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Gentamicin is an aminoglycoside antibiotic with a rapid bactericidal effect on the treatment of many infections. However, its use at high concentrations for more than 7 days causes nephrotoxic side effects. This study investigated the potential of Resatorvid and alpha lipoic acid (ALA) in mitigating gentamicin‐induced nephrotoxicity in rats, considering biochemical, histopathological, and molecular parameters. This study randomly distributed 34 Wistar albino rats into four groups: healthy control (n = 6), Gentamicin (80 mg/kg, n = 7), Gentamicin + Sham (%10 hydroalcoholic solution, n = 7), Gentamicin + Resatorvid (5 mg/kg, n = 7), and Gentamicin + ALA (100 mg/kg, n = 7). Resatorvid treatment led to a statistically significant decrease in urinary IL‐18, KIM‐1, and NGAL levels, whereas ALA treatment significantly reduced KIM‐1 levels compared to the gentamicin‐only group. Both Resatorvid and ALA showed partial reductions in urine creatinine levels. Moreover, treatments with Resatorvid and ALA resulted in statistically significant decreases in NRF‐2, CAS‐3, and NR4A2 expressions. However, only Resatorvid demonstrated a statistically significant decrease in NF‐B expression. These findings highlight the potential of Resatorvid in ameliorating gentamicin‐induced nephrotoxicity, thereby expanding the therapeutic utility of gentamicin and enhancing its efficacy against infections. [ABSTRACT FROM AUTHOR]

The aim of our study was to investigate the potential effects of alpha-lipoic acid (ALA) and resatorvid (RES) on gentamicin-induced hepatotoxicity. Thirty-four rats were divided into the following groups: Healthy control (n=6), Gentamicin (GNT, 80 mg/kg, n=7), GNT + Sham (10% hydroalcoholic solution, n=7), GNT + RES (5 mg/kg, n=7), and GNT + ALA (100 mg/kg, n=7). In the GNT group, a statistically significant increase in ALT levels and a significant decrease in total protein (TP) and albumin (TA) levels were observed compared to the control group. On the other hand, a significant increase in NRF-2, NF-κB, NR4A2 and CAS-3 expression was detected in the GNT group as compared to the control group. Simultaneous administration of RES or ALA with GNT led to a significant decrease in ALT levels compared to the GNT group. In addition, these treatments caused a significant increase in TP and TA levels. RES administration caused a significant decrease in gene expression compared to the GNT group. On the other hand, simultaneous ALA treatment with GNT caused a significant decrease in NRF-2, CAS-3 and NF-κB expression and partially reduced NR4A2 expression. These findings draw attention to the potential of RES or ALA to alleviate gentamicin-induced hepatotoxicity and to their increased efficacy in the treatment of infections. [ABSTRACT FROM AUTHOR]

Abstract Gentamicin is an aminoglycoside antibiotic with a rapid bactericidal effect on the treatment of many infections. However, its use at high concentrations for more than 7 days causes nephrotoxic side effects. This study investigated the potential of Resatorvid and alpha lipoic acid (ALA) in mitigating gentamicin‐induced nephrotoxicity in rats, considering biochemical, histopathological, and molecular parameters. This study randomly distributed 34 Wistar albino rats into four groups: healthy control (n = 6), Gentamicin (80 mg/kg, n = 7), Gentamicin + Sham (%10 hydroalcoholic solution, n = 7), Gentamicin + Resatorvid (5 mg/kg, n = 7), and Gentamicin + ALA (100 mg/kg, n = 7). Resatorvid treatment led to a statistically significant decrease in urinary IL‐18, KIM‐1, and NGAL levels, whereas ALA treatment significantly reduced KIM‐1 levels compared to the gentamicin‐only group. Both Resatorvid and ALA showed partial reductions in urine creatinine levels. Moreover, treatments with Resatorvid and ALA resulted in statistically significant decreases in NRF‐2, CAS‐3, and NR4A2 expressions. However, only Resatorvid demonstrated a statistically significant decrease in NF‐B expression. These findings highlight the potential of Resatorvid in ameliorating gentamicin‐induced nephrotoxicity, thereby expanding the therapeutic utility of gentamicin and enhancing its efficacy against infections.