J Vis Exp. 2026 Aug 4;(234). doi: 10.3791/71556.
ABSTRACT
Intracerebral hemorrhage (ICH) is a neurological disorder associated with high mortality and disability rates and can lead to severe neurological injury. This study investigated the role and underlying mechanism of FGD5-AS1 in ICH. In vitro and in vivo models of ICH were established. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure FGD5-AS1 and miR-93-5p expression. Neurological deficits were assessed using the modified Neurological Severity Score (mNSS), and cerebral edema was evaluated using the dry-wet weight method. Enzyme-linked immunosorbent assay (ELISA) was used to measure inflammatory cytokines and oxidative stress markers. Cell viability was evaluated using a cell viability and proliferation assay kit. The interaction between FGD5-AS1 and miR-93-5p was examined using dual-luciferase reporter assays and Pearson correlation analysis. Experimental ICH was accompanied by elevated FGD5-AS1 expression in both animal and cellular models. Suppression of FGD5-AS1 alleviated brain swelling, improved neurological performance, reduced inflammatory and oxidative injury, and enhanced endothelial cell survival. Inhibition of miR-93-5p diminished these protective effects, supporting a regulatory interaction between the two molecules. FGD5-AS1 negatively regulated miR-93-5p expression, and inhibition of miR-93-5p attenuated the effects observed following FGD5-AS1 knockdown. These results indicate that FGD5-AS1 may contribute to ICH-associated brain injury through regulation of miR-93-5p and that the FGD5-AS1/miR-93-5p axis may represent a potential target for further investigation in experimental ICH.
PMID:42612047 | DOI:10.3791/71556