Alternate Pathways Preserve Tumor Necrosis Factor-α Production After Nuclear Factor-κB Inhibition in Neonatal Cerebral Hypoxia–Ischemia | Zendy

Cora H. Nijboer | Zendy; Cobi J. Heijnen | Zendy; Floris Groenendaal | Zendy; Frank van Bel | Zendy; Annemieke Kavelaars | Zendy

Open Access

Alternate Pathways Preserve Tumor Necrosis Factor-α Production After Nuclear Factor-κB Inhibition in Neonatal Cerebral Hypoxia–Ischemia

Author(s) -

Cora H. Nijboer,

Cobi J. Heijnen,

Floris Groenendaal,

Frank van Bel,

Annemieke Kavelaars

Publication year - 2009

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.109.560250

Subject(s) - medicine , ischemia , hypoxia (environmental) , tumor necrosis factor α , necrosis , tumor necrosis factor alpha , pharmacology , oxygen , chemistry , organic chemistry

Nuclear factor-kappaB (NF-kappaB) is an important regulator of inflammation and apoptosis. We showed previously that NF-kappaB inhibition by intraperitoneal TAT-NBD treatment strongly reduced neonatal hypoxic-ischemic (HI) brain damage. Neuroprotection by TAT-NBD was not associated with inhibition of cerebral cytokine production. We investigated how tumor necrosis factor-alpha (TNF-alpha) production is maintained after NF-kappaB inhibition and whether TNF-alpha contributes to brain damage.

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