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尿流梗阻小鼠模型肾脏的脂质组学研究。

Lipidomic study of kidney in a mouse model with urine flow obstruction.

机构信息

Faculty of Health Sciences, Hokkaido University, Kita-12 Nishi-5, Kita-ku, Sapporo, 060-0812, Japan.

Department of Anatomy, Histology and Physiology, Faculty of Animal Science and Veterinary Medicine, Sher-e-Bangla Agricultural University, Dhaka, 1207, Bangladesh.

出版信息

Sci Rep. 2024 Aug 5;14(1):18042. doi: 10.1038/s41598-024-68270-5.

DOI:10.1038/s41598-024-68270-5
PMID:39098953
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11298537/
Abstract

Obstructed urine flow is known to cause structural and functional kidney damage leading to renal fibrosis. However, limited information is available on the change in kidney lipids during urinary tract obstruction. In this study, we investigated the change in lipidome in a mouse model with unilateral ureteral obstruction (UUO). The establishment of the UUO model was confirmed by histopathological examination using transmission electron microscopy. Untargeted liquid chromatography/mass spectrometry was carried out over a time course of 4 and 7 days. Compared to the sham control, the UUO kidney at 7 days showed dilatation of the renal tubule with loss of brush borders and thickening of the capillary endothelium. In the kidney lipidomes obtained from the UUO 7 days group compared to the control, a significant decrease of ceramide, sphingomyelin, phosphatidylcholine, lysophospholipids, and phosphatidylethanolamine was observed, whereas cholesteryl esters, free fatty acids, phosphatidylglycerol, and cardiolipins were significantly increased. The present study revealed the disturbed lipid metabolism in the UUO model, which may provide a clue to potential lipid pathways and therapeutic targets for the early stage of renal fibrosis.

摘要

尿路梗阻已知可导致结构和功能肾损伤，进而导致肾纤维化。然而，关于尿路梗阻期间肾脏脂质的变化，相关信息有限。在这项研究中，我们研究了单侧输尿管梗阻 (UUO) 小鼠模型中脂质组的变化。通过透射电子显微镜的组织病理学检查证实了 UUO 模型的建立。在 4 天和 7 天的时间过程中进行了非靶向液相色谱/质谱分析。与假手术对照组相比，UUO 第 7 天的肾脏表现为肾小管扩张，刷状缘丧失，毛细血管内皮增厚。与对照组相比，从 UUO 第 7 天组的肾脏脂质组中观察到神经酰胺、鞘磷脂、磷脂酰胆碱、溶血磷脂和磷脂酰乙醇胺显著减少，而胆固醇酯、游离脂肪酸、磷脂酰甘油和心磷脂显著增加。本研究揭示了 UUO 模型中脂质代谢的紊乱，这可能为早期肾纤维化的潜在脂质途径和治疗靶点提供线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/d29178cd62c8/41598_2024_68270_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/7a04916044b6/41598_2024_68270_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/7144ab83d214/41598_2024_68270_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/9f5f4734e071/41598_2024_68270_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/18548e0208ed/41598_2024_68270_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/99ae5b7cb95f/41598_2024_68270_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/d29178cd62c8/41598_2024_68270_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/7a04916044b6/41598_2024_68270_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/7144ab83d214/41598_2024_68270_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/9f5f4734e071/41598_2024_68270_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/18548e0208ed/41598_2024_68270_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/99ae5b7cb95f/41598_2024_68270_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6677/11298537/d29178cd62c8/41598_2024_68270_Fig6_HTML.jpg

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Lipidomic Analysis Reveals the Protection Mechanism of GLP-1 Analogue Dulaglutide on High-Fat Diet-Induced Chronic Kidney Disease in Mice.脂质组学分析揭示GLP-1类似物度拉糖肽对高脂饮食诱导的小鼠慢性肾病的保护机制。
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