《Scientific Reports》：岩藻多糖具有延缓慢性肾衰的活性
原标题：岩藻多糖通过抑制CD44信号通路抑制肾小管间质纤维化
①岩藻多糖（fucoidan）是褐藻来源的以岩藻糖为主要组成单糖的一种硫酸化多糖，研究证明岩藻多糖具有治疗糖尿病肾病及延缓慢性肾衰的活性；
②肾小管间质纤维化是慢性肾炎的决定因素，本研究评价了岩藻多糖对肾小管间质化的抑制作用；
③患有慢性肾炎的小鼠每天服用10-100mg/kg的岩藻多糖，持续六周，观察小鼠的肾脏功能及肾炎病情。
④实验结果：服用100mg/kg岩藻多糖的小鼠肾脏功能得到显著改善，同时肾小管间质化得到抑制，通过机理研究发现，岩藻多糖能够抑制CD44, β-catenin及
TGF-β蛋白的表达，从而抑制间质纤维化，改善慢性肾炎。
⑤结论：岩藻多糖具有治疗糖尿病肾病及延缓慢性肾衰的活性。
延伸阅读
Sci. Rep. 7, 40183; doi: 10.1038/srep40183 (2017).
Oligo-fucoidan prevents renal tubulointerstitial fbrosis by inhibiting the CD44 signal pathway
Abstract:
Tubulointerstitial fbrosis is recognized as a key determinant of progressive chronic kidney disease (CKD). Fucoidan, a sulphated polysaccharide extracted from brown seaweed, exerts benefcial effects in some nephropathy models. The present study evaluated the inhibitory effect of oligo-fucoidan (800 Da) on renal tubulointerstitial fbrosis. We established a mouse CKD model by right nephrectomy with transient ischemic injury to the left kidney. Six weeks after the surgery, we fed the CKD mice oligo-fucoidan at 10, 20, and 100 mg/kg/d for 6 weeks and found that the oligo-fucoidan doses less than 100 mg/kg/d improved renal function and reduced renal tubulointerstitial fbrosis in CKD mice. Oligofucoidan also inhibited pressure-induced fbrotic responses and the expression of CD44, β-catenin, and TGF-β in rat renal tubular cells (NRK-52E). CD44 knockdown downregulated the expression of β-catenin and TGF-β in pressure-treated cells. Additional ligands for CD44 reduced the anti-fbrotic effect of oligofucoidan in NRK-52E cells. These data suggest that oligo-fucoidan at the particular dose prevents renal tubulointerstitial fbrosis in a CKD model. The anti-fbrotic effect of oligo-fucoidan may result from interfering with the interaction between CD44 and its extracellular ligands.
First Authors:
Cheng-Hsien Chen
Correspondence:
Tso-Hsiao Chen
All Authors:
Cheng-Hsien Chen, Yuh-Mou Sue, Chung-Yi Cheng, Yen-Cheng Chen, Chung-Te Liu, Yung-Ho Hsu, Pai-An Hwang, Nai-Jen Huang & Tso-Hsiao Chen
2017-01-18 Article
