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Last update 08 May 2025

Sepsis-Associated Encephalopathy

Last update 08 May 2025

Basic Info

Synonyms

Associated Delirium, Sepsis, Associated Deliriums, Sepsis, Associated Encephalopathies, Sepsis

+ [27]

Introduction

Acute neurological dysfunction during severe SEPSIS in the absence of direct brain infection characterized by systemic inflammation and BLOOD BRAIN BARRIER perturbation.

Drugs associated with Sepsis-Associated Encephalopathy

Ginsenoside Rh2

Target-

Mechanism-

Active Org.

Shanghai Changzheng Hospital

Originator Org.

Shanghai Changzheng Hospital

Active Indication

Sepsis-Associated Encephalopathy

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Sepsis-Associated Encephalopathy

ChiCTR2400094558

/ SuspendedNot ApplicableIIT

Study on the Diagnostic and Prognostic Value of Peripheral Blood GBP5 Combined with Brain Injury Markers in Sepsis - Associated Encephalopathy

Start Date31 Dec 2024

Sponsor / Collaborator

The First People's Hospital of Lianyungang

ChiCTR2400090497

/ SuspendedEarly Phase 1IIT

The Diagnostic and Therapeutic Role of Klotho in Sepsis-Associated Encephalopathy and Its Mechanism Research

Start Date06 Oct 2024

Sponsor / Collaborator

The Third Hospital of Hebei Medical University

ChiCTR2400086446

/ SuspendedNot ApplicableIIT

A prospective cohort study of long-term cognitive dysfunction associated with sepsis

Start Date01 Sep 2024

Sponsor / Collaborator-

100 Clinical Results associated with Sepsis-Associated Encephalopathy

100 Translational Medicine associated with Sepsis-Associated Encephalopathy

0 Patents (Medical) associated with Sepsis-Associated Encephalopathy

1,073

Literatures (Medical) associated with Sepsis-Associated Encephalopathy

01 Dec 2025·Inflammation Research

Pericytes mediate neuroinflammation via Fli-1 in endotoxemia and sepsis in mice

Article

Author: Wang, Guirong ; Fan, Hongkuan ; Liu, Liu ; Halushka, Perry V ; Trojanowska, Maria ; Ergul, Adviye ; Li, Pengfei

AbstractBackgroundSepsis-associated encephalopathy (SAE) often results from neuroinflammation. Recent studies have shown that brain platelet-derived growth factor receptor β (PDGFRβ) cells, including pericytes, may act as early sensors of infection by secreting monocyte chemoattractant protein-1 (MCP-1), which transmits inflammatory signals to the central nervous system. The erythroblast transformation-specific (ETS) transcription factor Friend leukemia virus integration 1 (Fli-1) plays a critical role in inflammation by regulating the expression of key cytokines, including MCP-1. However, the role of pericyte Fli-1 in neuroinflammation during sepsis remains largely unknown.MethodsWT and pericyte-specific Fli-1 knockout mice were subjected to endotoxemia through LPS injection or sepsis via cecal ligation and puncture (CLP). In vitro, Fli-1 was knocked down using small interfering RNA in cultured mouse brain pericytes, followed by LPS stimulation.ResultsElevated Fli-1 levels were observed in isolated brain pericytes 2 h after LPS administration, in brain tissues 4 h after CLP, and in cultured mouse brain pericytes 2 h after LPS stimulation in vitro. In endotoxemic mice, pericyte-specific Fli-1 knockout reduced expression of MCP-1 and IL-6 in brain tissue 2 h after LPS injection. At 24 h post-LPS administration, protein levels of MCP-1 and IL-6, and microglia activation were suppressed in pericyte-Fli-1 knockout mice. Additionally, Fli-1 deficiency in pericytes significantly reduced MCP-1 and IL-6 mRNA levels in the brain tissue 4 h after CLP. Moreover, in cultured brain pericytes, Fli-1 knockdown markedly decreased MCP-1 and IL-6 levels after LPS stimulation. Notably, LPS stimulation increased Fli-1 levels via TLR4-Myd88 signaling, which subsequently led to elevated production of MCP-1 in brain pericytes.ConclusionsFli-1 in pericytes may serve as a crucial mediator of neuroinflammation during sepsis by directly regulating pivotal cytokines such as MCP-1 and IL-6. Therefore, Fli-1 has the potential to serve as a therapeutic target in SAE and other neuroinflammatory disorders.

01 Oct 2025·Biomaterials

Magnesium hexacyanoferrate mitigates sepsis-associated encephalopathy through inhibiting microglial activation and neuronal cuproptosis

Article

Author: Wang, Hongwei ; Ren, Xiangyi ; Xia, Yuzhong ; Chen, Gezi ; Zhang, Yabing ; Ji, Penghao ; Liu, Panmiao ; Wang, Yong ; Wang, Zhongyu ; Yu, Hai ; Zhao, Di ; Xin, Juan ; Huo, Minfeng ; Wei, Hua ; Yang, Jianjun

Sepsis-associated encephalopathy (SAE) is a severe neurological complication stemming from sepsis, characterized by cognitive impairment. The underlying mechanisms involve oxidative stress, neuroinflammation, and disruptions in copper/iron homeostasis. This study introduces magnesium hexacyanoferrate (MgHCF) as a novel compound and explores its therapeutic potential in SAE. Our investigation reveals that MgHCF features intriguing properties in effectively scavenging reactive oxygen species (ROS), and chelating excess copper and iron. Treatment with MgHCF significantly attenuates microglia activation, and protects neuronal cells from oxidative damage and cytotoxicity induced by activated microglia in vitro and in vivo. Furthermore, the cognitive impairment in SAE mice is effectively alleviated by MgHCF treatment, mechanically through a reduction in the copper/iron-responsive histone methylation, and neuronal cuproptosis. These findings suggest MgHCF as a promising therapeutic agent for SAE, targeting the copper/iron signaling pathway to alleviate neuroinflammation, and neuronal cuproptosis.

01 Jul 2025·Experimental Neurology

Astrocytic N-myc downstream-regulated gene 2 is involved in neural injury induced by sepsis-associated encephalopathy

Article

Author: Gu, Tingting ; Liu, Bingjie ; Liu, Qingzhen ; Zhang, Lidong ; Yin, Anqi ; Xu, Chang ; Qu, Haoran

SAE is a systemic inflammatory response syndrome resulting from severe infection, which can progress to multiorgan dysfunction and mortality. Astrocytic-specific NDRG2, a stress response gene, has been implicated in regulating astrocyte reactivity and glutamate homeostasis in various neurological disorders. In this study, we initially investigated the expression and functional role of NDRG2 in SAE. Our results demonstrated that the upregulation of NDRG2 primarily inhibited Na⁺/K⁺-ATPase β1 and EAAT2, subsequently leading to glutamate toxicity and then induced astrocyte activation, neuronal dysfunction, and cellular apoptosis, ultimately leading to cognitive impairment. The deficiency of NDRG2 significantly mitigated these detrimental changes, including astrocytic activation, impaired glutamate clearance, and cognitive deficits in SAE, partly through the modulation of Na⁺/K⁺-ATPase β1. Our findings may provide new strategies for the intervention and treatment of patients with SAE in the future.

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Sepsis-Associated Encephalopathy

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