Zhang Aihong, Hao Shuang, Bi Jing, Bao Yongming, Zhang Xiuli, An Lijia, Jiang Bo
School of Environmental and Biological Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Exp Toxicol Pathol. 2009 Sep;61(5):461-9. doi: 10.1016/j.etp.2008.10.010. Epub 2008 Dec 10.
The aim of this study was to investigate whether catalpol could facilitate recovery from lipopolysaccharide (LPS)-induced cognitive deficits and protect brain mitochondrial function from LPS-induced acute systemic inflammation. In the study, except control group, mice were challenged with a single dose of LPS (100 microg/mouse, i.p.) to mimic an acute peripheral infection. The results showed that LPS enhanced nuclear factor kappa B (NF-kappaB) activation and induced a loss in mitochondrial integrity as shown by a significant decrease in membrane potential and increase in mitochondrial permeability transition pore opening. Pretreatment with catalpol (10 mg/kg d, i.p.) for 10d before injection of LPS reversed the memory deficits induced by LPS, protected brain mitochondrial function, and attenuated LPS-induced NF-kappaB activation. Taken together, these data indicate that catalpol may possess therapeutic potential against LPS-induced acute systemic inflammation by attenuating NF-kappaB activation and protecting mitochondrial function in cerebral cortex and hippocampus.
本研究的目的是探讨梓醇是否能促进脂多糖（LPS）诱导的认知缺陷的恢复，并保护脑线粒体功能免受LPS诱导的急性全身炎症的影响。在该研究中，除对照组外，小鼠接受单剂量LPS（100微克/小鼠，腹腔注射）以模拟急性外周感染。结果显示，LPS增强了核因子κB（NF-κB）的激活，并导致线粒体完整性丧失，表现为膜电位显著降低和线粒体通透性转换孔开放增加。在注射LPS前10天用梓醇（10毫克/千克·天，腹腔注射）预处理可逆转LPS诱导的记忆缺陷，保护脑线粒体功能，并减弱LPS诱导的NF-κB激活。综上所述，这些数据表明梓醇可能通过减弱NF-κB激活并保护大脑皮层和海马体中的线粒体功能，对LPS诱导的急性全身炎症具有治疗潜力。
