Up-regulation of miR-137 can inhibit PTN in target manner to regulate PTN/PTPRZ pathway to prevent cognitive dysfunction caused by propofol.

OBJECTIVE

To explore the effects of miR-137 on cognitive dysfunction in rats induced by propofol (PRO).

METHODS

Male SD rats and SK-N-SH cells were purchased, and control and PRO groups were set up in the rats, and the same groups were set up in the cells. On the basis of the PRO group, miR-137 and PTN were up-regulated or down-regulated, and cognitive dysfunction and cell biological functions in each group were detected.

RESULTS

The cognitive function of rats induced by PRO might be affected. We observed that the escape latency of PRO group was significantly prolonged, with significantly lower percentage of time for target platform exploration and times of crossing the platform, while over-expression of miR-137 or knock down of PTN could change the above results. Under PRO intervention, the expression of miR-137 in SK-N-SH cells decreased in a dose-dependent manner, while the expression and protein level of PTN in SK-N-SH cells increased in a dose-dependent manner. Cytotoxicity test yielded a 30 μM concentration of PRO as the optimal experimental concentration. When miR-137 and PTN were up-regulated or down-regulated, PRO-induced cell apoptosis, proliferation and PTN/PTPRZ pathway protein phosphorylation level were effectively reversed. Dual luciferase reporter confirmed that miR-137 and PTN have targeted relationship.

CONCLUSION

Up-regulation of miR-137 can at least partially regulate PTN/PTPRZ pathway through the inhibition of PTN in a targeted manner, effectively inhibit cell apoptosis, and protect cognitive dysfunction caused by PRO.