J Vis Exp. 2026 Jul 3;(233). doi: 10.3791/71332.
ABSTRACT
Acute cerebral infarction causes irreversible injury in the infarct core and secondary damage in surrounding ischemic tissue, where apoptosis-related signaling may contribute to lesion progression. This study evaluated whether inhibition of microRNA-423-5p is associated with improved early outcomes in a rat model of permanent middle cerebral artery occlusion. Adult male Sprague-Dawley rats were assigned to Sham, permanent middle cerebral artery occlusion, permanent middle cerebral artery occlusion plus negative-control adenovirus, or permanent middle cerebral artery occlusion plus microRNA-423-5p-interfering adenovirus groups. A stereotactic intracerebroventricular injection was performed 72 h before occlusion. Neurological deficits were assessed 24 h after surgery using the Zea Longa score; infarct volume was quantified by 2,3,5-triphenyltetrazolium chloride staining; Bax and Bcl-2 protein expression were evaluated by Western blotting; and microRNA-423-5p expression was measured by quantitative real-time polymerase chain reaction. Bioinformatic prediction was also summarized to contextualize BAX as a potential microRNA-423-5p-associated apoptosis-related gene. microRNA-423-5p inhibition was associated with lower neurological deficit scores, reduced infarct volume, decreased Bax expression, increased Bcl-2 expression, and reduced microRNA-423-5p abundance in ischemic brain tissue. These findings support a preliminary association between inhibition of microRNA-423-5p and reduced injury severity after permanent cerebral ischemia. However, direct target validation and direct apoptosis assays are required to define the underlying mechanism.
PMID:42475301 | DOI:10.3791/71332