Desflurane attenuates renal ischemia-reperfusion injury by modulating ITGB1/CD9 and reducing oxidative stress in tubular epithelial cells.

OBJECTIVE

Renal ischemia-reperfusion (I/R) injury triggers significant oxidative stress and inflammation, leading to tubular epithelial cell (TEC) damage. This study investigates the protective role of Desflurane (DFE) in renal I/R by modulating the ITGB1/CD9 signaling pathway and mitigating oxidative damage.

METHODS

Single-cell RNA sequencing (scRNA-seq) and transcriptome analysis identified ITGB1 as a key regulatory gene in TECs during renal I/R. The effects of DFE on ITGB1/CD9 expression were evaluated through in vitro experiments using RT-qPCR, Western blot, and TUNEL assays. A mouse model of renal I/R was employed to assess renal function and oxidative stress markers under DFE treatment.

RESULTS

DFE reduced ITGB1 and CD9 expression, resulting in decreased TEC apoptosis and enhanced proliferation. In vivo, DFE-treated mice exhibited improved renal function, with significantly lower serum creatinine and blood urea nitrogen (BUN) levels. Additionally, DFE reduced oxidative stress, as indicated by decreased malondialdehyde (MDA) and myeloperoxidase (MPO) activity, alongside increased superoxide dismutase (SOD) activity.

CONCLUSION

DFE confers renal protection against I/R by modulating the ITGB1/CD9 axis and reducing oxidative stress, offering a promising therapeutic strategy for mitigating kidney damage.