Department of Physiology, Trakya University School of Medicine, Edirne, Turkey.
Department of Pathology, Trakya University School of Medicine, Edirne, Turkey.
Balkan Med J. 2018 Jan 20;35(1):68-76. doi: 10.4274/balkanmedj.2017.0040. Epub 2017 Sep 13.
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.
To investigate the nephroprotective mechanism of baicalin on myoglobinuric acute kidney injury.
Animal experimentation.
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.
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.
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.
肌红蛋白尿性急性肾损伤是一种由于骨骼肌损伤而发展成的尿毒症综合征。自由基和一氧化氮在肌红蛋白尿性急性肾损伤的发病机制中起着重要作用。黄芩苷具有多种生物活性，包括抗菌、抗炎和抗氧化特性，是一种有效的自由基清除剂。
研究黄芩苷对肌红蛋白尿性急性肾损伤的肾保护机制。
动物实验。
在我们的研究中，雄性 Sprague Dawley 大鼠分为 4 组。对照组（n=8）、黄芩苷组（n=8）、肌红蛋白尿性急性肾损伤组（n=10）和肌红蛋白尿性急性肾损伤+黄芩苷组（n=10）。在接受肌肉注射前，大鼠被剥夺 24 小时的水。对照组和黄芩苷组肌肉注射生理盐水（8ml/kg），肌红蛋白尿性急性肾损伤组和肌红蛋白尿性急性肾损伤+黄芩苷组给予 50%甘油 8ml/kg。1 小时后，对照组和肌红蛋白尿性急性肾损伤组腹腔内注射生理盐水，黄芩苷组和肌红蛋白尿性急性肾损伤+黄芩苷组给予 200mg/kg 黄芩苷。甘油注射后 24 小时，采集尿液和血液样本，麻醉下腹腔内注射后采集大鼠肾脏。
我们发现，与对照组相比，肌红蛋白尿性急性肾损伤组血清样本中肌酐、尿素、一氧化氮、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、肌酸激酶、肾组织中丙二醛、一氧化氮、诱导型一氧化氮合酶和内皮型一氧化氮合酶浓度升高（p<0.05）。肌红蛋白尿性急性肾损伤+黄芩苷组与肌红蛋白尿性急性肾损伤组相比，肾组织中一氧化氮和谷胱甘肽水平显著降低（p<0.05）。其他参数之间没有显著差异。
我们的结果没有显示黄芩苷对肌红蛋白尿性急性肾损伤有任何保护作用，可能是因为本实验中实验性肌红蛋白尿性急性肾损伤的不同有效因素与其他实验模型不同。此外，需要详细研究以阐明不同剂量和治疗时间的黄芩苷在甘油诱导的急性肾损伤模型中的作用。
