慢性不可预测的轻度应激会增加血清醛固酮,但不影响皮质酮水平,并诱发年轻成年雄性大鼠肝脂肪变性和肾损伤

IF 2.9 4区 生物学 Q3 CELL BIOLOGY Journal of Molecular Histology Pub Date : 2024-04-07 DOI:10.1007/s10735-024-10188-3
Eliut Pérez Sánchez, Adriana Corona-Pérez, Omar Arroyo-Helguera, Ida Soto Rodríguez, Senobia Rosalía Cruz Lumbreras, Jorge Rodríguez-Antolín, Cuevas Romero Estela, Leticia Nicolás-Toledo
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引用次数: 0

摘要

摘要 压力通常与青少年的焦虑和抑郁症状有关。压力与代谢综合征和炎症有关。本研究假设醛固酮比皮质酮更能促进慢性压力-肝脏脂肪变性和纤维化,以及年轻成年大鼠的肾脏炎症和纤维化。将 32 只出生 51 天的年轻成年雄性 Wistar 大鼠分为四组(每组 8 只):对照组(C)、慢性不可预测轻度应激组(CUMS)、对照组加车辆组(C加veh)、CUMS加选择性醛固酮阻断剂依普利酮组(CUMS加EP)。出生后第 51 天,在应激试验开始前两小时通过胃管口服依普利酮。每天在不同时间进行一次CUMS范式,四周内不重复应激序列。对肾脏炎症和纤维化以及肝糖原、三酰甘油和纤维化水平进行了测定。对尿液和血清中的皮质酮、醛固酮、钠和肌酐浓度进行了测定。CUMS 组显示血清醛固酮水平较高,但不影响皮质酮水平,尿钠增加,肾小管萎缩,肾小球硬化,存在炎症和纤维化,但不影响肌酐,肝脏中糖原含量、三酰甘油和中度纤维化增加,使用依普利酮治疗可防止炎症、纤维化、糖原和三酰甘油。我们的研究结果表明,慢性应激诱导的醛固酮比皮质酮更能促进肝脂肪变性和肾损伤。依普利酮的预防作用支持了我们的假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Chronic unpredictable mild stress increases serum aldosterone without affecting corticosterone levels and induces hepatic steatosis and renal injury in young adult male rats

Stress is often associated with anxiety and depressive symptoms in adolescents. Stress is associated with components of metabolic syndrome and inflammation. The present study hypothesizes that aldosterone, more than corticosterone, promotes chronic stress-hepatic steatosis and fibrosis, as well as renal inflammation and fibrosis in young adult rats. Thirty-two young adult male Wistar rats of 51 days old were divided into four groups (n = 8 per group): Control (C), chronic unpredictable mild stress (CUMS), control plus vehicle (C plus veh), CUMS plus eplerenone, a selective aldosterone blocker (CUMS plus EP). On postnatal day 51, eplerenone was administered orally through a gastric tube two hours before the start of the stress test. The CUMS paradigm was administered once daily at different times, with no repetition of the stressor sequence for four weeks. Renal inflammation and fibrosis were measured, as well as liver glycogen, triacylglycerol, and fibrosis levels. The serum concentrations of corticosterone, aldosterone, sodium, and creatinine were measured in urine and serum. The CUMS group showed a high level of serum aldosterone without affecting the level of corticosterone, increased urinary sodium, tubular atrophy, glomerular sclerosis, the presence of inflammation, and fibrosis, without affecting creatinine, increased glycogen content, triacylglycerol, and moderate fibrosis in the liver, and treatment with eplerenone prevented the inflammation, fibrosis, glycogen, and triacylglycerol. Our results show that chronic stress-induced aldosterone promotes hepatic steatosis and renal injury more than corticosterone. The prevention by eplerenone supports our hypothesis.

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来源期刊
Journal of Molecular Histology
Journal of Molecular Histology 生物-细胞生物学
CiteScore
5.90
自引率
0.00%
发文量
68
审稿时长
1 months
期刊介绍: The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.
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Editorial: New perspectives from the new Editor-in-Chief of Journal of Molecular Histology. Correction: Dendrobine alleviates oleic acid-induced lipid accumulation by inhibiting FOS/METTL14 pathway. Correction: Zinc-alkaline phosphatase at sites of aortic calcification. PODXL promotes malignant progression of hepatocellular carcinoma by activating PI3K/AKT pathway. Biotoxicity of paraquat to lung cells mediated by endoplasmic reticulum-mitochondria interaction.
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