Therapeutic Potential of Meloxicam in Ameliorating Sepsis-Induced Renal Injury Through the PI3K/AKT Pathway

Abstract

Infectious ureteral stones often lead to sepsis. This study investigated the effect of meloxicam on renal injury caused by sepsis. A sepsis kidney injury model was established using lipopolysaccharide (LPS). HK-2 cells were divided into three groups: control, LPS, and LPS+Mel. The expression of TNF-α, IL-6, Bcl-2, and Bax mRNA and protein were detected using PCR and Western blot. The inflammation of HK-2 cells was observed using IL-1β immunofluorescence. Apoptosis was investigated using LDH content, TUNEL staining, and flow cytometry. The viability of HK-2 cells was detected using a CCK-8 assay. The protein expression of the PI3K/AKT pathway was examined to investigate the mechanism of action of Mel. LPS treatment increased TNF-α, IL-6, and Bax expression while decreasing Bcl-2 expression. However, Mel treatment reversed these effects. Mel also decreased the number of TUNEL-positive cells and the apoptotic rate and LDH content in the LPS+Mel group. Additionally, Mel up-regulated the p-PI3K and p-AKT expression, indicating that Mel inhibits inflammation and apoptosis of HK-2 cells treated with LPS by activating the PI3K/AKT pathway. In conclusion, Mel could inhibit inflammation and apoptosis of HK-2 cells treated with LPS via activation of PI3K/AKT pathway.