ASK1 inhibitor NQDI‑1 decreases oxidative stress and neuroapoptosis via the ASK1/p38 and JNK signaling pathway in early brain injury after subarachnoid hemorrhage in rats.

ABSTRACT: Oxidative stress and neuroapoptosis are key pathological processes after subarachnoid hemorrhage (SAH). The present study evaluated the anti‑oxidation and anti‑apoptotic neuroprotective effects of the apoptosis signal‑regulating kinase 1 (ASK1) inhibitor ethyl‑2,7‑dioxo‑2,7‑dihydro‑3H‑naphtho(1,2,3‑de)quinoline‑1‑carboxylate (NQDI‑1) in early brain injury (EBI) following SAH in a rat model. A total of 191 rats were used and the SAH model was induced using monofilament perforation. Western blotting was subsequently used to detect the endogenous expression levels of proteins. Immunofluorescence was then used to confirm the nerve cellular localization of ASK1. Short‑term neurological function was assessed using the modified Garcia scores and the beam balance test 24 h after SAH, whereas long‑

SUBMITTER: Duan J 

PROVIDER: S-EPMC9879074 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature