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A novel preventive mechanism of gentamicin-induced nephrotoxicity by atorvastatin.

Atorvastatin (ATO) inhibited the synthesis of non-steroidal isoprenoid compounds and possessed pleiotropic effect. However, the detailed mechanism of ATO in preventing gentamicin (GM)-induced renal injury remained obscure. Although underlying multifaceted mechanisms involving in GM-induced nephrotoxicity were well known, further work on elucidating the essential mechanism was needed. By using fluorogenic derivatization-liquid chromatography tandem mass spectrometry proteomic method (FD-LC-MS/MS method), we investigated the effects and mechanisms of ATO treatment on GM-induced nephrotoxicity rats. Consequently, 49 differentially expressed proteins were identified. The most significant mechanisms of nephrotoxicity caused by GM were mitochondrial dysfunction, fatty acid metabolism and oxidative stress. Their upstream regulator was also found to be PPARα. The proteins involving in GM nephrotoxicity were sodium-hydrogen exchanger regulatory factor (SLC9A3R1), cathepsin V (CTSV), macrophage Migration Inhibitory Factor (MIF) and RhoGDP dissociation inhibitor alpha (ARHGDIA). After ATO intervention, we observed a reverse enrichment pattern of the expression of them, especially in CTSV and SLC9A3R1 (p-value<0.05). We predicted ATO may improve abnormal phospholipid metabolism and phospholipidosis caused by GM and also alleviate cell volume homeostasis and reverse the interference of GM to the transporter. Furthermore, proteomic results also provided clues for GM-induced nephrotoxicity biomarkers such as CTSV and transthyretin.