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硫代乙酰胺诱导的急性肝性脑病大鼠三羧酸代谢物失衡表明不完全恢复。

Tricarboxylic Acid Metabolite Imbalance in Rats with Acute Thioacetamide-Induced Hepatic Encephalopathy Indicates Incomplete Recovery.

机构信息

Centre for Strategic Planning and Management of Medical and Biological Health Risks, Federal Medical Biological Agency of The Russian Federation, Moscow 119121, Russia.

Valiev Institute of Physics and Technology of the Russian Academy of Sciences, Moscow 117218, Russia.

出版信息

Int J Mol Sci. 2023 Jan 10;24(2):1384. doi: 10.3390/ijms24021384.

DOI:10.3390/ijms24021384
PMID:36674898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9861856/
Abstract

Exposure to the toxin thioacetamide (TAA) causes acute hepatic encephalopathy (HE), changes in the functioning of systemic organs, and an imbalance in a number of energy metabolites. The deferred effects after acute HE development are poorly understood. The study considers the balance of the tricarboxylic acid (TCA) cycle metabolites in the blood plasma, liver, kidneys, and brain tissues of rats in the post-rehabilitation period. The samples of the control (n = 3) and TAA-induced groups of rats (n = 13) were collected six days after the administration of a single intraperitoneal TAA injection at doses of 200, 400, and 600 mg/kg. Despite the complete physiological recovery of rats by this date, a residual imbalance of metabolites in all the vital organs was noted. The results obtained showed a trend of stabilizing processes in the main organs of the animals and permit the use of these data both for prognostic purposes and the choice of potential therapeutic agents.

摘要

接触硫代乙酰胺(TAA)会导致急性肝性脑病(HE)、全身器官功能改变以及多种能量代谢物失衡。急性 HE 发展后的延迟效应知之甚少。本研究考虑了恢复期大鼠血浆、肝脏、肾脏和脑组织中三羧酸(TCA)循环代谢物的平衡。对照组(n = 3)和 TAA 诱导组大鼠(n = 13)的样本在单次腹腔注射 TAA 剂量为 200、400 和 600 mg/kg 后 6 天采集。尽管到目前为止,大鼠的生理机能已经完全恢复,但所有重要器官中的代谢物仍存在残余失衡。研究结果表明,动物主要器官中的稳定过程呈稳定趋势,这使得这些数据既可以用于预后目的,也可以用于选择潜在的治疗药物。

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