Propofol can suppress renal ischemia-reperfusion injury through the activation of PI3K/AKT/mTOR signal pathway

Renal ischemia/reperfusion injury (IRI) remains one of the most diseases in clinic. The purpose of this study was to investigate the potential role and mechanism of propofol in protecting mice kidney from IRI. Renal I/R model was established in C57/BL6 mice by clamping bilateral renal pedicles for 35 min. The mice were randomly divided into four groups: sham group, IR group, IR + Propofol group, and IR + Propofol+LY294002 group. Histological assessment of kidney was conducted by HE staining and the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) of each group were measured. Expressions of inflammatory factors (IL-6, TNF-α) were detected by qRT-PCR and immunoblotting. The expression levels of cleaved Caspasse-3, PI3K, Akt, p-Akt, mTOR, and p-mTOR within renal tissue samples were measured by Western Blot. The levels BUN, Cr and morphological damage score increased significantly after renal IRI. However, such changes could be prevented by propofol. Besides, IRI reduced renal expressions of PI3K, p-Akt, p-mTOR, and increased the levels of IL-6, TNF-α，cl-caspase-3 in kidney, After propofol treatment, these changes were significantly alleviated, but the use of PI3K inhibitor LY294002 could reverse the effects of propofol. Propofol can protect renal IRI partially by reducing apoptosis and release of inflammatory cytokines, which is possibly involved in the modulation of the PI3K/AKT/mTOR signaling pathway. Our data suggested that propofol may play certain positive roles in protecting the kidney from IRI.