Fucoidan from <i>Laminaria japonica</i> Inhibits Expression of GLUT9 and URAT1 via PI3K/Akt, JNK and NF-κB Pathways in Uric Acid-Exposed HK-2 Cells
Yu Zhang,
Xiaohui Tan,
Zhen Lin,
Fangping Li,
Chunyan Yang,
Haiying Zheng,
Lingyu Li,
Huazhong Liu,
Jianghua Shang
Affiliations
Yu Zhang
College of Chemistry and Environmental Science, Guangdong Ocean University, Zhanjiang 524088, China
Xiaohui Tan
College of Chemistry and Environmental Science, Guangdong Ocean University, Zhanjiang 524088, China
Zhen Lin
College of Chemistry and Environmental Science, Guangdong Ocean University, Zhanjiang 524088, China
Fangping Li
College of Chemistry and Environmental Science, Guangdong Ocean University, Zhanjiang 524088, China
Chunyan Yang
Guangxi Key Laboratory of Buffalo Genetics, Reproduction and Breeding, Guangxi Buffalo Research Institute, Chinese Academy of Agricultural Sciences, Nanning 530001, China
Haiying Zheng
Guangxi Key Laboratory of Buffalo Genetics, Reproduction and Breeding, Guangxi Buffalo Research Institute, Chinese Academy of Agricultural Sciences, Nanning 530001, China
Lingyu Li
Guangxi Key Laboratory of Buffalo Genetics, Reproduction and Breeding, Guangxi Buffalo Research Institute, Chinese Academy of Agricultural Sciences, Nanning 530001, China
Huazhong Liu
College of Chemistry and Environmental Science, Guangdong Ocean University, Zhanjiang 524088, China
Jianghua Shang
Guangxi Key Laboratory of Buffalo Genetics, Reproduction and Breeding, Guangxi Buffalo Research Institute, Chinese Academy of Agricultural Sciences, Nanning 530001, China
This work aimed to investigate the effect of fucoidan (FPS) on urate transporters induced by uric acid (UA). The results showed that UA stimulated the expression of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) in HK-2 cells, and FPS could reverse the effect. Moreover, UA could activate NF-κB, JNK and PI3K/Akt pathways, but both pathway inhibitors and FPS inhibited the UA-induced activation of these three pathways. These data suggested that FPS effectively inhibited the expression induction of reabsorption transporters URAT1 and GLUT9 by UA, through repressing the activation of NF-κB, JNK and PI3K/Akt signal pathways in HK-2 cells. The in vitro research findings support the in vivo results that FPS reduces serum uric acid content in hyperuricemia mice and rats through inhibiting the expression of URAT1 and GLUT9 in renal tubular epithelial cells. This study provides a theoretical basis for the application of FPS in the treatment of hyperuricemia.
