Hyperbilirubinemia Protects against Aging-Associated Inflammation and Metabolic Deterioration

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60461373%3A22330%2F16%3A43901855" target="_blank" >RIV/60461373:22330/16:43901855 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/67985823:_____/16:00465951 RIV/00216208:11110/16:10327684 RIV/00023761:_____/16:N0000030 RIV/00064165:_____/16:10327684

Výsledek na webu

<a href="https://www.hindawi.com/journals/omcl/2016/6190609/" target="_blank" >https://www.hindawi.com/journals/omcl/2016/6190609/</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1155/2016/6190609" target="_blank" >10.1155/2016/6190609</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Hyperbilirubinemia Protects against Aging-Associated Inflammation and Metabolic Deterioration

Popis výsledku v původním jazyce

Mild constitutive hyperbilirubinemia is associated with a reduced risk of cardiovascular diseases, diabetes, and cancer. Since these pathologies are associated with aging, inflammation, and oxidative stress, we investigated whether hyperbilirubinemia interferes with ROS homeostasis in cell cultures and with inflammation, senescence, and mitochondrial dysfunction in aged rats. Human embryonic kidney cells and rat primary fibroblasts showed a dose-dependent decrease in the ratio of oxidized/reduced glutathione, intracellular H2O2 levels, and mitochondrial ROS production, with increasing bilirubin concentrations in the culture media. Compared to their normobilirubinemic siblings, aged hyperbilirubinemic Gunn rats showed significantly smaller amounts of visceral fat, better glucose tolerance, and decreased serum levels of proinflammatory cytokines TNF alpha, IL-1 beta, and IL-18. Simultaneously, livers from Gunn rats showed decreased expression of senescence markers and cell cycle inhibitors p21 and p16. Mitochondria from aged Gunn rats showed higher respiration and lower H2O2 production compared to controls. In conclusion, we demonstrated that mildly elevated serum bilirubin is generally associated with attenuation of oxidative stress and with better anthropometric parameters, decreased inflammatory status, increased glucose tolerance, fewer signs of cellular senescence, and enhanced mitochondrial function in aged rats.

Název v anglickém jazyce

Hyperbilirubinemia Protects against Aging-Associated Inflammation and Metabolic Deterioration

Popis výsledku anglicky

Mild constitutive hyperbilirubinemia is associated with a reduced risk of cardiovascular diseases, diabetes, and cancer. Since these pathologies are associated with aging, inflammation, and oxidative stress, we investigated whether hyperbilirubinemia interferes with ROS homeostasis in cell cultures and with inflammation, senescence, and mitochondrial dysfunction in aged rats. Human embryonic kidney cells and rat primary fibroblasts showed a dose-dependent decrease in the ratio of oxidized/reduced glutathione, intracellular H2O2 levels, and mitochondrial ROS production, with increasing bilirubin concentrations in the culture media. Compared to their normobilirubinemic siblings, aged hyperbilirubinemic Gunn rats showed significantly smaller amounts of visceral fat, better glucose tolerance, and decreased serum levels of proinflammatory cytokines TNF alpha, IL-1 beta, and IL-18. Simultaneously, livers from Gunn rats showed decreased expression of senescence markers and cell cycle inhibitors p21 and p16. Mitochondria from aged Gunn rats showed higher respiration and lower H2O2 production compared to controls. In conclusion, we demonstrated that mildly elevated serum bilirubin is generally associated with attenuation of oxidative stress and with better anthropometric parameters, decreased inflammatory status, increased glucose tolerance, fewer signs of cellular senescence, and enhanced mitochondrial function in aged rats.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

—

Projekt

<a href="/cs/project/GPP305%2F12%2FP388" target="_blank" >GPP305/12/P388: Mitochondriální DNA u tumorů a metabolického syndromu</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2016

Kód důvěrnosti údajů

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

Název periodika

Oxidative Medicine and Cellular Longevity

ISSN

1942-0900

e-ISSN

—

Svazek periodika

Neuveden

Číslo periodika v rámci svazku

léto 2016

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

"nestrankovano"

Kód UT WoS článku

000381431600001

EID výsledku v databázi Scopus

2-s2.0-84986247533