Balkan Medical Journal (Feb 2018)
The Effects of Baicalin on Myoglobinuric Acute Renal Failure in Rats
Abstract
Background: Myoglobinuric acute kidney injury is a uremic syndrome that develops due to damage of skeletal muscle. Free radicals and nitric oxide play an important role in the pathogenesis of myoglobinuric acute kidney injury. Baicalin has multiple bioactivities, including antimicrobial, anti-inflammatory and antioxidant properties and is a potent free radical scavenger. Aims: To investigate the nephroprotective mechanism of baicalin on myoglobinuric acute kidney injury. Study Design: Animal experimentation. Methods: In our study, male Sprague Dawley rats were divided into 4 groups. Control (n=8), Baicalin (n=8), myoglobinuric acute kidney injury (n=10) and myoglobinuric acute kidney injury + baicalin (n=10). The rats were deprived of water for 24 hours before receiving intramuscular injection. The control and baicalin groups were injected intramuscularly with saline (8 ml/kg), and the myoglobinuric acute kidney injury and myoglobinuric acute kidney injury + baicalin groups were given 50% glycerol 8 ml/kg. One hour later, the control and myoglobinuric acute kidney injury groups received saline intraperitoneally, and the baicalin and myoglobinuric acute kidney injury + baicalin groups were given 200 mg/kg baicalin. Twenty-four hours after the glycerol injection, urine and blood samples were taken, and the kidneys of the rats were harvested under intraperitoneally injections of anaesthesia. Results: We found that the levels of creatinine, urea, nitric oxide, alanine transaminase, aspartate aminotransferase, creatine kinase in serum samples, malondialdehyde, nitric oxide, inducible nitric oxide synthase, and endothelial nitric oxide synthase concentrations in renal tissue were increased in the myoglobinuric acute kidney injury group compared with the control group (p<0.05). The nitric oxide and glutathione levels in the kidney were significantly decreased in the myoglobinuric acute kidney injury + baicalin group compared with the myoglobinuric acute kidney injury group (p<0.05). There were no significant differences between any other parameters. Conclusion: Our results did not show any protective effect of baicalin on myoglobinuric acute kidney injury, possibly because the different effective factors in the pathogenesis of experimental myoglobinuric acute kidney injury used in this experiment deviate from other experimental models. Moreover, detailed studies are needed to clarify the effects of baicalin in different doses and treatment durations in glycerol-induced acute kidney injury model
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