Background: Sepsis-induced acute kidney injury (AKI) is a singularly grievous and life-threatening syndrome. Its pathogenesis is closely related to inflammatory response, apoptosis, oxidative stress, and ferroptosis. Cation transport regulator-like protein 1 (CHAC1), as a proapoptic factor, may be involved in apoptosis, oxidative stress, and ferroptosis. This study aimed to explore the role of CHAC1 in the lipopolysaccharide (LPS)-induced the human renal proximal tubular epithelial (HK-2) cells. Methods: HK-2 cells were challenged with LPS to construct a model of sepsis-induced AKI in vitro. The role of CHAC1 in the LPS-induced HK-2 cells was explored using Western blot assay, cell counting kit-8 (CCK-8), flow cytometry, and colorimetric assays. Additionally, N-acetyl cysteine (NAC) was incubated with HK-2 cells to define deeply the relation between oxidative stress and apoptosis or ferroptosis. Results: The expression of CHAC1 was enhanced in the kidney tissues of mice with sepsis--induced multiple organ dysfunction syndrome (MODS), through the Gene Expression Omnibus database (GSE60088 microarray dataset), and in the LPS-induced HK-2 cells. The cell viability was significantly reduced by LPS treatment, which was at least partly restored by the transfection of siCHAC1#1 and siCHAC1#2 but not siNC. In addition, down-regulation of CHAC1 counteracted the LPS-induced reactive oxygen species level and malonaldehyde concentrations while restored the LPS-induced glutathione concentrations. Meanwhile, interference of CHAC1 neutralized LPS-induced apoptosis rate, and the relative level of cleaved poly(ADP-ribose) polymerase (PARP)/PARP, and cleaved caspase-3/caspase-3. In addition, silencing of CHAC1 recovered the LPS-induced enhanced protein level of glutathione peroxidase 4 (GPx4) whereas antagonized the LPS-induced relative protein level of ACSL4 and that of iron. Moreover, application of NAC inverted the effect of CHAC1 on apoptosis and ferroptosis in HK-2 cells. Conclusion: CHAC1 exacerbated ferroptosis and apoptosis by enhancing oxidative stress in LPS-induced HK-2 cells.

Acute respiratory distress syndrome (ARDS) is one of the more serious diseases in human lung disease. Reducing its incidence rate is an important task in current clinical research. Dynamic monitoring of serum protein in patients will help to achieve the early diagnosis and treatment of ARDS. In this study, a protein monitoring model based on artificial neural network is proposed. First, surface enhanced laser desorption ionization time-of-flight mass spectrometry is used for protein detection, and then BP neural network is used for protein classification and content analysis. In the experimental analysis, serum samples from patients with acute respiratory distress syndrome in our hospital from November 2020 to August 2021 were selected for experimental testing. The experimental results show that the serum protein monitoring model based on BP neural network has low error and high convergence ability and can monitor individual protein in protein monitoring, and the area under the ROC curve in diagnostic performance reaches 0.854. The above results show that the artificial neural network has a good effect on the dynamic monitoring of serum protein in acute respiratory distress syndrome, and the diagnostic performance evaluation can reach 0.854, which has the ability to significantly improve the clinical diagnosis and treatment of acute respiratory distress syndrome.