Chlorogenic acid prevents vancomycin-induced nephrotoxicity without compromising vancomycin antibacterial properties

Area of Science:

• Pharmacology
• Nephrology
• Biochemistry

Background:

• Vancomycin (VCM) is a critical antibiotic for gram-positive infections.
• VCM use is limited by significant nephrotoxic side effects.
• Novel strategies are needed to mitigate VCM-induced kidney damage.

Purpose of the Study:

• To investigate the protective effects of chlorogenic acid (CA) against VCM-induced nephrotoxicity in a rat model.
• To elucidate the underlying mechanisms of CA's renoprotective action.

Main Methods:

• A rat model was used to induce nephrotoxicity with VCM.
• Animals were co-administered chlorogenic acid (CA) or vehicle.
• Kidney function markers (BUN, creatinine), oxidative stress indicators (MDA, NO), antioxidant enzyme activities, inflammatory markers (NF-κB, TNF-α, ILs), and apoptotic markers were assessed.

Main Results:

• CA co-administration prevented VCM-induced increases in blood urea nitrogen and serum creatinine.
• CA significantly attenuated VCM-induced oxidative and nitrosative stress, preserving antioxidant enzyme activities and glutathione levels.
• CA inhibited VCM-induced inflammatory responses and apoptosis markers.

Conclusions:

• Chlorogenic acid demonstrates significant renoprotective effects against vancomycin-induced nephrotoxicity in rats.
• CA mitigates VCM nephrotoxicity by reducing oxidative stress, inflammation, and apoptosis.
• CA's protective action does not interfere with vancomycin's in vitro antibacterial activity.