Objective To investigate the effects and mechanisms of fatty acid binding protein 4(FABP4)on ferroptosis in human renal tubular epithelial cells(HK-2)treated with hypoxia/reoxygenation(H/R).Methods HK-2 cells were cultured in vitro and subjected to hypoxia for 24 hours followed by reoxygenation for different durations(1,3,6 h).The messenger RNA(mRNA)and protein levels of FABP4 in HK-2 cells were detected at each time point using real-time fluorescent quantitative polymerase chain reaction and Western blotting.Small interfering RNA(siRNA)technology was used to silence the expression of FABP4 gene in HK-2 cells,which were then treated with H/R(24 h of hypoxia and 6 h of reoxygenation)or treated with the Nrf2 inhibitor ML385.Cell proliferation activity was assessed using cell counting kit-8(CCK-8).Lactate dehydrogenase(LDH)levels were measured by enzyme-linked immune absorbent assay.Malondialdehyde(MDA),glutathione(GSH)and ferrous ion(Fe2+)levels were determined by biochemical technology.Reactive oxygen species(ROS)levels were detected using the 2',7'-dichlorodihydrofluorescein diacetate fluorescence probe.Protein expression levels of FABP4,nuclear factor E2-related factor 2(Nrf2),heme oxygenase-1(HO-1),glutathione peroxidase 4(GPX4)and solute carrier family 7 member 11(SLC7A11)were measured by Western blotting.Results The mRNA and protein levels of FABP4 in HK-2 cells increased with prolonged reoxygenation time(all P<0.05).H/R treatment reduced cell proliferation activity,increased LDH levels in the cell supernatant,and elevated MDA,Fe2+and ROS levels in HK-2 cells while decreasing GSH levels and the protein levels of Nrf2,HO-1,GPX4 and SLC7A11(all P<0.05).Silencing FABP4 enhanced the proliferation activity of H/R-treated HK-2 cells(P<0.05),reduced MDA,Fe2+and ROS levels,increased GSH levels,and elevated the protein levels of Nrf2,HO-1,GPX4 and SLC7A11(all P<0.05).However,these beneficial effects of FABP4 silencing on H/R-induced ferroptosis in HK-2 cells were reversed by co-treatment with ML385.Conclusions Silencing FABP4 alleviated H/R-induced ferroptosis in HK-2 cells,possibly by activating the Nrf2/GPX4 axis.

Objective To investigate the effects and mechanisms of fatty acid binding protein 4(FABP4)on ferroptosis in human renal tubular epithelial cells(HK-2)treated with hypoxia/reoxygenation(H/R).Methods HK-2 cells were cultured in vitro and subjected to hypoxia for 24 hours followed by reoxygenation for different durations(1,3,6 h).The messenger RNA(mRNA)and protein levels of FABP4 in HK-2 cells were detected at each time point using real-time fluorescent quantitative polymerase chain reaction and Western blotting.Small interfering RNA(siRNA)technology was used to silence the expression of FABP4 gene in HK-2 cells,which were then treated with H/R(24 h of hypoxia and 6 h of reoxygenation)or treated with the Nrf2 inhibitor ML385.Cell proliferation activity was assessed using cell counting kit-8(CCK-8).Lactate dehydrogenase(LDH)levels were measured by enzyme-linked immune absorbent assay.Malondialdehyde(MDA),glutathione(GSH)and ferrous ion(Fe2+)levels were determined by biochemical technology.Reactive oxygen species(ROS)levels were detected using the 2',7'-dichlorodihydrofluorescein diacetate fluorescence probe.Protein expression levels of FABP4,nuclear factor E2-related factor 2(Nrf2),heme oxygenase-1(HO-1),glutathione peroxidase 4(GPX4)and solute carrier family 7 member 11(SLC7A11)were measured by Western blotting.Results The mRNA and protein levels of FABP4 in HK-2 cells increased with prolonged reoxygenation time(all P<0.05).H/R treatment reduced cell proliferation activity,increased LDH levels in the cell supernatant,and elevated MDA,Fe2+and ROS levels in HK-2 cells while decreasing GSH levels and the protein levels of Nrf2,HO-1,GPX4 and SLC7A11(all P<0.05).Silencing FABP4 enhanced the proliferation activity of H/R-treated HK-2 cells(P<0.05),reduced MDA,Fe2+and ROS levels,increased GSH levels,and elevated the protein levels of Nrf2,HO-1,GPX4 and SLC7A11(all P<0.05).However,these beneficial effects of FABP4 silencing on H/R-induced ferroptosis in HK-2 cells were reversed by co-treatment with ML385.Conclusions Silencing FABP4 alleviated H/R-induced ferroptosis in HK-2 cells,possibly by activating the Nrf2/GPX4 axis.

Objective:To explorethe the clinical manifestations, treatment and prognosis of anastomotic pseudoaneurysm after renal transplantation caused by infection.Methods:Clinical data of 1 recipient with pseudoaneurysm after renal transplantation due to Pseudomonas aeruginosa infection were retrospectively analysed and combined with a literature review. Results:At Month 2 post-transplantation, the recipient developed right lower abdominal pain, and contrast-enhanced ultrasound examination showed a pseudoaneurysm at the artery anastomosis. Anti-infection and anti-rejection therapy had no obvious effect, and therefore next surgical exploration was performed. A size4.0 cm×3.5cm pseudoaneurysm was found intraoperatively at the graft renal artery anastomosis.After graft was evaluated as having no preservation value, the transplanted kidney and pseudoaneurysm were resected. Bacterial culture indicated Pseudomonas aeruginosa infection.The recipient recovered well and waited for next transplantation. Conclusions:Pseudoaneurysm of transplanted kidney is a very rare complication after renal transplantation, and caused by infection of Pseudomonas aeruginosa is more rarer, It has not been reported in mainland China.This type of recipient has the characteristics of high graft inactivation rate and high mortality rate. Timely surgical resection can effectively prevent the deterioration of disease.