School of Food Science and Engineering, Wuhan Polytechnic University, Wuhan, 430023, China.
Food Funct. 2018 Nov 14;9(11):5778-5790. doi: 10.1039/c8fo01480a.
Clinically, Chaenomeles sinensis (Thouin) Koehne (C. sinensis) has been used to treat hyperuricemia and gout. However, the exact mechanism of action is still unknown. In the present study, the ethyl acetate fraction of C. sinensis fruit extract (CSF-E) was separated. Potassium oxonate (PO)-induced hyperuricemic mice and normal mice were administered with CSF-E at 60, 120 and 180 mg kg-1, respectively for 7 days. Serum uric acid, creatinine and BUN levels, liver oxidative damage, and serum and hepatic XOD activities were primarily measured using assay kits. The evaluation of its nephroprotective effects was carried out by renal histopathological analysis. Simultaneously, renal protein levels of organic anion transporters, such as mURAT1 and mOAT1, were detected using western blotting to elucidate the possible mechanisms. The results showed that CSF-E could significantly inhibit XOD activities in both serum and liver (p < 0.05), decreasing uric acid, creatinine and BUN levels in serum, and increasing levels in the excretion of uric acid by down-regulated of mURAT1 and up-regulated mOAT1 protein expression of kidney in hyperuricemic mice. Moreover, PO-induced alterations in the levels of MDA, hepatic SOD and GSH-Px activities and renal inflammation damage in hyperuricemic mice were effectively recovered by CSF-E at 120 mg kg-1. CSF-E possessed anti-hyperuricemic and nephroprotective effects by suppressing XOD activity, improving renal function and regulating renal mURAT1 and mOAT1 protein expression, which resulted in beneficial effects on hyperuricemia and gout prevention.
临床上,木瓜(Thouin)Koehne(C. sinensis)已被用于治疗高尿酸血症和痛风。然而,其确切作用机制尚不清楚。本研究对木瓜果实提取物的乙酸乙酯部分(CSF-E)进行了分离。用氧嗪酸钾(PO)诱导高尿酸血症小鼠和正常小鼠,分别灌胃 60、120 和 180 mg kg-1 CSF-E,连续 7 天。采用试剂盒检测血清尿酸、肌酐和 BUN 水平、肝氧化损伤以及血清和肝 XOD 活性。通过肾组织病理分析评价其肾保护作用。同时,采用 Western blot 检测肾有机阴离子转运体(如 mURAT1 和 mOAT1)的蛋白水平,以阐明可能的机制。结果表明,CSF-E 可显著抑制血清和肝中 XOD 活性(p<0.05),降低高尿酸血症小鼠血清中尿酸、肌酐和 BUN 水平,增加尿酸排泄量,下调 mURAT1,上调 mOAT1 蛋白表达。此外,CSF-E(120 mg kg-1)可有效恢复 PO 诱导的高尿酸血症小鼠 MDA、肝 SOD 和 GSH-Px 活性以及肾炎症损伤水平的变化。CSF-E 通过抑制 XOD 活性、改善肾功能和调节肾 mURAT1 和 mOAT1 蛋白表达,发挥抗高尿酸血症和肾保护作用,有利于预防高尿酸血症和痛风。