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口服海藻糖可改善艾杜糖醛酸2-硫酸酯酶缺陷小鼠的II型黏多糖贮积症的组织学和行为症状。

Oral trehalose improves histological and behavior symptoms of mucopolysaccharidosis type II in iduronate 2-sulfatase deficient mice.

作者信息

Lee Hyesook, Han Jung-Hwa, Jeong Roo Gam, Kang Yun Jeong, Choi Byung Hyun, Kim Seo Rin, Cheon Chong Kun, Hur Jin, Lee Soo Yong

机构信息

Department of Convergence Medicine, Pusan National University School of Medicine, Yangsan, Gyeongsangnam-do, 50612, Republic of Korea.

Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Gyeongsangnam-do, 50612, Republic of Korea.

出版信息

Sci Rep. 2025 Feb 10;15(1):4882. doi: 10.1038/s41598-025-88362-0.

Abstract

Mucopolysaccharidosis type II (MPS II) is caused by a deficiency in iduronate-2-sulfatase (Ids), an enzyme that catabolizes glycosaminoglycan (GAG). Ids insufficiency results in the accumulation of GAG in various organs, ultimately resulting in multisystemic disease. Trehalose, a non-reducing disaccharide, has shown protective effects against various diseases. However, its potential utility through oral administration in MPS II has not yet been explored. In the present study, to investigate the efficacy of oral trehalose in Ids-knock-out (KO) mice, Ids-KO and wild type (WT) mice were treated with 2% trehalose dissolved in distilled water ad libitum for 24 weeks. Histological analysis revealed that almost all tissues from Ids-KO mice exhibited abnormal changes, including large vacuolization, inflammatory cell infiltration, and GAG deposition. However, oral administration of trehalose significantly suppressed GAG levels, vacuolization, inflammation and apoptosis in the spleen and brain. Additionally, oral trehalose considerably improved cognitive functions, such as short-term spatial learning and working memory, alongside limited improvements in walking capacity in Ids-KO mice. These results suggest that oral trehalose can reduce GAG accumulation, vacuolization and the number of apoptotic and inflammatory cells in pathological tissues including the brain, ultimately considerably improving spontaneous alteration behavior and could be a promising treatment option for MPS II.

摘要

II型黏多糖贮积症(MPS II)是由艾杜糖醛酸-2-硫酸酯酶(Ids)缺乏引起的,Ids是一种分解代谢糖胺聚糖(GAG)的酶。Ids功能不足会导致GAG在各个器官中蓄积,最终引发多系统疾病。海藻糖是一种非还原性二糖,已显示出对多种疾病具有保护作用。然而,其通过口服给药对MPS II的潜在效用尚未得到探索。在本研究中,为了研究口服海藻糖对Ids基因敲除(KO)小鼠的疗效,将Ids-KO小鼠和野生型(WT)小鼠用溶解于蒸馏水中的2%海藻糖随意喂养24周。组织学分析显示,Ids-KO小鼠的几乎所有组织都出现了异常变化,包括大空泡化、炎性细胞浸润和GAG沉积。然而,口服海藻糖显著抑制了脾脏和大脑中的GAG水平、空泡化、炎症和细胞凋亡。此外,口服海藻糖在Ids-KO小鼠中显著改善了认知功能,如短期空间学习和工作记忆,同时对行走能力也有有限的改善。这些结果表明,口服海藻糖可以减少包括大脑在内的病理组织中的GAG蓄积、空泡化以及凋亡和炎性细胞数量,最终显著改善自发改变行为,可能是MPS II的一种有前景的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ca/11811122/73b3f7feb753/41598_2025_88362_Fig1_HTML.jpg

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