17β-estradiol suppresses hyperoxia-induced apoptosis of oligodendrocytes through paired-immunoglobulin-like receptor B.

Hyperoxia is a high risk factor for neurodevelopmental disorders and can cause nerve cell death. 17β‑Estradiol (E2) has been demonstrated as a neuroprotective agent. In the present study, the effect of hyperoxia on rat oligodendrocyte precursor cells (OPCs) in vivo and the neuroprotective effects of E2 on these cells were investigated. OPCs were treated with various concentrations of E2 and were harvested for reverse transcription‑quantitiative polymerase chain reaction (RT‑qPCR) analysis at various time‑points. RT‑qPCR analysis demonstrated that paired immunoglobin‑like receptor B (PriB) PriB mRNA expression levels were markedly decreased following treatment with 10(‑6), 10(‑7) and 10(‑8) M E2. Cells treated with 10(‑7) M E2 for 24 h were selected for subsequent experiments. PriB was silenced with small interfering (si)RNA and the effects of E2 treatment and silencing of PriB on the viability and apoptosis of OPCs under hyperoxic stimulation was detected using 3‑(4,5‑dimethyl‑2‑thiazolyl)‑2,5‑diphenyl‑2‑H‑tetrazoliu‑bromide (MTT) assay and flow cytometry analysis. The results revealed that hyperoxia induced apoptosis in OPCs and decreased their viability. Hyperoxia also induced the expression of caspases‑3 and ‑8, and Fas cell surface death receptor (Fas). E2 treatment markedly downregulated the expression of PirB. E2 treatment or PirB silencing markedly decreased hyperoxia‑induced apoptosis, increased cell viability and decreased the expression of caspases‑3 and ‑8, and Fas in OPCs, indicating that E2 protects OPCs from hyperoxia‑induced apoptosis, predominantly through the downregulation of PirB The results of the present study provide a theoretical basis for the reasonable use of oxygen in Neonatal Intensive Care Units.