N-tert-Butyl-α-phenylnitrone (PBN) (25-100 µM) treatment leads to a significant decrease in 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)-induced intracellular ROS accumulation. N-tert-Butyl-α-phenylnitrone also attenuates AAPH-induced cytotoxicity, matrix degradation, and apoptosis. N-tert-Butyl-α-phenylnitrone suppresses AAPH-induced activation of ERK/MAPK pathway. N-tert-Butyl-α-phenylnitrone has the potenial for intervertebral disc degeneration (IDD) research.

N-tert-Butyl-α-phenylnitrone (PBN; 100 mg/kg; intraperitoneal injection; twice a day; C57Bl/6 mice) treatment not only abolishes the LPS-induced lipid peroxidation, nitrotyrosine residue levels, and GSH depletion, but also decreases the incidence of external malformations.