未经证实:尿酸肾病(UN)是高尿酸血症(HUA)的并发症,这对人们的生活有很大的影响。这里,我们评估了桑黄总黄酮(TFPI)的体内治疗潜力,并研究了TFPI的体外抗UN作用。
UNASSIGNED:ICR小鼠腹膜内注射草酸钾诱发高尿酸血症。TFPI干预后,我们评估了血清尿酸(UA)和肌酐(CR)的水平,肝脏中黄嘌呤氧化酶(XOD)和腺苷脱氨酶(ADA)的含量。探讨TFPI对UN的作用及其分子机制,我们用尿酸单钠(MSU)处理HK-2细胞,以研究TFPI对细胞凋亡和炎症的影响。此外,为了探讨TFPI对尿酸转运的作用机制,我们评估了尿酸转运体ABCG2与炎症信号通路TLR4-NLRP3之间的关系。
未经证实:在模型小鼠中,TFPI显着降低了UA和Cr的水平,这可能与XOD酶活性的抑制有关。在HK-2细胞中,TFPI对MSU的反应能有效抑制细胞凋亡和TLR4-NLRP3信号通路的激活,促进ABCG2的表达。
UNASSIGNED:TFPI通过靶向TLR4受体和NLRP3炎性体,显著抑制炎症因子的释放,促进ABCG2的表达。并有针对性地抑制XOD酶活性,降低尿酸水平,抑制UN的发展。
UNASSIGNED: Uric acid nephropathy (UN) is a complication of hyperuricemia (HUA), which has a great impact on people\'s lives. Here, we evaluated the therapeutic potential of total flavonoids of Phellinus igniarius (TFPI) in vivo and studied the anti UN effect of TFPI in vitro.
UNASSIGNED: Hyperuricemia was induced by intraperitoneal injection of potassium oxonate in ICR mice. After intervention with TFPI, we evaluated the levels of serum uric acid (UA) and creatinine (CR), and the contents of xanthine oxidase (XOD) and adenosine deaminase (ADA) in liver. To explore the effect and molecular mechanism of TFPI on UN, we treated HK-2 cells with monosodium urate (MSU) to study the effect of TFPI on apoptosis and inflammation. In addition, to explore the mechanism of TFPI on uric acid transport we evaluated the relationship between uric acid transporter ABCG2 and inflammatory signaling pathway TLR4-NLRP3.
UNASSIGNED: In the model mice, TFPI significantly decreased the levels of UA and Cr, which may be related to the inhibition of XOD enzyme activity. In HK-2 cells, the response of TFPI to MSU can effectively inhibit apoptosis and activation of TLR4-NLRP3 signaling pathway and promote the expression of ABCG2.
UNASSIGNED: TFPI can significantly inhibit the release of inflammatory factors and promote the expression of ABCG2 by targeting TLR4 receptor and NLRP3 inflammasome. And targeted inhibition of XOD enzyme activity to reduce uric acid level and inhibit the development of UN.