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胆汁酸代谢分析为盐敏感性高血压大鼠血管内皮损伤的研究提供了新见解。

Bile Acid Metabolism Analysis Provides Insights into Vascular Endothelial Injury in Salt-Sensitive Hypertensive Rats.

作者信息

Zeng Baihan, Peng Xile, Chen Li, Liu Jiao, Xia Lina

机构信息

School of Health Preservation and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.

出版信息

Metabolites. 2024 Aug 16;14(8):452. doi: 10.3390/metabo14080452.

Abstract

As an unhealthy dietary habit, a high-salt diet can affect the body's endocrine system and metabolic processes. As one of the most important metabolites, bile acids can prevent atherosclerosis and reduce the risk of developing cardiovascular diseases. Therefore, in the present study, we aimed to reveal the bile acid metabolism changes in salt-sensitive hypertension-induced vascular endothelial injury. The model was established using a high-salt diet, and the success of this procedure was confirmed by detecting the levels of the blood pressure, vascular regulatory factors, and inflammatory factors. An evaluation of the histological sections of arterial blood vessels and kidneys confirmed the pathological processes in these tissues of experimental rats. Bile acid metabolism analysis was performed to identify differential bile acids between the low-salt diet group and the high-salt diet group. The results indicated that the high-salt diet led to a significant increase in blood pressure and the levels of endothelin-1 (ET-1) and tumor necrosis factor-α (TNF-α). The high-salt diet causes disorders in bile acid metabolism. The levels of four differential bile acids (glycocholic acid, taurolithocholic acid, tauroursodeoxycholic acid, and glycolithocholic acid) significantly increased in the high-salt group. Further correlation analysis indicated that the levels of ET-1 and TNF-α were positively correlated with these differential bile acid levels. This study provides new evidence for salt-sensitive cardiovascular diseases and metabolic changes caused by a high-salt diet in rats.

摘要

作为一种不健康的饮食习惯,高盐饮食会影响人体的内分泌系统和代谢过程。胆汁酸作为最重要的代谢产物之一,可以预防动脉粥样硬化并降低患心血管疾病的风险。因此,在本研究中,我们旨在揭示盐敏感性高血压诱导的血管内皮损伤中胆汁酸代谢的变化。使用高盐饮食建立模型,并通过检测血压、血管调节因子和炎症因子的水平来确认该过程的成功。对动脉血管和肾脏的组织切片进行评估,证实了实验大鼠这些组织中的病理过程。进行胆汁酸代谢分析以确定低盐饮食组和高盐饮食组之间的差异胆汁酸。结果表明,高盐饮食导致血压以及内皮素-1(ET-1)和肿瘤坏死因子-α(TNF-α)水平显著升高。高盐饮食会导致胆汁酸代谢紊乱。高盐组中四种差异胆汁酸(甘氨胆酸、牛磺石胆酸、牛磺熊去氧胆酸和甘氨石胆酸)的水平显著升高。进一步的相关性分析表明,ET-1和TNF-α的水平与这些差异胆汁酸水平呈正相关。本研究为大鼠高盐饮食引起的盐敏感性心血管疾病和代谢变化提供了新的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5012/11356606/397e1d5caa1d/metabolites-14-00452-g001.jpg

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