Anti-hyperuricemic and nephroprotective effect of geniposide in chronic hyperuricemia mice
文献类型： 外文期刊
作者： Liu, Chao 1 ; Zhou, Hou-ning 1 ; Zhang, Rui-rui 1 ; Wang, Xin-kun 1 ; He, Sheng-wen 2 ; Zhang, Jin-bao 3 ; Guo, Xu 1 ; Wa 1 ;
作者机构： 1.Shandong Acad Agr Sci, Key Lab Agroprod Proc Technol Shandong Prov, Key Lab Novel Food Resources Proc, Minist Agr & Rural Affairs,Inst Agrofood Sci & Te, 202 Gongye North Rd, Jinan 250100, Shandong, Peoples R China
2.Weifang Med Univ, Sch Publ Hlth & Management, 7166 Baotong Rd, Weifang 261053, Shandong, Peoples R China
3.Weifang Med Univ, Sch Biosci & Technol, 7166 West Baotong Rd, Weifang 261053, Shandong, Peoples R China
关键词： Geniposide; Hyperuricemia; Renal dysfunction; Renal inflammation; Nephroprotective effects
期刊名称：JOURNAL OF FUNCTIONAL FOODS （ 影响因子：4.451； 五年影响因子：4.907 ）
ISSN： 1756-4646
年卷期： 2019 年 61 卷
页码：
收录情况： SCI
摘要： Hyperuricemia is a key risk factor for kidney disease. Geniposide possesses various pharmacological activities, however, to our knowledge, no previous work investigated the therapeutic effect of geniposide on urate nephropathy. The present study established a chronic hyperuricemia model using a combination of adenine and ethambutol administration. The potential beneficial effects and mechanisms of geniposide on hyperuricemia and nephropathy were also investigated. The results demonstrated that geniposide significantly decreased SUA levels via inhibition of the XOD activity and increasing the excretion of urinary uric acid. Geniposide also markedly improved kidney damage related to hyperuricemia. Further investigation indicated that geniposide improved the symptoms of nephropathy via decreasing the production of proinflammatory cytokines, including IL-1 beta, PG-E-2, and TNF-alpha, and inhibiting the expression of TGF-1 beta. The molecular mechanism of action may be associated with suppression of TLR4/MyD88 signaling and NLRP3 inflammasome activation to reduce IL-1 beta and TNF-alpha production respectively in hyperuricemic mice.
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