Oxidative Stress, Metabolic Impairment and Neuroinflammation are Associated With Target Organ Damage in SHRSP

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F25%3A00641851" target="_blank" >RIV/61388963:_____/25:00641851 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/67985823:_____/25:00643939 RIV/61388971:_____/25:00643939 RIV/00216208:11110/25:10506740

Výsledek na webu

<a href="https://doi.org/10.33549/physiolres.935659" target="_blank" >https://doi.org/10.33549/physiolres.935659</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.33549/physiolres.935659" target="_blank" >10.33549/physiolres.935659</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Oxidative Stress, Metabolic Impairment and Neuroinflammation are Associated With Target Organ Damage in SHRSP

Popis výsledku v původním jazyce

Stroke-prone spontaneously hypertensive rats (SHRSP) are widely used as a model to study cerebral small vessel disease (CSVD) and its association with chronic hypertension. This study investigated the relationship between metabolic, cardiovascular, and neuronal comorbidities in 32-week-old SHRSP rats versus Wistar-Kyoto (WKY) controls, with a focus on oxidative stress, inflammation, and metabolic alterations. Despite hypertension and cardiac and renal hypertrophy, no significant cerebral vascular changes or microbleeds and no cerebral edema were detected in SHRSP. NMR-based urinary metabolomics revealed reduced gut microbiome-derived metabolites, such as p-cresylglucuronide, hippurate, and phenylacetylglycine, alongside increases in methylamine and dimethylamine. These findings reflect gut dysbiosis and altered microbial composition in hypertensive conditions. Elevated markers of oxidative stress, including thiobarbituric acid-reactive substances, and increased expression of NADPH oxidase (NOX) 2 and NOX4 in peripheral tissues suggested oxidative damage in SHRSP rats. Astrocytic hyperreactivity, indicated by increased expression of glial fibrillary acidic protein in brain cortex and hippocampus, was suggestive of neuroinflammatory responses. Our findings highlight complex interplay between hypertension, metabolism, and neuroinflammation while underscoring the variability in SHRSP models.

Název v anglickém jazyce

Oxidative Stress, Metabolic Impairment and Neuroinflammation are Associated With Target Organ Damage in SHRSP

Popis výsledku anglicky

Stroke-prone spontaneously hypertensive rats (SHRSP) are widely used as a model to study cerebral small vessel disease (CSVD) and its association with chronic hypertension. This study investigated the relationship between metabolic, cardiovascular, and neuronal comorbidities in 32-week-old SHRSP rats versus Wistar-Kyoto (WKY) controls, with a focus on oxidative stress, inflammation, and metabolic alterations. Despite hypertension and cardiac and renal hypertrophy, no significant cerebral vascular changes or microbleeds and no cerebral edema were detected in SHRSP. NMR-based urinary metabolomics revealed reduced gut microbiome-derived metabolites, such as p-cresylglucuronide, hippurate, and phenylacetylglycine, alongside increases in methylamine and dimethylamine. These findings reflect gut dysbiosis and altered microbial composition in hypertensive conditions. Elevated markers of oxidative stress, including thiobarbituric acid-reactive substances, and increased expression of NADPH oxidase (NOX) 2 and NOX4 in peripheral tissues suggested oxidative damage in SHRSP rats. Astrocytic hyperreactivity, indicated by increased expression of glial fibrillary acidic protein in brain cortex and hippocampus, was suggestive of neuroinflammatory responses. Our findings highlight complex interplay between hypertension, metabolism, and neuroinflammation while underscoring the variability in SHRSP models.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Physiological Research

ISSN

0862-8408

e-ISSN

1802-9973

Svazek periodika

74

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

17

Strana od-do

779-795

Kód UT WoS článku

001631813000008

EID výsledku v databázi Scopus

2-s2.0-105020870523