Abstract
The renoprotective effect of thymol (TML) was investigated in rats challenged with gentamicin (GN). Rats received TML (20 mg/kg/day, p.o.) for 15 days, and GN (80 mg/kg/day, i.p.) starting from the 8th day. TML significantly lowered serum creatinine and neutrophil gelatinase-associated lipocalin, and renal malondialdehyde, nitric oxide, tumor necrosis factor-α, interleukin-18, Bax, caspase-3, and caspase-9 in GN-challenged rats. In addition, TML caused a significant increment of renal total antioxidant capacity in rats received GN. Moreover, TML significantly ameliorated GN-induced histopathological kidney tissue injury, and significantly decreased nuclear factor-κB p65 and kidney injury molecule-1 expressions in kidneys of GN-challenged rats. It was concluded that TML guarded against CN-induced nephrotoxicity in rats via inhibition of oxidative stress, inflammation, and apoptosis.
Highlights
Gentamicin (GN), an antibiotic related to aminoglycosides, is commonly used to treat serious infections caused by aerobic Gram-negative bacilli
Administration of GN (80 mg/kg/day, i.p.) for 8 days resulted in significant increases of serum creatinine and neutrophil gelatinase-associated lipocalin (NGAL) (p < 0.05) in comparison with the control values (Fig. 1A)
TML caused significant decrements of renal nuclear factor-κB (NF-κB) p65 and kidney injury molecule-1 (KIM-1) expressions (p < 0.05) in rats challenged with GN (Figs 3, 4)
Summary
Gentamicin (GN), an antibiotic related to aminoglycosides, is commonly used to treat serious infections caused by aerobic Gram-negative bacilli. Despite its efficacy in bacterial eradication, GN-induced nephrotoxicity is considered a major adverse effect which limits its usefulness (Hayward et al 2018; Srisung et al 2017). A well-built evidence proposes that increased manufacturing of reactive oxygen species (ROS) and reactive nitrogen species (RNS), are implicated in GN-induced AKI.
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