LncRNA PCED1B-AS1 Inhibits Sepsis-Induced Acute Kidney Injury by Promoting Transformation of Macrophages from M1 to M2 Type via Regulating the miR-361-3p/SOCS1 Axis.

Purpose: A common complication observed in septic patients under intensive care is acute kidney injury (AKI), which is characterized by acute onset and strong inflammation, resulting in poor clinical outcomes for patients. This study aims to explore the expression status of PCED1B-AS1 in sepsis-induced AKI and to preliminarily investigate the molecular mechanism by which PCED1B-AS1 affects AKI. Patients and Methods: This study included 105 healthy individuals and 220 patients with sepsis (110 patients with AKI and 110 non-AKI patients). The levels of PCED1B-AS1 were examined by RT-qPCR. Macrophage polarization was induced by LPS treatment of RAW264.7 cells, and an in vitro renal injury model was established using HK-2 cells. Cell proliferation ability was evaluated by CCK-8 assay, apoptosis was detected by flow cytometry, and the levels of inflammatory factors were assessed using ELISA kits. The dual-luciferase assay was used to verify the interrelationship among the PCED1B-AS1/miR-361-3p/SOCS1 axis. Results: PCED1B-AS1 was downregulated in sepsis patients without AKI and further reduced in AKI patients. PCED1B-AS1 could differentiate healthy individuals from non-AKI sepsis patients and identify AKI patients. Additionally, low PCED1B-AS1 expression correlated with poor AKI prognosis. Overexpression of PCED1B-AS1 promoted the polarization of M1 macrophages to M2 by regulating the miR-361-3p/SOCS1 axis, thereby inhibiting apoptosis and inflammatory responses in HK-2 cells. Conclusion: PCED1B-AS1 may serve as a potential diagnostic and prognostic marker and inhibit sepsis-induced AKI by promoting transformation of macrophages from M1 to M2 type via regulating the miR-361-3p/SOCS1 axis.