Molecular hydrogen attenuates sepsis-induced cognitive dysfunction through regulation of tau phosphorylation

Qi, Bo; Song, Yu; Chen, Chen; Zhao, Lina; Ma, Wanjie; Meng, Shuqi; Zhuang, Xiaoli; Lin, Huayi; Liang, Jing; Cui, Yan; Xie, Keliang

doi:10.1016/j.intimp.2022.109603

Cited by 10 publications

(3 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In animal experiments, it was observed that the levels of ptau and ptau key kinases were elevated in the hippocampus of CLP mice. Studies have also found decreased dendritic spine density and the number of normal hippocampal neurons in CLP mice, indicating damage to neuronal synapses ( Qi et al, 2023 ). Glutamate serves as the foremost excitatory neurotransmitter within the central nervous system, while the critical function of ionotropic glutamate receptors (NMDAR) involves the regulation of neuronal survival and synaptic plasticity.…”

Section: Pathogenesis Of Sepsis-associated Encephalopathymentioning

confidence: 99%

The role of the peripheral system dysfunction in the pathogenesis of sepsis-associated encephalopathy

Zhang,

Chen,

et al. 2024

Front. Microbiol.

View full text Add to dashboard Cite

Sepsis is a condition that greatly impacts the brain, leading to neurological dysfunction and heightened mortality rates, making it one of the primary organs affected. Injury to the central nervous system can be attributed to dysfunction of various organs throughout the entire body and imbalances within the peripheral immune system. Furthermore, central nervous system injury can create a vicious circle with infection-induced peripheral immune disorders. We collate the pathogenesis of septic encephalopathy, which involves microglial activation, programmed cell death, mitochondrial dysfunction, endoplasmic reticulum stress, neurotransmitter imbalance, and blood–brain barrier disruption. We also spotlight the effects of intestinal flora and its metabolites, enterocyte-derived exosomes, cholinergic anti-inflammatory pathway, peripheral T cells and their cytokines on septic encephalopathy.

show abstract

Section: Pathogenesis Of Sepsis-associated Encephalopathymentioning

confidence: 99%

The role of the peripheral system dysfunction in the pathogenesis of sepsis-associated encephalopathy

Zhang,

Chen,

et al. 2024

Front. Microbiol.

View full text Add to dashboard Cite

show abstract

“…Moreover, a higher expression of brain-derived neurotrophic factor (BDNF), one of the neuronal growth factors, was observed due to the modified methylation of its promoter [ 58 ]. Another study on the hippocampi of mice showed a decreased level of phosphorylated tau protein and an improvement in cognitive functions after H 2 inhalation [ 59 ].…”

Section: Hydrogenmentioning

confidence: 99%

Exploring Neuroprotective Agents for Sepsis-Associated Encephalopathy: A Comprehensive Review

Krzyzaniak,

Krion,

Szymczyk

et al. 2023

IJMS

View full text Add to dashboard Cite

Sepsis is a life-threatening condition resulting from an inflammatory overreaction that is induced by an infectious factor, which leads to multi-organ failure. Sepsis-associated encephalopathy (SAE) is a common complication of sepsis that can lead to acute cognitive and consciousness disorders, and no strict diagnostic criteria have been created for the complication thus far. The etiopathology of SAE is not fully understood, but plausible mechanisms include neuroinflammation, blood–brain barrier disruption, altered cerebral microcirculation, alterations in neurotransmission, changes in calcium homeostasis, and oxidative stress. SAE may also lead to long-term consequences such as dementia and post-traumatic stress disorder. This review aims to provide a comprehensive summary of substances with neuroprotective properties that have the potential to offer neuroprotection in the treatment of SAE. An extensive literature search was conducted, extracting 71 articles that cover a range of substances, including plant-derived drugs, peptides, monoclonal antibodies, and other commonly used drugs. This review may provide valuable insights for clinicians and researchers working in the field of sepsis and SAE and contribute to the development of new treatment options for this challenging condition.

show abstract

“…Sepsis is a systemic inflammatory response syndrome caused by the disorder of the body's immune response to infection, which can eventually develop into multiple organ dysfunction and lead to death (1)(2)(3)(4). Because the lack of effective targeted treatment measures, the mortality rate of sepsis can be as high as 28% to 40% and has become the number one common cause of death in intensive care unit worldwide.…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of Dexmedetomidine on the Liver Injury in Sepsis Through Inhibition of Necroptosis

Meng,

Zhang

et al. 2024

Shock

Self Cite

View full text Add to dashboard Cite

Background Sepsis-induced liver injury leads to extensive necroptosis in hepatocytes, which is the main factor of liver dysfunction. This study aims to investigate the protective effect of dexmedetomidine (DEX) on septic liver and to explore whether its molecular mechanism is related to the modulation of necroptosis. Methods The model of septic liver injury was induced by cecal ligation and puncture (CLP) in rats. DEX and necrostatin-1(Nec-1), a specific antagonist of necroptosis, were administered 1 h before CLP. The levels of arterial blood gas (ABG), serum AST and ALT were measured at 6, 12 and 24 h after CLP. The survival rate was observed 24 h after CLP. Liver pathological changes and apoptosis, the contents of IL-6 and TNF-α in liver tissue homogenates, the ROS content in liver tissue, and the expression levels of RIP1, RIP3, MLKL and HMGB1 were detected. Results At 6, 12, and 24 h after CLP, the levels of ALT and AST levels increased, and liver enzyme levels gradually increased with the progression of sepsis. In ABG analysis, PaO2 gradually decreased and lactic acid concentration gradually increased during these three time periods. The morphological impairment of liver tissues, increased apoptosis, elevated inflammatory factors (IL-6 and TNF-α), increased ROS level and necroptosis components (RIP1, RIP3, MLKL and HMGB1) were all observed in sepsis rats. However, these injuries can be ameliorated by pretreatment with DEX. Meanwhile, Nec-1 pretreatment also reduced the expression of RIP1, RIP3, MLKL, HMGB1, and ROS level. Conclusion Our study suggests that DEX alleviates septic liver injury, and the mechanism is associated with the inhibition of necroptosis.

show abstract

Molecular hydrogen attenuates sepsis-induced cognitive dysfunction through regulation of tau phosphorylation

Cited by 10 publications

References 43 publications

The role of the peripheral system dysfunction in the pathogenesis of sepsis-associated encephalopathy

The role of the peripheral system dysfunction in the pathogenesis of sepsis-associated encephalopathy

Exploring Neuroprotective Agents for Sepsis-Associated Encephalopathy: A Comprehensive Review

The Protective Effect of Dexmedetomidine on the Liver Injury in Sepsis Through Inhibition of Necroptosis

Contact Info

Product

Resources

About