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<p>To investigate the role of endothelial glycocalyx (eGC) degradation in mediating the progression from systemic inflammation to neuroinflammation and cognitive impairment in aged rats, and to explore the protective effects of the mitochondrial-targeted peptide SS-31. Aged male Wistar rats (24&#xa0;months) were assigned to four groups: Vehicle, LPS, LPS + SS-31, and SS-31 alone. Systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS). SS-31 was administered 30&#xa0;min prior to LPS injection in the LPS + SS-31 group. Serum levels of eGC degradation products (syndecan-1 [SDC-1], hyaluronic acid [HA], heparan sulfate [HS]) and inflammatory markers (IL-1β, TNF-α) in hippocampus were measured using ELISA. Hippocampal levels of postsynaptic density 95 (PSD-95) were also assessed. LPS-induced systemic inflammation led to significant increases in serum levels of SDC-1, HA, and HS, correlating with elevated hippocampal IL-1β and TNF-α levels and reduced PSD-95 expression. These findings suggest that eGC degradation facilitates the transfer of systemic inflammation to the brain, contributing to neuroinflammation.&#xa0;SS-31 pretreatment attenuated eGC degradation, reduced neuroinflammation, and restored PSD-95 levels, suggesting its potential protective role. eGC degradation is a key intermediary linking systemic inflammation to neuroinflammation and cognitive decline in aged rats. SS-31 may serve as a promising preventive strategy by preserving eGC integrity and mitigating neuroinflammatory processes.</p>

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Endothelial Glycocalyx Degradation as a Mediator of Neuroinflammation and Cognitive Impairment in Aged Rats: Protective Role of SS-31

  • 期刊论文

  • 发表日期：

    2025年11月17日

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  • Min-Hui Kan,
  • Yang Liu,
  • Fan-Qi Meng,
  • Long Fan,
  • Yan Wu,
  • Tian-Long Wang

摘要

To investigate the role of endothelial glycocalyx (eGC) degradation in mediating the progression from systemic inflammation to neuroinflammation and cognitive impairment in aged rats, and to explore the protective effects of the mitochondrial-targeted peptide SS-31. Aged male Wistar rats (24 months) were assigned to four groups: Vehicle, LPS, LPS + SS-31, and SS-31 alone. Systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS). SS-31 was administered 30 min prior to LPS injection in the LPS + SS-31 group. Serum levels of eGC degradation products (syndecan-1 [SDC-1], hyaluronic acid [HA], heparan sulfate [HS]) and inflammatory markers (IL-1β, TNF-α) in hippocampus were measured using ELISA. Hippocampal levels of postsynaptic density 95 (PSD-95) were also assessed. LPS-induced systemic inflammation led to significant increases in serum levels of SDC-1, HA, and HS, correlating with elevated hippocampal IL-1β and TNF-α levels and reduced PSD-95 expression. These findings suggest that eGC degradation facilitates the transfer of systemic inflammation to the brain, contributing to neuroinflammation. SS-31 pretreatment attenuated eGC degradation, reduced neuroinflammation, and restored PSD-95 levels, suggesting its potential protective role. eGC degradation is a key intermediary linking systemic inflammation to neuroinflammation and cognitive decline in aged rats. SS-31 may serve as a promising preventive strategy by preserving eGC integrity and mitigating neuroinflammatory processes.