磷脂酰胆碱和磷脂酰乙醇胺水平降低与脓毒症相关性脑病中的炎症激活相关。
Reduced phosphatidylcholine and phosphatidylethanolamine levels correlate with inflammatory activation in sepsis-associated encephalopathy.
作者信息
Qin Mubing, Yu Shiyuan, Lu Xin, Gong Chao, Song Zengrui, Zhu Huadong, Gao Yanxia, Li Yi
机构信息
Emergency Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.
Emergency Department, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
出版信息
Eur J Med Res. 2025 Aug 31;30(1):828. doi: 10.1186/s40001-025-03115-z.
BACKGROUND
Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis, often leading to poor neurological outcomes. Lipid molecules are increasingly recognized for their potential involvement in both sepsis and cognitive impairment. However, the relationship between lipidomic alterations and SAE remains incompletely understood. This study aims to investigate lipidomic changes in patients with SAE and explore potential associations between lipid metabolism and the development of SAE.
METHODS
Sepsis patients without pre-existing central nervous system disorders were prospectively enrolled. SAE was defined as a positive result on the Confusion Assessment Method for the ICU (CAM-ICU) or a Glasgow Coma Scale (GCS) score < 15. Blood samples were collected at enrollment and upon any change in cognitive status. Cerebrospinal fluid (CSF) samples were collected based on the physician assessment. Lipid metabolites were analyzed using high-performance liquid chromatography coupled with mass spectrometry.
RESULTS
A total of 98 sepsis patients were enrolled, with 39 classified into the SAE group and 59 into the non-SAE group. Plasma levels of phosphatidylethanolamines (PE) and phosphatidylcholines (PC) were significantly decreased in SAE patients. Among these, LPC (18:2), LPC (16:0), LPE (22:6), and LPE (20:4) showed the most notable reductions. Additionally, 3-hydroxy-3-methylglutaryl coenzyme A(HMG-CoA) levels were decreased in SAE patients, while proinflammatory cytokines such as IFN-γ, IL-1ra, MCP-1, and IP-10 were elevated.
CONCLUSION
Reduced levels of PC and PE lipids in SAE patients may reflect underlying inflammatory processes. The observed downregulation of HMG-CoA and upregulation of IP-10 and MCP-1 suggest a potential therapeutic role for statins in the management of SAE. Clinical Trial Registry number and website where it was obtained: Clinical Trial NCT04230447 (Registration Date: 01/02/2021; https://www.
CLINICALTRIALS
gov/study/NCT04230447?cond=Sepsis%20Associated%20Encephalopathy&rank=4 ).
背景
脓毒症相关脑病（SAE）是脓毒症的一种严重并发症，常导致不良的神经学预后。脂质分子在脓毒症和认知障碍中的潜在作用日益受到认可。然而，脂质组学改变与SAE之间的关系仍未完全明确。本研究旨在调查SAE患者的脂质组学变化，并探索脂质代谢与SAE发生之间的潜在关联。
方法
前瞻性纳入无既往中枢神经系统疾病的脓毒症患者。SAE定义为重症监护病房意识模糊评估法（CAM-ICU）结果为阳性或格拉斯哥昏迷量表（GCS）评分<15。在入组时及认知状态出现任何变化时采集血样。根据医生评估采集脑脊液（CSF）样本。使用高效液相色谱-质谱联用技术分析脂质代谢物。
结果
共纳入98例脓毒症患者，其中39例分为SAE组，59例分为非SAE组。SAE患者血浆中磷脂酰乙醇胺（PE）和磷脂酰胆碱（PC）水平显著降低。其中，溶血磷脂酰胆碱（LPC，18:2）、溶血磷脂酰胆碱（LPC，16:0）、溶血磷脂酰乙醇胺（LPE，22:6）和溶血磷脂酰乙醇胺（LPE，20:4）降低最为显著。此外，SAE患者3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）水平降低，而促炎细胞因子如干扰素-γ、白细胞介素-1受体拮抗剂（IL-1ra）、单核细胞趋化蛋白-1（MCP-1）和干扰素诱导蛋白10（IP-10）升高。
结论
SAE患者PC和PE脂质水平降低可能反映潜在的炎症过程。观察到的HMG-CoA下调以及IP-10和MCP-1上调表明他汀类药物在SAE治疗中可能具有潜在作用。临床试验注册号及获取网址：临床试验NCT04230447（注册日期：2021年2月1日；https://www.CLINICALTRIALS.gov/study/NCT04230447?cond=Sepsis%20Associated%20Encephalopathy&rank=4 ）。
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