Probiotics ameliorate renal ischemia-reperfusion injury by modulating the phenotype of macrophages through the IL-10/GSK-3β/PTEN signaling pathway.
Animals
Down-Regulation
/ drug effects
Glycogen Synthase Kinase 3 beta
/ metabolism
Interleukin-10
/ metabolism
Kidney
/ drug effects
Macrophages
/ drug effects
Male
PTEN Phosphohydrolase
/ metabolism
Phenotype
Probiotics
/ pharmacology
Rats
Rats, Wistar
Reperfusion Injury
/ drug therapy
Signal Transduction
/ drug effects
Up-Regulation
/ drug effects
IL-10/GSK-3β/PTEN signaling pathway
Macrophage phenotype
Probiotics
Renal ischemia-reperfusion injury
Journal
Pflugers Archiv : European journal of physiology
ISSN: 1432-2013
Titre abrégé: Pflugers Arch
Pays: Germany
ID NLM: 0154720
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
19
06
2018
accepted:
02
10
2018
revised:
26
09
2018
pubmed:
15
11
2018
medline:
17
4
2020
entrez:
15
11
2018
Statut:
ppublish
Résumé
After renal ischemic reperfusion injury, a series of pathological changes, such as impaired intestinal barrier function, intestinal flora, and endotoxin translocation, are caused by intestinal ischemia and hypoxia, which then trigger systemic inflammatory responses and affect the condition and prognosis of the patients. In this study, a rat model of ischemia-reperfusion injury was established by examining changes in renal function, intestinal barrier function, inflammatory index, oxidative stress, and macrophage phenotypes to evaluate the effect of probiotic VSL#3 on renal ischemia-reperfusion injury. The results showed that, after VSL#3 intervention, the levels of BUN, Scr, Cys C, PRO, and NGAL were all significantly decreased compared with the I/R group, while the value of Ccr showed a significant increase. In addition, the concentrations of MPO, IL-1β, TNF-α, IL-6, ED-1, and PCNA were all significantly lower than those in the I/R group, while the levels of endotoxin, DOA, and D-lactic acid were significantly decreased. Furthermore, the proteins associated with intestinal barrier functions, such as ZO-1, Occludin, and Claudin-1, were significantly upregulated compared with the I/R group. Overall, the VSL#3 intervention group was able to maintain the required number of beneficial intestinal flora and to inhibit the proliferation of harmful bacteria. At the same time, the VSL#3 intervention could also prevent the decrease in the levels of CAT, GSH-PX, H
Identifiants
pubmed: 30426249
doi: 10.1007/s00424-018-2213-1
pii: 10.1007/s00424-018-2213-1
doi:
Substances chimiques
Interleukin-10
130068-27-8
Glycogen Synthase Kinase 3 beta
EC 2.7.11.1
PTEN Phosphohydrolase
EC 3.1.3.67
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
573-581Références
Bone. 2013 Jul;55(1):126-31
pubmed: 23419777
Mediators Inflamm. 2014;2014:901530
pubmed: 25132736
Am J Physiol Renal Physiol. 2015 Jan 1;308(1):F69-75
pubmed: 25377911
Atherosclerosis. 2015 Sep;242(1):56-64
pubmed: 26184694
Nat Rev Nephrol. 2016 Dec;12(12):714
pubmed: 27818505
Biomed Res Int. 2014;2014:210901
pubmed: 24955347
Exp Ther Med. 2016 Sep;12(3):1367-1372
pubmed: 27588057
Cytokine. 2014 Sep;69(1):29-38
pubmed: 25022959
J Ginseng Res. 2016 Apr;40(2):196-202
pubmed: 27158241
Int J Mol Med. 2018 May;41(5):2640-2650
pubmed: 29436597
Br J Nutr. 2017 Jan;117(1):93-107
pubmed: 28102115
J Surg Res. 2016 Jun 15;203(2):324-30
pubmed: 27363640
Cell Signal. 2014 Oct;26(10):2096-106
pubmed: 24975844
J Am Soc Nephrol. 2014 Feb;25(2):292-304
pubmed: 24309188
Am J Physiol Heart Circ Physiol. 2017 Nov 1;313(5):H988-H999
pubmed: 28822969
Kidney Dis (Basel). 2015 Sep;1(2):138-46
pubmed: 27536674
Nat Rev Nephrol. 2015 Aug;11(8):445
pubmed: 26077741
Nat Rev Nephrol. 2016 Dec;12(12):715
pubmed: 27748388