Receptor-interacting protein kinase-3 (RIPK3): a new biomarker for necrotising enterocolitis in preterm infants.

OBJECTIVE: This study aimed to evaluate the role of receptor-interacting protein kinase-3 (RIPK3) in the diagnosis, estimation of disease severity, and prognosis of premature infants with necrotising enterocolitis (NEC). METHODS: RIPK3, lactic acid (LA), and C-reactive protein (CRP) levels were measured in the peripheral blood of 108 premature infants between 2019 and 2023, including 24 with stage II NEC, 18 with stage III NEC and 66 controls. Diagnostic values of the indicators for NEC were evaluated via receiver operating characteristic (ROC) curve analysis. RESULTS: Plasma RIPK3 and LA levels upon NEC suspicion in neonates with stage III NEC were 32.37 ± 16.20 ng/mL. The ROC curve for the combination of RIPK3, LA, CRP for NEC diagnosis were 0.925. The time to full enteral feeding (FEFt) after recovery from NEC was different between two expression groups of plasma RIPK3 (RIPK3 < 20.06 ng/mL and RIPK3 ≥ 20.06 ng/mL). CONCLUSION: Plasma RIPK3 can be used as a promising marker for the diagnosis and estimation of disease severity of premature infants with NEC and for the guidance on proper feeding strategies after recovery from NEC.

[Effect of glucose regulated protein 78 gene silencing on hyperoxia-induced apoptosis in alveolar epithelial cells].

OBJECTIVE: To investigate the effect and possible mechanism of small interfering RNA (siRNA)-mediated glucose regulated protein 78 (GRP78) gene silencing on hyperoxia-induced apoptosis of alveolar epithelial cells. METHODS: Human lung adenocarcinoma A549 cells in vitro were transfected with siRNA by Lipofectamine(TM)2000. Cells were divided into untransfected group, scrambled siRNA group and GRP78-siRNA group. A model of hyperoxia-induced cell injury was established by 95% oxygen. After 48 hours, the mRNA and protein levels of GRP78 and C/EBP homologous protein (CHOP) were detected respectively by real-time PCR and Western blotting, and cell apoptosis was measured by flow cytometry. RESULTS: By GRP78 siRNA interference, the mRNA and protein levels of GRP78 decreased significantly, while CHOP increased significantly. The apoptosis rate of A549 cells was elevated significantly. CONCLUSION: GRP78 gene silencing may enhance the CHOP apoptotic pathway and promote apoptosis in alveolar epithelial cells induced by hyperoxia, suggesting the potential value of GRP78 as a therapeutic target for the clinical treatment of bronchopulmonary dysplasia.