Anti-inflammatory effects of palm11-PrRP31 in a rat model of lipopolysaccharide-induced acute inflammation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F25%3A00618014" target="_blank" >RIV/61388963:_____/25:00618014 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/67985823:_____/25:00618243 RIV/00216208:11110/25:10500000

Výsledek na webu

<a href="https://doi.org/10.1530/JME-24-0090" target="_blank" >https://doi.org/10.1530/JME-24-0090</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1530/JME-24-0090" target="_blank" >10.1530/JME-24-0090</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Anti-inflammatory effects of palm11-PrRP31 in a rat model of lipopolysaccharide-induced acute inflammation

Popis výsledku v původním jazyce

Lipopolysaccharides (LPS) are major components of gram-negative bacteria. LPS not only induce endotoxemia and inflammation but also contribute to various diseases. In experimental settings, LPS administration serves as a model for acute inflammatory responses. This study aimed to evaluate the anti-inflammatory potential and mechanism of action of palmitoylated prolactin-releasing peptide (palm11-PrRP31) in a rat model of LPS-induced inflammation. Palm11-PrRP31 has demonstrated efficacy in mitigating LPS-induced weight loss and anorexia, emphasizing its potential protective effects. The cytokine profiles revealed a consistent reduction in tumor necrosis factor α, highlighting the potent anti-inflammatory effects of palm11-PrRP31. The peptide also modulated key cytokines and chemokines in the plasma, liver and hypothalamus, reflecting its broad-spectrum anti-inflammatory properties. Palm11-PrRP31 also effectively attenuated the expression levels of Toll-like receptor 4 signaling components in the liver, suggesting its ability to suppress the activation of these pathways during LPS-induced inflammation. These anti-inflammatory effects were specific to palm11-PrRP31, whereas natural PrRP31 had a minimal impact. In conclusion, this study reveals the efficacy of palm11-PrRP31 in modulating LPS-induced inflammation, offering insights into its immunomodulatory properties. The ability of the peptide to suppress proinflammatory responses and attenuate relevant signaling pathways indicates its potential use as a therapeutic agent for inflammatory disorders.

Název v anglickém jazyce

Anti-inflammatory effects of palm11-PrRP31 in a rat model of lipopolysaccharide-induced acute inflammation

Popis výsledku anglicky

Lipopolysaccharides (LPS) are major components of gram-negative bacteria. LPS not only induce endotoxemia and inflammation but also contribute to various diseases. In experimental settings, LPS administration serves as a model for acute inflammatory responses. This study aimed to evaluate the anti-inflammatory potential and mechanism of action of palmitoylated prolactin-releasing peptide (palm11-PrRP31) in a rat model of LPS-induced inflammation. Palm11-PrRP31 has demonstrated efficacy in mitigating LPS-induced weight loss and anorexia, emphasizing its potential protective effects. The cytokine profiles revealed a consistent reduction in tumor necrosis factor α, highlighting the potent anti-inflammatory effects of palm11-PrRP31. The peptide also modulated key cytokines and chemokines in the plasma, liver and hypothalamus, reflecting its broad-spectrum anti-inflammatory properties. Palm11-PrRP31 also effectively attenuated the expression levels of Toll-like receptor 4 signaling components in the liver, suggesting its ability to suppress the activation of these pathways during LPS-induced inflammation. These anti-inflammatory effects were specific to palm11-PrRP31, whereas natural PrRP31 had a minimal impact. In conclusion, this study reveals the efficacy of palm11-PrRP31 in modulating LPS-induced inflammation, offering insights into its immunomodulatory properties. The ability of the peptide to suppress proinflammatory responses and attenuate relevant signaling pathways indicates its potential use as a therapeutic agent for inflammatory disorders.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30202 - Endocrinology and metabolism (including diabetes, hormones)

Projekt

<a href="/cs/project/LX22NPO5104" target="_blank" >LX22NPO5104: Národní institut pro výzkum metabolických a kardiovaskulárních onemocnění</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

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

Název periodika

Journal of Molecular Endocrinology

ISSN

0952-5041

e-ISSN

1479-6813

Svazek periodika

74

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

13

Strana od-do

e240090

Kód UT WoS článku

001518868900002

EID výsledku v databázi Scopus

2-s2.0-85219015100