Low molecular weight fucoidan protects renal tubular cells from injury induced by albumin overload.

Low molecular weight fucoidan protects renal tubular cells from injury induced by albumin overload.
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低分子量岩藻依聚糖可保护肾小管细胞免受白蛋白超载引起的损伤

DOI:
10.1038/srep31759
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发表时间:
2016-08-22
期刊:
影响因子:
4.6
通讯作者:
Yang B
Yang B
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Jia Y;Sun Y;Weng L;Li Y;Zhang Q;Zhou H;Yang B

文献摘要

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蛋白尿是慢性肾脏病(CKD)进行性肾损害的致病和加重因素。本研究旨在探讨低分子岩藻糖胶(LMWF)对白蛋白超负荷所致肾功能和肾小管上皮细胞损伤的保护作用。经10 mg/g牛血清白蛋白处理后,129S2/Sv小鼠出现肾功能障碍、形态改变以及炎症和纤维化相关蛋白的过度表达。在体外近端肾小管上皮细胞模型中,LMWF(100 mg/kg)可剂量依赖性地抑制白蛋白超载所致的促炎症因子和促纤维化因子的过度表达、氧化应激和细胞凋亡。这些实验结果表明,LMWF通过抑制炎症、纤维化、氧化应激和细胞凋亡来保护白蛋白超负荷所致的肾损伤,提示LMWF可能是一种有前途的预防CKD的候选药物。
Albuminuria is a causative and aggravating factor for progressive renal damage in chronic kidney disease (CKD). The aim of this study was to determine if low molecular weight fucoidan (LMWF) could protect renal function and tubular cells from albumin overload caused injury. Treatment with 10 mg/g bovine serum albumin caused renal dysfunction, morphological changes, and overexpression of inflammation and fibrosis associated proteins in 129S2/Sv mice. LMWF (100 mg/kg) protected against kidney injury and renal dysfunction with decreased blood creatinine by 34% and urea nitrogen by 25%, increased creatinine clearance by 48%, and decreased significantly urinary albumin concentration.In vitroproximal tubule epithelial cell (NRK-52E) model showed that LMWF dose-dependently inhibited overexpression of proinflammatory and profibrotic factors, oxidative stress and apoptosis caused by albumin overload. These experimental results indicate that LMWF protects against albumin overload caused renal injury by inhibiting inflammation, fibrosis, oxidative stress and apoptosis, which suggests that LMWF could be a promising candidate drug for preventing CKD.