Platelet rich plasma alleviates OGD/R injury in N2a cell by enhancing autophagy through the miR‑223/PAQR3 pathway.

Our study constructed an in vitro model of cerebral ischemia/reperfusion (I/R) injury to evaluate the protective effect of platelet rich plasma (PRP) on I/R injury and uncover the mechanism behind it. Firstly, N2a cells were exposed in the condition of oxygen and glucose deprivation/reperfusion (OGD/R) to construct a model of cerebral I/R in vitro. MTT assay was employed to access the effects of PRP in N2a cell OGD/R injury. Then, we evaluated the role of the expression of miR‑223, progestin and adipoQ receptors 3 (PAQR3) and autophagy markers in the neuroprotective effect of PRP by qPCR and western blot. And the effect of miR‑223/PAQR3 axis regulated autophagy in the neuroprotection of PRP was verified by overexpressing miR‑223 and PAQR3. Finally, the interaction between miR‑223 and PAQR3 was analyzed by the luciferase reporter gene. The results showed that after OGD/R treatment of N2a cells, the expression of miR‑223 increased and the expression of PAQR3 and autophagy decreased. PRP improved cells damage caused by OGD/R in N2a cell, and reduced the expression of miR‑223 in cells, increased PAQR3 and autophagy. The luciferase reporter assay was used to prove that miR‑223 could target PAQR3 directly. Overexpression of miR‑223 could eliminate the improvement effect of PRP on OGD/R cells, but at the same time, overexpression of PAQR3 restored the protection of PRP from cell damage. Our research found that in the OGD/R injury in vitro model, PRP inhibited the expression of miR‑223 and enhanced autophagy to attenuate the injury by increasing the expression of PAQR3.