High-temperature requirement serine protease A2 inhibitor UCF-101 ameliorates damaged neurons in traumatic brain-injured rats by the AMPK/NF-κB pathway.

ABSTRACT: Traumatic brain injury (TBI) leads to permanent damage, including neurological deficits, cognitive deficits, and cerebral edema. The specific inhibitor of serine protease Omi/high-temperature requirement A2 (Omi/HtrA2), UCF-101, exerts neuroprotective effects, but its role in TBI remains unclear. Eighty-four male Sprague Dawley rats were randomized to control, TBI, UCF-101 of low dose (1.5 μmol/kg), middle dose (3.0 μmol/kg), and high dose (6.0 μmol/kg), Compound C (AMPK inhibitor, 20 mg/kg), and high dose + Compound C groups. TBI rat modeling was operated by the controlled cortical impact method. Modified neurological severity score (mNSS) cognitive function, cerebral edema index, hematoxylin-eosin staining, TUNEL staining for apoptosis, ethidium bromide staining for blood-brain barrier (

SUBMITTER: Qiu TW 

PROVIDER: S-EPMC11889502 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature