文献类型：期刊文献

英文题名：The Emerging Evidence for a Protective Role of Fucoidan from Laminaria japonica in Chronic Kidney Disease-Triggered Cognitive Dysfunction

作者：Ma, Zhihui[1];Yang, Zhiyou[1,2];Feng, Xinyue[1];Deng, Jiahang[1];He, Chuantong[1];Li, Rui[1];Zhao, Yuntao[1];Ge, Yuewei[3];Zhang, Yongping[1];Song, Cai[1];Zhong, Saiyi[1,2]

机构：[1]Guangdong Ocean Univ, Guangdong Prov Key Lab Aquat Prod Proc & Safety, Coll Food Sci & Technol,Guangdong Prov Engn Lab M, Guangdong Prov Engn Technol Res Ctr Seafood,Key L, Zhanjiang 524088, Peoples R China;[2]Dalian Polytech Univ, Collaborat Innovat Ctr Seafood Deep Proc, Dalian 116034, Peoples R China;[3]Guangdong Pharmaceut Univ, Key Lab Digital Qual Evaluat Chinese Mat Med Stat, Guangzhou 510006, Peoples R China

年份：2022

卷号：20

期号：4

外文期刊名：MARINE DRUGS

收录：SCI-EXPANDED(收录号：WOS:000785416100001)、、WOS

基金：This research was funded by the National Natural Science Foundation of China (grant number 81803753), Special Funds for Science and Technology Development of Zhanjiang City (grant number 2018A01046), Natural Science Foundation of Guangdong Province of China (grant number 2020A1515010779), Scientific Research Foundation of Guangdong Ocean University (grant number R19035), and The Innovative Team Program of High Education of Guangdong Province (2021KCXTD021).

语种：英文

外文关键词：chronic kidney disease; fucoidan; cognitive dysfunction; neuroinflammation; oxidative stress; GSK3 beta-Nrf2-HO-1 signaling; microglial polarization

外文摘要：This study aimed to explore the mechanism of fucoidan in chronic kidney disease (CKD)-triggered cognitive dysfunction. The adenine-induced ICR strain CKD mice model was applied, and RNA-Seq was performed for differential gene analysis between aged-CKD and normal mice. As a result, fucoidan (100 and 200 mg kg(-1)) significantly reversed adenine-induced high expression of urea, uric acid in urine, and creatinine in serum, as well as the novel object recognition memory and spatial memory deficits. RNA sequencing analysis indicated that oxidative and inflammatory signaling were involved in adenine-induced kidney injury and cognitive dysfunction; furthermore, fucoidan inhibited oxidative stress via GSK3 beta-Nrf2-HO-1 signaling and ameliorated inflammatory response through regulation of microglia/macrophage polarization in the kidney and hippocampus of CKD mice. Additionally, we clarified six hallmarks in the hippocampus and four in the kidney, which were correlated with CKD-triggered cognitive dysfunction. This study provides a theoretical basis for the application of fucoidan in the treatment of CKD-triggered memory deficits.