Abstract / Summary
Liver transplantation, the sole curative for end-stage hepatopathy, is compromised by ischemia–reperfusion-elicited immunoinflammatory cascades that undermine graft viability, mandating sensitive, specific, noninvasive circulating markers. This study examines lncRNA FTX and miR-381-3p expression in hepatic ischemia–reperfusion injury (HIRI) after liver transplantation, confirming that lncRNA FTX regulates hepatocyte injury by sponging miR-381-3p via ceRNA. This study included 72 healthy individuals as controls alongside 68 HIRI patients. An H/R cellular insult was generated in AML12 monolayers. qPCR served to detect lncRNA FTX, miR-381-3p, and NFKBIA mRNA expression. Proliferation rates were gauged by CCK-8 and Edu, and apoptotic populations were scored via flow cytometry. The culture supernatants were assayed for inflammatory factors by ELISA. Oxidative stress indicators were evaluated using standard biochemical kits. Reduced expression of lncRNA FTX and NFKBIA and elevated miR-381-3p expression were observed in post-transplant HIRI. Combined clinical and molecular cellular data validated the dual targeting of lncRNA FTX and NFKBIA by miR-381-3p, which showed a notable negative correlation with the two targets. LncRNA FTX overexpression alone alleviated H/R-induced proliferation arrest, apoptosis, inflammation, and oxidative stress. This protection was reversed by miR-381-3p mimic but restored upon NFKBIA co-transfection. Hence, lncRNA FTX functioned through sponging miR-381-3p and upregulating NFKBIA. LncRNA FTX may sponge miR-381-3p to derepress NFKBIA, potentially restraining inflammation and oxidative stress and alleviating HIRI after liver transplantation. This finding extends our knowledge of non-coding regulatory networks in HIRI and offers preliminary mechanistic evidence for the FTX/miR-381-3p/NFKBIA axis; further validation in larger independent cohorts is required to assess its translational value.