Background::CD5L (CD5 molecular-like) plays an important role in lipid metabolism and immune regulation. This study aimed to investigate the roles of CD5L on liver hepatocellular carcinoma (LIHC).Methods::We analyzed the CD5L mRNA expression and its potential prognostic value based on The Cancer Genome Atlas and Gene Expression Omnibus databases. Immunohistochemical analysis was used to investigate the CD5L levels in LIHC tissues. Serum CD5L levels in LIHC were detected by enzyme-linked immunosorbent assay. Cell Counting Kit-8 (CCK-8) assay was used to investigate the effect of CD5L treatment on HepG2 and QSG-7701 cell proliferation. CD5L expression correlated genes were exhumed based on the LinkedOmics. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses for CD5L associated genes were performed. The correlation between CD5L and tumor immune infiltration was analyzed by using Tumor Immune Estimation Resource (TIMER) 2.0.Results::CD5L mRNA and protein levels were significantly decreased in LIHC tumor tissue compared with non-tumor control tissues. Moreover, serum CD5L levels were significantly lower in LIHC patients than that in healthy subjects. Gene Expression Profiling Interactive Analysis 2 and Kaplan-Meier plotter analysis showed that a high-CD5L expression was correlated with favorable overall survival in LIHC patients, except the LIHC patients with hepatitis virus. CCK-8 results showed that CD5L treatment significantly decreased HepG2 cell proliferation in a concentration-dependent manner, and CD5L treatment had no effect on the proliferation of non-tumor hepatocyte line QSG-7701. CD5L associated genes were enriched in the immune response biological process, and CD5L expression levels were positively correlated with the immune infiltrates of CD8 + T cell and M1 macrophage cells but negatively correlated with CD4 + T cells and M0 macrophage cell infiltration. Conclusions::Exogenous CD5L inhibits cell proliferation of hepatocellular carcinoma. CD5L may act as a role of prognostic marker.

Objective: To explore the effects and mechanisms of NADPH oxidase 4(NOX4) and nucleotide-binding oligomeric structural domain protein-like receptor protein 3(NLRP3) inflammasome on aging-associated renal injury in mice. Methods: The 6, 16, 20, and 24-month-old mice were used in this study. The levels of serum creatinine(SCr) and blood urea nitrogen(BUN) were detected by the kit. Frozen sections of kidney tissue were used to detect the levels of β-Galactosidase(β-Gal) and reactive oxygen species(ROS). The pathological changes of the kidney were observed by H&E, PAS, and Masson staining. The expressions of collagen Ⅳ and NLRP3 were detected by immunohistochemistry. Western blot was used to detect the expression of related proteins in the NOX4-NLRP3 signaling pathway in kidney tissues. Results: The results showed that, compared with 6-month-old mice, the levels of BUN and SCr in serum, β-Gal activity, and ROS level in the renal cortex increased, the glomerular and tubular injury was mild, and there was no obvious renal fibrosis change in 16-month-old mice. However, in 20 and 24-month-old mice, these indexes increased, the damage of glomeruli and renal tubules increased, and renal fibrosis appeared. In addition, expression of NOX4 and NLRP3 inflammasome-associated proteins mediating ROS production was upregulated in the kidneys of 20-and 24-month-old mice. Conclusion The NOX4-NLRP3 signaling pathway may activate and promote renal aging and renal fibrosis during aging.