OBJECTIVE: To investigate the expression and significance of miR-423-5p in ischemic stroke to provide a new basis for the diagnosis and treatment of cerebral infarction. STUDY DESIGN: The Gene Expression Omnibus (GEO) database collected stroke-related data sets. Meta analysis was performed using the meta package of R 4.1.0 software. Target genes were predicted and enriched by miRWalk and KOBAS databases. A rat model of cerebral ischemia was established. Expression level of miR-423-5p in serum was detected by qRT-PCR. IL-1β, IL-6, and TNF-α were detected by ELISA. TUNEL was used to detect the apoptosis of brain tissue. CISH detected the expression and location of miR-423-5p in brain tissue. RESULTS: Seven qualified data sets were included in the analysis, and the high expression of miR-423-5p was the main trend in the stroke group. There was no heterogeneity, no publication bias, and low sensitivity among the data sets. Meta results indicated that the expression data of miR-423-5p in these studies was stable and reliable. Target genes predicted by the database mainly regulated inflammatory signaling pathways. After the establishment of rat brain injury model, it was found that serum miR-423-5p level in the model group was significantly higher than that in the normal group. At the same time, serum levels of aspirin treatment group and miR-423-5p silencing group were also higher than the normal group. In addition, compared with the normal group, the contents of IL-1β, IL-6, and TNF-α in other groups were significantly increased, and the apoptosis rate was also significantly increased. miR-423-5p expression in the cytoplasmic region in the model group, aspirin treatment group, and miR-423-5p silencing group was significantly higher than that in the normal group. CONCLUSION: These results indicated that the increased expression level of miR-423-5p predicted the occurrence and progression of cerebral infarction and may be a potential biomarker for the diagnosis of cerebral infarction. © Science Printers and Publishers, Inc.