Inhibition of mast cell tryptase attenuates neuroinflammation via PAR-2/p38/NF kappa B pathway following asphyxial cardiac arrest in rats


Ocak U., Ocak P., Huang L., Xu W., Zuo Y., Li P., ...More

JOURNAL OF NEUROINFLAMMATION, vol.17, no.1, 2020 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 17 Issue: 1
  • Publication Date: 2020
  • Doi Number: 10.1186/s12974-020-01808-2
  • Journal Name: JOURNAL OF NEUROINFLAMMATION
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, CINAHL, EMBASE, MEDLINE, Veterinary Science Database, Directory of Open Access Journals
  • Keywords: Asphyxia, Cardiac arrest, Cognitive, Global brain ischemia, Mast cell, Neuroinflammation, PAR-2, Tryptase, PROTEASE-ACTIVATED RECEPTORS, GLOBAL CEREBRAL-ISCHEMIA, INTRACEREBRAL HEMORRHAGE, MICROGLIA ACTIVATION, COLLAGEN-SYNTHESIS, BRAIN, SURVIVAL, PATHOPHYSIOLOGY, RESUSCITATION, INFILTRATION
  • Bursa Uludag University Affiliated: No

Abstract

Background: Cardiac arrest survivors suffer from neurological dysfunction including cognitive impairment. Cerebral mast cells, the key regulators of neuroinflammation contribute to neuroinflammation-associated cognitive dysfunction. Mast cell tryptase was demonstrated to have a proinflammatory effect on microglia via the activation of microglial protease-activated receptor-2 (PAR-2). This study investigated the potential anti-neuroinflammatory effect of mast cell tryptase inhibition and the underlying mechanism of PAR-2/p-p38/NF kappa B signaling following asphyxia-induced cardiac arrest in rats.