Loss of lncRNA UCA1 ameliorates the injury managed by cerebral ischemia-reperfusion by sponging miR-18a-5p.

Introduction: Acute ischemic stroke (AIS) is a disease with high morbidity and mortality in the clinic. The current experiments aimed to study the effects of UCA1 interfering miR-18a-5p on cerebral ischemia-reperfusion (CI/R).

Material and methods: For rat models undergoing middle cerebral artery infarction (MCAO) surgery, the expression of UCA1 and miR-18a-5p was evaluated by qRT-PCR, and underlying function was identified by detecting infarct size, neurological scores, and inflammation. Luciferase report was applied to verify the relationship between UCA1 and miR-18a-5p. In the cell models, the impacts of UCA1 and miR-18a-5p were validated by CCK-8 assay, flow cytometry analysis, and ELISA. In patients with AIS, Pearson correlation was carried out to unveil the association between UCA1 and miR-18a-5p.

Results: The expression of UCA1 was at high levels and miR-18a-5p was at low levels in AIS patients. UCA1 knockdown showed a protective role in infarct size, neurofunction, and inflammation via binding miR-18a-5p. MiR-18a-5p participated in the regulation of UCA1 on cell viability, cell apoptosis, lactate dehydrogenase (LDH) levels, and inflammation. In patients with AIS, overexpression of UCA1 and underexpression of miR-18a-5p had a reverse correlation.

Conclusions: Elimination of UCA1 was favourable to the recovery of the rat model and cells from CI/R damage by efficaciously sponging miR-18a-5p.