Shi Hui, Liang Xiaoshan, Huang Liwen, Luo Zhigang, Tan Long
Department of Nutrition and Food Hygiene, School of Public Health, Tianjin Medical University, Tianjin 300070, China.
Shanghai Kangshi Food Technology Co. , Ltd. , Shanghai 201103, China.
Wei Sheng Yan Jiu. 2020 Sep;49(5):802-808. doi: 10.19813/j.cnki.weishengyanjiu.2020.05.019.
To investigate the effects of electrolytic drinking water on the hyperuricemia and the potential mechanism.
The 6-week-old SD rats were induced as the animal model with hyperuricemia by yeast extract(10 g/kg) and adenine(100 g/kg) gavage(twice per day) combined with oxygen oxazine acid potassium(300 mg/kg, the 1(st), 5(th) and 10~(th )day) i. p. Then the rats were supplied electrolytic drinking water in different dosages(1 mL, 2 mL and 3 mL) by gavage for 7 days. Weight was measured at regular intervals. The 24-hour urine was sampled by metabolic cage for the measurements of uric acid, creatinine and urea nitrogen levels. The parameters for the uric acid clearance were calculated. The serum was sampled after execution for the determination of serum uric acid, creatinine. The activities of xanthine oxidase and adenine dehydrogenase were detected. The morphological measurements of stomach and kidney were completed.
The hyperuricemia model was successfully induced by this method. In the intervention, the pH of urine was significantly elevated along with the electrolytic drinking water intake(P<0. 01). The excretion of uric acid in the rats with hyperuricemia was significantly increased while administrated with electrolytic drinking water. The effects of improving uric acid excretion were enhanced along with the intake of electrolytic drinking water. The levels of serum uric acid(group Model, Model+Treatment 1, Model+Treatment 2 and Model+Treatment 3: 693. 7 μmol/L, 668. 1 μmol/L, 642. 5 μmol/L, 633. 1 μmol/L), urine uric acid(5740. 0 μmol/L, 5894. 1 μmol/L, 5562. 3 μmol/L, 5083. 2 μmol/L) and urea nitrogen(11. 40 mmol/L, 10. 47 mmol/L, 9. 54 mmol/L, 8. 93 mmol/L) were significantly decreased in the model rats with high dose intervention(P<0. 05). Clearance of uric acid was obviously increased(9. 27%, 10. 40%, 10. 44%, 11. 13%, P<0. 05). However, no pathological change was observed among the three groups with intervention.
The electrolytic drinking water intake is benefit for the excretion of uric acid of hyperuricemia rat. Enhancing alkalization of urine is considered as the important mechanism of the beneficial effects.
探讨电解水对高尿酸血症的影响及其潜在机制。
将6周龄的SD大鼠通过酵母提取物（10 g/kg）和腺嘌呤（100 g/kg）灌胃（每天2次）联合腹腔注射氧嗪酸钾（300 mg/kg，第1、5、10天）诱导为高尿酸血症动物模型。然后通过灌胃给予大鼠不同剂量（1 mL、2 mL和3 mL）的电解水，持续7天。定期测量体重。用代谢笼采集24小时尿液，检测尿酸、肌酐和尿素氮水平。计算尿酸清除率参数。处死大鼠后采集血清，测定血清尿酸、肌酐。检测黄嘌呤氧化酶和腺嘌呤脱氢酶的活性。完成胃和肾脏的形态学测量。
该方法成功诱导了高尿酸血症模型。在干预过程中，随着电解水摄入量的增加，尿液pH值显著升高（P<0.01）。给予电解水后，高尿酸血症大鼠的尿酸排泄显著增加。随着电解水摄入量的增加，改善尿酸排泄的效果增强。高剂量干预的模型大鼠血清尿酸（模型组、模型+治疗1组、模型+治疗2组和模型+治疗3组：693.7 μmol/L、668.1 μmol/L、642.5 μmol/L、633.1 μmol/L）、尿尿酸（5740.0 μmol/L、5894.1 μmol/L、5562.3 μmol/L、5083.2 μmol/L）和尿素氮（11.40 mmol/L、10.47 mmol/L、9.54 mmol/L、8.93 mmol/L）水平显著降低（P<0.05）。尿酸清除率明显增加（9.27%、10.40%、10.44%、11.13%，P<0.05）。然而，干预的三组中均未观察到病理变化。
摄入电解水有利于高尿酸血症大鼠尿酸的排泄。增强尿液碱化被认为是其有益作用的重要机制。
