CLEC5A Knockdown Reduces Oxidative Stress and Inflammation Caused by Lipopolysaccharide in Renal Tubular Epithelial Cells via the NF-κB/NLRP3 Signaling Pathway

Sepsis-related acute kidney injury (S-AKI) is a severe condition characterized by rapid onset and high mortality. Thus, identifying effective treatments for S-AKI is of critical importance. Lipopolysaccharide (LPS) was used to activate HK-2 cells to mimic S-AKI <i>in vitro</i>. Lentiviral transfection was performed to knock down C-type lectin domain family 5 member A (CLEC5A) expression, and protein immunoblotting was used to detect changes in CLEC5A expression. Cell damage was evaluated using the cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH) kit, cellular inflammatory factor levels were determined using the enzyme-linked immunosorbent assay (ELISA), and oxidative stress signs were detected using the kit. Western blotting was used to detect the expression of NF-κB/NLRP3 (NLR family, pyrin domain-containing protein 3) pathway, and NF-κB activator was used to detect whether knockdown of CLEC5A acts through the NF-κB/NLRP3 pathway. LPS stimulated the expression of CLEC5A in HK-2 cells. Knockdown of CLEC5A could inhibit the LPS-induced decrease in HK-2 cell viability and increased LDH release. Knockdown of CLEC5A could inhibit the LPS-induced increase in HK-2 cell release of inflammatory factors. Knockdown of CLEC5A could inhibit LPS-induced oxidative stress. CLEC5A knockdown can prevent the NF-κB/NLRP3 signaling pathway from being activated, and NF-κB activation can undo the effects of CLEC5A knockdown. Knockdown of CLEC5A can ameliorate renal tubular damage and lessen inflammation and oxidative stress via reducing NF-κB/NLRP3 activation.