Inhibition of mast cell tryptase attenuates neuroinflammation via PAR-2/p38/NF kappa B pathway following asphyxial cardiac arrest in rats
JOURNAL OF NEUROINFLAMMATION, cilt.17, sa.1, 2020 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 17 Sayı: 1
- Basım Tarihi: 2020
- Doi Numarası: 10.1186/s12974-020-01808-2
- Dergi Adı: JOURNAL OF NEUROINFLAMMATION
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, CINAHL, EMBASE, MEDLINE, Veterinary Science Database, Directory of Open Access Journals
- Anahtar Kelimeler: 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 Uludağ Üniversitesi Adresli: Evet
Özet
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.