Kallistatin deficiency exacerbates neuronal damage after cardiac arrest.

ABSTRACT: The purpose of study was to evaluate that kallistatin deficiency causes excessive production of reactive oxygen species and exacerbates neuronal injury after cardiac arrest. For in vitro study, kallistatin knockdown human neuronal cells were given ischemia-reperfusion injury, and the oxidative stress and apoptosis were evaluated. For clinical study, cardiac arrest survivors admitted to the ICU were divided into the good (CPC 1-2) and poor (CPC 3-5) 6-month neurological outcome groups. The serum level of kallistatin, Nox-1, H₂O₂ were measured. Nox-1 and H₂O₂ levels were increased in the kallistatin knockdown human neuronal cells with ischemia-reperfusion injury (p < 0.001) and caspase-3 was elevated and apoptosis was promoted (SERPINA4 siRNA: p < 

SUBMITTER: Kim H 

PROVIDER: S-EPMC10881987 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature