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Ginsenoside Rc Targets ROCK2 to Inhibit NF-κB Activation and Alleviate Cognitive Dysfunction in Septic Encephalopathy

Wei Wang1, Lv-Yue Wang2, Yan-Yan Zhao3

  • 1Department of Neurology, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, 210018, China. ww_2046@126.com.

Applied Biochemistry and Biotechnology
|September 18, 2025
PubMed
Summary

Ginsenoside Rc (GRc) alleviates septic encephalopathy (SE) by targeting the ROCK2/NF-κBp65 pathway. This study reveals GRc

Keywords:
Ginsenoside RcMolecular dockingNF-κBP65ROCK2Septic encephalopathy

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Immunology

Background:

  • Septic encephalopathy (SE) is a severe complication of systemic inflammatory response syndrome with limited therapeutic options.
  • Ginsenoside Rc (GRc), a herbal compound, shows neuroprotective potential but its role in SE is unknown.
  • Rho-associated kinase (ROCK) is implicated in sepsis, but its precise mechanism in SE requires elucidation.

Purpose of the Study:

  • To investigate the therapeutic potential of GRc in a murine model of SE.
  • To explore the ROCK-mediated mechanisms underlying SE pathogenesis and GRc's anti-septic effects.
  • To identify molecular targets of GRc in the context of SE.

Main Methods:

  • Established a murine model of SE using lipopolysaccharide (LPS) induction.
  • Assessed cognitive function using the Morris water maze and open-field tests.
  • Examined ROCK2 protein expression and NF-κBp65 phosphorylation in SE mice.
  • Evaluated the effect of GRc treatment on ROCK2 expression, NF-κBp65 phosphorylation, and inflammatory cytokine secretion.

Main Results:

  • GRc treatment significantly improved cognitive impairment in SE mice.
  • GRc reduced ROCK2 protein expression in LPS-induced SE.
  • GRc suppressed the phosphorylation of NF-κBp65, a downstream target of ROCK2.
  • GRc mitigated the secretion of pro-inflammatory cytokines.

Conclusions:

  • The ROCK2/NF-κBp65 signaling axis plays a critical role in the pathophysiology of SE.
  • GRc demonstrates significant therapeutic potential for SE by targeting the ROCK2/NF-κBp65 pathway.
  • GRc exerts its beneficial effects by directly binding to ROCK2, inhibiting NF-κBp65 phosphorylation, and reducing inflammation.