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在关键时期暴露于过量蔗糖的大鼠会发生炎症，并表现出血管平滑肌细胞的分泌表型。

Rats Exposed to Excess Sucrose During a Critical Period Develop Inflammation and Express a Secretory Phenotype of Vascular Smooth Muscle Cells.

作者信息

Guarner-Lans Verónica, Soria-Castro Elizabeth, Cano-Martínez Agustina, Rubio-Ruiz María Esther, Zarco Gabriela, Carreón-Torres Elizabeth, Grimaldo Oscar, Castrejón-Téllez Vicente, Pérez-Torres Israel

机构信息

Department of Physiology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, Tlalpan, Mexico City 14080, Mexico.

Department of Cardiovascular Biomedicine, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, Tlalpan, Mexico City 14080, Mexico.

出版信息

Metabolites. 2024 Oct 17;14(10):555. doi: 10.3390/metabo14100555.

DOI:10.3390/metabo14100555
PMID:39452936
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11509398/
Abstract

BACKGROUND

Neonatal rats that receive sucrose during a critical postnatal period (CP, days 12 to 28) develop hypertension by the time they reach adulthood. Inflammation might contribute to changes during this period and could be associated with variations in the vascular smooth muscle (VSMC) phenotype.

OBJECTIVE

We studied changes in inflammatory pathways that could underlie the expression of the secretory phenotype in the VSMC in the thoracic aorta of rats that received sucrose during CP.

METHODS

We analyzed histological changes in the aorta and the expression of the COX-2, TLR4, iNOS, eNOS, MMP-2 and -9, and β- and α-actin, the quantities of TNF-α, IL-6, and IL-1β using ELISA, and the levels of fatty acids using gas chromatography.

RESULTS

The aortic wall presented disorganization, decellularization, and wavy elastic fibers and an increase in the lumen area. The α- and β-actin expressions were decreased, while COX-2, TLR4, TNF-α, and the activity of IL-6 were increased. Oleic acid was increased in CP in comparison to the control group.

CONCLUSIONS

There is transient hypertension at the end of the CP that is accompanied by inflammation and a change in the phenotype of VSMC to the secretory phenotype. The inflammatory changes could act as epigenetic signals to determine the development of hypertension when animals reach adulthood.

摘要

背景

在关键的出生后时期（CP，第12至28天）接受蔗糖的新生大鼠成年后会出现高血压。炎症可能在这一时期的变化中起作用，并且可能与血管平滑肌（VSMC）表型的变化有关。

目的

我们研究了在CP期间接受蔗糖的大鼠胸主动脉VSMC中，可能是分泌表型表达基础的炎症途径的变化。

方法

我们分析了主动脉的组织学变化、COX-2、TLR4、iNOS、eNOS、MMP-2和-9以及β-和α-肌动蛋白的表达，使用酶联免疫吸附测定法检测TNF-α、IL-6和IL-1β的量，并使用气相色谱法检测脂肪酸水平。

结果

主动脉壁出现结构紊乱、脱细胞和波浪状弹性纤维，管腔面积增加。α-和β-肌动蛋白表达降低，而COX-2、TLR4、TNF-α和IL-6的活性增加。与对照组相比，CP组油酸增加。

结论

CP末期存在短暂性高血压，伴有炎症以及VSMC表型向分泌表型的转变。炎症变化可能作为表观遗传信号，决定动物成年后高血压的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/f8fb9559fabf/metabolites-14-00555-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/6fc6c896b69c/metabolites-14-00555-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/146724e5d7f4/metabolites-14-00555-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/298581baeab1/metabolites-14-00555-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/8c5224d8c136/metabolites-14-00555-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/c9626a3c7516/metabolites-14-00555-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/6086805a118c/metabolites-14-00555-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/dde0e28c9f42/metabolites-14-00555-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/f8fb9559fabf/metabolites-14-00555-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/6fc6c896b69c/metabolites-14-00555-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/146724e5d7f4/metabolites-14-00555-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/298581baeab1/metabolites-14-00555-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/8c5224d8c136/metabolites-14-00555-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/c9626a3c7516/metabolites-14-00555-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/6086805a118c/metabolites-14-00555-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/dde0e28c9f42/metabolites-14-00555-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773b/11509398/f8fb9559fabf/metabolites-14-00555-g008.jpg

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