Fang Li1, Yaping Liu2, Yongyan Xie2, Zhiyong Liu3, Guoming Zou4. 1. Jiangxi Maternal and Child Health Hospital, Nanchang 330006, China. 2. Jiangxi University of Traditional Chinese Medicine, Nanchang 330003, China. 3. Jiangxi University of Traditional Chinese Medicine, Nanchang 330003, China. 469241547@qq.com. 4. Jiangxi University of Traditional Chinese Medicine, Nanchang 330003, China. zouguoming1@163.com.
Abstract
BACKGROUND: This study investigates the effect of epigallocatechin gallate (EGCG) from tea leaves on hyperuricemia and explores the underlying mechanisms in vitro and in vivo. METHODS: The effects of EGCG on proliferation of BRL 3A rat liver cells were evaluated by CCK8 and after stimulation by xanthine the uric acid and xanthine oxidase (XOD) levels were evaluated by a kit; In an in vivo experiment, rats were treated with oxonic acid potassium salt combined with ethylamine pyrimidine to induce high uric acid hematic disease (7 days), The serum uric acid levels and XOD levels were evaluated by a kit, The expressions of OTA1 and GLUT9 were detected by RT-qPCR and Immunohistochemical. RESULTS: EGCG had no effect on proliferation, and significantly reduced serum uric acid levels and inhibited XOD activity (P<0.05). The rat model exhibited a significant rise in blood uric acid levels (54.59 mg/dL), and EGCG significantly reduced the high level of serum uric acid and inhibited XOD activity in the serum and liver tissues (P<0.05). RT-PCR showed that EGCG significantly increased mOAT1 expression in the kidney tissues and reduced mGLUT9 expression (P<0.05). Immunohistochemical results showed that EGCG significantly increased OAT1 expression in the kidney tissues and decreased GLUT9 expression (P<0.05). CONCLUSIONS: These results demonstrate that EGCG has obvious anti-hyperuricemia effects in vitro and in vivo via the inhibition of XOD activity and GLUT9 expression and the promotion of OAT1 expression.
BACKGROUND: This study investigates the effect of epigallocatechin gallate (EGCG) from tea leaves on hyperuricemia and explores the underlying mechanisms in vitro and in vivo. METHODS: The effects of EGCG on proliferation of BRL 3A rat liver cells were evaluated by CCK8 and after stimulation by xanthine the uric acid and xanthine oxidase (XOD) levels were evaluated by a kit; In an in vivo experiment, rats were treated with oxonic acid potassium salt combined with ethylamine pyrimidine to induce high uric acidhematic disease (7 days), The serum uric acid levels and XOD levels were evaluated by a kit, The expressions of OTA1 and GLUT9 were detected by RT-qPCR and Immunohistochemical. RESULTS:EGCG had no effect on proliferation, and significantly reduced serum uric acid levels and inhibited XOD activity (P<0.05). The rat model exhibited a significant rise in blood uric acid levels (54.59 mg/dL), and EGCG significantly reduced the high level of serum uric acid and inhibited XOD activity in the serum and liver tissues (P<0.05). RT-PCR showed that EGCG significantly increased mOAT1 expression in the kidney tissues and reduced mGLUT9 expression (P<0.05). Immunohistochemical results showed that EGCG significantly increased OAT1 expression in the kidney tissues and decreased GLUT9 expression (P<0.05). CONCLUSIONS: These results demonstrate that EGCG has obvious anti-hyperuricemia effects in vitro and in vivo via the inhibition of XOD activity and GLUT9 expression and the promotion of OAT1 expression.