冲击引起的器官损伤和死亡率方面发挥着关键的保护作用.
- 这些发现突出了HO-1作为败血症和相关疾病的潜在治疗点.
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