Isoflurane regulates the level of HOXA11-AS and affects oxidative stress and inflammation in liver ischemia-reperfusion injury.

BACKGROUND

Isoflurane exhibits protective roles on ischemia-reperfusion injury (IRI), but whether isoflurane can alleviate the inflammation and oxidative stress of LIRI remains unknown.

AIM: To explore the effects of isoflurane treatment and HOXA11 antisense long noncoding RNA (HOXA11-AS) expression on LIRI.

METHODS

AML12 cells were used to construct a hypoxia-reoxygenation (H/R) model. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was employed to test the HOXA11-AS level, microRNA-130b-3p, and phosphatase and tensin homolog (PTEN). Cell viability was detected using the cell counting kit-8 (CCK-8) kit. The content of intracellular inflammatory factors was detected using the enzyme‑linked immunosorbent assay (ELISA) kit. The positive rate of reactive oxygen species (ROS) was detected using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA), and the contents of malondialdehyde (MDA) and superoxide dismutase (SOD) enzyme activities were detected using specialized kits. The dual luciferase reporter gene assay was used to verify the targeting relationship.

RESULTS

In the H/R model, the levels of HOXA11-AS and PTEN were increased, miR-130b-3p was decreased, cell viability was reduced, inflammatory factors level and oxidative stress were aggravated. The results showed an opposite trend with isoflurane pre-treatment. However, after HOXA11-AS overexpression, cell damage was further aggravated. HOXA11-AS is a molecular sponge for miR-130b-3p. It was revealed that the cell viability was improved, the inflammatory response and oxidative stress were weakened after transfection with miR-130b-3p mimic.

CONCLUSION

Isoflurane pretreatment reduced the level of HOXA11-AS, increased the level of miR-130b-3p, enhanced cell viability, and decreased cellular inflammatory factors level and oxidative stress in H/R model.