Knockdown of lncRNA TUG1 attenuates cerebral ischemia/reperfusion injury through regulating miR-142-3p.

Abstract

Cerebral ischemia-reperfusion injury (CI/RI) is one of the most common diseases of the central nervous system. At present, there is no specific treatment for CI/RI. It is necessary to explore the mechanism of CI/RI and find new ways to prevent and treat CI/RI. An oxygen and glucose deprivation/recovery (OGD/R) model was established to evaluate the effects of mouse astrocytes (MA-C) cell viability and apoptosis of stepwise exposure to oxygen and glucose deprivation followed by their replenishment. This assessment included using taurine upregulated gene 1-small interfering RNAs (TUG1-siRNA) transfection to determine the effects of TUG1 knockdown on MA-C survival and apoptosis. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to evaluate TUG1 and miR-142-3p expression levels. The luciferase gene reporter assay was performed to validate that miR-142-3p is a TUG1 target. Accordingly, the effects of miR-142-3p knockdown on TUG1-induced MA-C apoptosis were determined using flow cytometry. Methyl thiazolyl tetrazolium (MTT) method was used to detect cell growth viability. Western blotting analysis was performed to detect the expression levels of apoptosis-related proteins. TUG1 was upregulated, while miR-142-3p was downregulated in the OGD/R model of MA-C cells. Inhibiting the expression of TUG1 could protect MA-C cells and reverse the decrease in growth viability and increasing apoptosis of MA-C cells caused by OGD/R stimulation. On the other hand, the inhibition of miR-142-3p offset the effect of TUG1 knockdown on cell viability and apoptosis. Inhibition of OGD/R-induced increases in TUG1 expression that in turn reduces miR-142-3p upregulation may suppress reperfusion-induced losses in cell viability.