Abstract
Our study aimed to assess the effect of liposomal epigallocatechin-gallate (LEGCG) compared with epigallocatechin-gallate (EGCG) solution on hepatic toxicity induced by gentamicin (G) administration in rats. Five groups were evaluated, a control group (no G administration) and four groups that received G (1 mL, i.p, 80 mg/kg b.w. (body weight/day), for 7 days) to which we associated daily administration 30 min before G of EGCG (G-EGCG, 2.5 mg/0.1 kg b.w.), LEGCG (G-LEGCG, 2.5 mg/0.1 kg b.w.) or silymarin (100 mg/kg b.w./day). The nitro-oxidative stress (NOx), catalase (CAT), TNF-α, transaminases, creatinine, urea, metalloproteinase (MMP) 2 and 9, and liver histopathological changes were evaluated. LEGCG exhibited better efficacy than EGCG, improving the oxidant/antioxidant balance (p = 0.0125 for NOx and 0.0032 for CAT), TNF-α (p < 0.0001), MMP-2 (p < 0.0001), aminotransferases (p = 0.0001 for AST and 0.0136 for ALT), creatinine (p < 0.0001), urea (p = 0.0006) and histopathologic liver changes induced by gentamicin. Our study demonstrated the beneficial effect of EGCG with superior results of the liposomal formulation for hepatoprotection in experimental hepatic toxicity induced by gentamicin.
Highlights
Introduction published maps and institutional affilGentamicin (G) is an aminoglycoside commonly used in clinical practice
The administration of EGCG, liposomal epigallocatechin-gallate (LEGCG) and silymarin decreases the damage of gentamicin on hepatic function with best results attributed to silymarin (Table 1)
Our study showed a significant increase of NOx after gentamicin administration, proving the presence of nitro-oxidative stress due to gentamicin toxicity (Table 4, Figure 2)
Summary
Introduction published maps and institutional affilGentamicin (G) is an aminoglycoside commonly used in clinical practice. Despite beneficial effects against bacterial infection, gentamicin-induced toxicity is one of the most critical side effects that require precaution when administering the drug. Due to their active participation in various metabolic pathways, the kidney and liver are exposed to damage associated with drug toxicity. Hepatotoxicity and nephrotoxicity are rare effects of gentamicin administration and are primarily associated with overdoses. Deciphering gentamicin-induced liver-toxicity associated mechanisms can be challenging due to the various and complex molecular mechanisms involved. The active role of the kidney and liver in different metabolic loops exposes these organs to oxidative-stress induced lesions [1]. Gentamicin-induced hepatotoxicity has been previously demonstrated iations
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