Gentisic acid mitigates gentamicin-induced nephrotoxicity in rats

Area of Science:

• Pharmacology
• Toxicology
• Nephrology

Background:

• Gentamicin (GEN) is an antibiotic known to cause nephrotoxicity.
• Oxidative stress and inflammation are key mechanisms in GEN-induced kidney injury.
• Gentisic acid (GA) is being investigated for its potential protective properties.

Purpose of the Study:

• To evaluate the protective effects of gentisic acid (GA) against gentamicin (GEN)-induced nephrotoxicity in rats.
• To assess the impact of GA on oxidative stress, inflammatory markers, and kidney function following GEN exposure.

Main Methods:

• Rats were administered varying doses of GA (25, 50, 100 mg/kg) orally for 14 days.
• Gentamicin (100 mg/kg) was administered intraperitoneally from day 8 to day 14.
• Serum and renal tissue markers of kidney injury, oxidative stress (MDA, GSH), inflammation (TNF-α, IL-1β), and antioxidant enzyme activities (CAT, SOD, GPx) were analyzed.

Main Results:

• GEN administration significantly increased markers of kidney injury (NGAL, KIM-1, BUN, Cr) and oxidative stress (MDA, NO).
• GEN exposure elevated inflammatory cytokines (TNF-α, IL-1β) and decreased antioxidant enzyme activities (CAT, SOD, GPx) in renal tissue.
• GA treatment significantly mitigated GEN-induced increases in kidney injury markers, oxidative stress, and inflammation, while restoring antioxidant enzyme activity.

Conclusions:

• Gentisic acid (GA) demonstrates significant nephroprotective effects against gentamicin (GEN)-induced kidney damage.
• GA ameliorates GEN-induced nephrotoxicity by alleviating oxidative stress and suppressing inflammatory responses.
• GA holds potential as a therapeutic agent to prevent or treat antibiotic-induced kidney injury.