Department of Immunobiology, College of Medicine, University of Arizona, Tucson, Arizona, USA.
Department of Pharmacology and Toxicology, R. Ken Coit College of Pharmacy, University of Arizona, Tucson, Arizona, USA; Coit Center for Longevity and Neurotherapeutics, R. Ken Coit College of Pharmacy, University of Arizona, Tucson, Arizona, USA; BIO5 Institute, College of Medicine, University of Arizona, Tucson, Arizona, USA.
J Lipid Res. 2024 Sep;65(9):100614. doi: 10.1016/j.jlr.2024.100614. Epub 2024 Aug 2.
Ischemic stroke remains a leading cause of mortality and long-term disability worldwide, necessitating efforts to identify biomarkers for diagnosis, prognosis, and treatment monitoring. The present study aimed to identify novel plasma biomarkers of neurodegeneration and inflammation in a mouse model of stroke induced by distal middle cerebral artery occlusion. Using targeted lipidomic and global untargeted metabolomic profiling of plasma collected from aged male mice 24 h after stroke and weekly thereafter for 7 weeks, we discovered distinct acute and chronic signatures. In the acute phase, we observed elevations in myelin-associated lipids, including sphingomyelin (SM) and hexosylceramide (HCER) lipid species, indicating brain lipid catabolism. In the chronic phase, we identified 12-hydroxyeicosatetraenoic acid (12-HETE) as a putative biomarker of prolonged inflammation, consistent with our previous observation of a biphasic pro-inflammatory response to ischemia in the mouse brain. These results provide insight into the metabolic alterations detectable in the plasma after stroke and highlight the potential of myelin degradation products and arachidonic acid derivatives as biomarkers of neurodegeneration and inflammation, respectively. These discoveries lay the groundwork for further validation in human studies and may improve stroke management strategies.
缺血性脑卒中仍然是全球范围内导致死亡和长期残疾的主要原因,因此需要努力寻找生物标志物,用于诊断、预后和治疗监测。本研究旨在通过对大脑中动脉远端阻塞诱导的老龄雄性小鼠脑卒中后 24 小时以及此后每周的血浆进行靶向脂质组学和全局非靶向代谢组学分析,来鉴定脑卒中后神经退行性变和炎症的新型血浆生物标志物。在急性期,我们观察到与髓鞘相关的脂质,包括神经鞘磷脂(SM)和己糖神经酰胺(HCER)脂质种类升高,表明脑脂质分解代谢。在慢性期,我们发现 12-羟基二十碳四烯酸(12-HETE)是一种潜在的延长炎症的生物标志物,这与我们之前观察到的小鼠脑缺血的双相促炎反应一致。这些结果提供了对脑卒中后可在血浆中检测到的代谢变化的深入了解,并突出了髓鞘降解产物和花生四烯酸衍生物分别作为神经退行性变和炎症生物标志物的潜力。这些发现为进一步在人类研究中进行验证奠定了基础,并可能改善脑卒中管理策略。