Halofuginone Alleviates Burn-Induced Hepatic and Renal Damage in Rats

The aim of this study was to evaluate the possible protective effects of halofuginone on burn-induced oxidative injury of the liver and kidney. For the induction of burn, backs of Wistar albino rats were shaved and exposed for 10 seconds to water bath at 90°C, whereas rats in the control group were exposed for 10 seconds at 25°C. Rats were then administered either saline (1 ml/kg) or halofuginone (100 μg/kg/day) intraperitoneally and decapitated at the 24th hour (early burn) or on the 7th day (late burn). Serum concentrations of creatinine, blood urea nitrogen, alanine aminotransferase, and aspartate aminotransferase were determined. Renal and hepatic tissue samples were used for microscopic analysis, and glutathione, malondialdehyde, and myeloperoxidase activity and chemiluminescence levels were measured. Halofuginone treatment improved renal functions in late burn group and hepatic functions in early burn group as demonstrated by decreased serum creatinine, blood urea nitrogen, and alanine aminotransferase levels. Increased serum lactate dehydrogenase level measured in late phase was reduced by halofuginone treatment. Generation of reactive oxygen metabolites measured by chemiluminescence, indicating burn-induced renal and hepatic oxidative injury in both the early and late burn groups, was reduced by halofuginone. Increased hepatic malondialdehyde levels accompanied with high microscopic damage scores were reversed by halofuginone in early burn group, while depleted renal glutathione levels were replenished. The present findings demonstrate that halofuginone preserved renal and hepatic functions and alleviated oxidative tissue damage insulted by burn trauma, suggesting an anti-inflammatory and antioxidant potential for halofuginone in providing protection against burn-induced renal and hepatic injury.