PhD Scientific Days 2017

Oral Presentations: Basic Sciences II.

Novel option for the treatment of renal hypoxic injury

Előadó neve

Lenart, Lilla

Előadó munkahelye

MTA-SE „Lendület” Diabetes Research Group, Budapest, Hungary

Előadó telefonszáma

+36205772890

Előadó e-mail címe

lenart.lillaa@gmail.com

Az előadás címe

Novel option for the treatment of renal hypoxic injury

Szerző(k) neve és munkahelye

Lilla Lenart(1), Judit Hodrea(1), Edgar Szkibinszkij(1,3), Dora B. Balogh(1,4),
Adam Hosszu(1,3), Adam Vannay(2,4), Laszlo Wagner(3),
Attila J. Szabo(4), Andrea Fekete(1,4)

MTA-SE „Lendület” Diabetes Research Group, Budapest, Hungary1
MTA-SE Pediatrics and Nephrology Research Group, Budapest, Hungary2
SE Department of Transplantation and Surgery, Budapest, Hungary3
SE 1st Department of Pediatrics, Budapest, Hungary4

Témacsoport

other

Szekció

Oral Presentations: Basic Sciences II.

Data of the presenter

Grants: LP008/2016, OTKA-, -K112629, K116928NNOTKA-114607, SUPPORTED BY THE ÚNKP-16-3-III NEW NATIONAL EXCELLENCE PROGRAM OF THE MINISTRY OF HUMAN CAPACITIES

Doctoral School: II. Clinical Medicine
Program: Prevention of Chronic Diseases in Childhood
Supervisor: Andrea Fekete
E-mail address: lenart.lillaa@gmail.com

Text of the abstract

Introduction: Although millions of patients suffer from end-stage renal disease, renal replacement therapy is the only therapeutic option. Graft function depends on the extent of ischemia/reperfusion injury (IRI) during transplantation.
It is known that the brain-derived neurotrophic factor (BDNF) plays a pivotal role in the mitigation of brain ischemic injury. Sigma-1 receptor (S1R) agonism has been shown to induce BDNF production in neuronal cells, however there is no data concerning the relation of BDNF and IRI leading to acute renal failure.

Aims: The aim of our study is to investigate the role of S1R agonism and BDNF in a rodent model of renal IRI.

Methods: Male Wistar rats were subjected to 50 min unilateral renal IRI, tissue samples were collected 24 hours after reperfusion. 30 min before the insult rats were treated i.p. with vehicle or S1R agonist FC03 (20 mg/bwkg). Sham-operated rats served as controls (n=8/group). Renal functional and structural parameters as well as inflammatory mediators were measured. Renal S1R and BDNF protein levels were determined.

Results: Impaired renal function and structural damage following IRI was ameliorated by S1R agonist FC03 treatment. Early and sensitive markers of acute kidney injury Kim1, Ngal and inflammatory mediators (IL-1α, IL-6, TNFα) were decreased in in FC03-treated kidneys. Our study is the first to show the presence of pro- and mature BDNF in the kidney. Both forms of BDNF were decreased in the kindey after IRI. Pro BDNF showed a rising tendency, while mature BDNF was markedy increased after FC03 treatment.

Conclusions: Our results could demonstrate the role of BDNF in the mitigation of renal IRI. Therapeutic modulation of the process could alleviate renal hypoxic injury, thus improving long-term graft function. Our study supports better understanding of the pathomechanism of hypoxic renal injury and the characterization of novel pathways for therapeutic intervention.

Kind

Szabad

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

1215

Authors (legacy)

Lilla Lenart(1), Judit Hodrea(1), Edgar Szkibinszkij(1,3), Dora B. Balogh(1,4),
Adam Hosszu(1,3), Adam Vannay(2,4), Laszlo Wagner(3),
Attila J. Szabo(4), Andrea Fekete(1,4)

MTA-SE „Lendület” Diabetes Research Group, Budapest, Hungary1
MTA-SE Pediatrics and Nephrology Research Group, Budapest, Hungary2
SE Department of Transplantation and Surgery, Budapest, Hungary3
SE 1st Department of Pediatrics, Budapest, Hungary4