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Naringenin Ameliorates Hyperuricemia by Regulating Renal Uric Acid Excretion via the PI3K/AKT Signaling Pathway and Renal Inflammation through the NF-KB Signaling Pathway

文献类型： 外文期刊

作者： Yang, Bendong 1 ; Xin, Meiling 1 ; Liang, Shufei 1 ; Huang, Yuhong 2 ; Li, Jingda 2 ; Wang, Chao 1 ; Liu, Chao 3 ; Song, Xinhua 1 ; Sun, Jinyue 3 ; Sun, Wenlong 1 ;

作者机构： 1.Shandong Univ Technol, Inst Biomed Res, Sch Life Sci & Med, Zibo 255000, Shandong, Peoples R China

2.Yangtze Univ, Coll Life Sci, Jingzhou 434100, Hubei, Peoples R China

3.Shandong Acad Agr Sci, Inst Agrofood Sci & Technol, Key Lab Novel Food Resources Proc, Key Lab Agroprod Proc Technol Shandong Prov,Minist, Jinan 250100, Shandong, Peoples R China

4.Shandong Qingyujiangxing Biotechnol Co Ltd, Zibo 255000, Shandong, Peoples R China

5.Weifang Med Univ, Sch Publ Hlth & Management, Weifang 261053, Shandong, Peoples R China

关键词： naringenin; hyperuricemia; urate transporter; uric acid excretion; renal inflammation

期刊名称：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY （ 影响因子：5.895； 五年影响因子：6.048 ）

ISSN： 0021-8561

年卷期：

页码：

收录情况： SCI

摘要： Hyperuricemia characterized by high serum levels of uric acid (UA, >6.8 mg/dL) is regarded as a common chronic metabolic disease. When used as a food supplement, naringenin might have various pharmacological activities, including antioxidant, free-radical-scavenging, and inflammation-suppressing activities. However, the effects of naringenin on hyperuricemia and renal inflammation and the underlying mechanisms remain to be elucidated. Here, we comprehensively examined the effects of naringenin on hyperuricemia and the attenuation of renal impairment. Mice were injected with 250 mg/kg of potassium oxonate (PO) and given 5% fructose water to induce hyperuricemia. The pharmacological effects of naringenin (10 and 50 mg/kg) and benzbromarone (positive control group, 20 mg/kg) on hyperuricemic mice were evaluated in vivo. The disordered expression of urate transporters in HK-2 cells was stimulated by 8 mg/dL UA, which was used to determine the mechanisms underlying the effects of naringenin in vitro. Naringenin markedly reduced the serum UA level in a dose-dependent manner and improved renal dysfunction. Moreover, the increased elimination of UA in urine showed that the effects of naringenin were associated with the regulation of renal excretion. Further examination indicated that naringenin reduced the expression of GLUT9 by inhibiting the PI3K/AKT signaling pathway and reinforced the expression of ABCG2 by increasing the abundance of PDZK1 in vivo and in vitro. Furthermore, sirius red staining and western blotting indicated that naringenin plays a protective role in renal injury by suppressing increases in the levels of pro inflammatory cytokines, including IL-6 and TNF-alpha, which contribute to the inhibition of the TLR4/NF-kappa B signaling pathway in vivo and in vitro. Naringenin supplementation might be a potential therapeutic strategy to ameliorate hyperuricemia by promoting UA excretion in the kidney and attenuating the inflammatory response by decreasing the release of inflammatory cytokines. This study shows that naringenin could be used as a functional food or dietary supplement for hyperuricemia prevention and treatment.

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