Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

A localized ischemic preconditioning regimen increases tumor necrosis factor a expression in a rat model of kidney ischemia-reperfusion injury

Khalid, Usman, Jenkins, Robert H., Pino-Chavez, Gilda, Bowen, Timothy, Fraser, Donald James ORCID: https://orcid.org/0000-0003-0102-9342 and Chavez, Rafael 2015. A localized ischemic preconditioning regimen increases tumor necrosis factor a expression in a rat model of kidney ischemia-reperfusion injury. Experimental and Clinical Transplantation 13 (6) , pp. 535-542. 10.6002/ect.2015.0039

Full text not available from this repository.

Abstract

OBJECTIVES: We evaluated a continuous, immediate, localized ischemic preconditioning regimen in a rat model of ischemia-reperfusion injury and assessed whether it attenuated injury at the histologic and molecular levels. MATERIALS AND METHODS: Fifteen adult male Lewis rats received sham operation, left unilateral warm ischemia (45 minutes of cross-clamping of the renal pedicle; ischemia-reperfusion injury group), or 15 minutes of ischemia followed by a 20-minute reperfusion period, 45 minutes of ischemia-reperfusion injury, and subsequent reperfusion (ischemic preconditioning/ischemia-reperfusion injury group). Kidney tissue was retrieved 48 hours later, sectioned, stained with hematoxylin and eosin, and examined. We used RNA extraction and real-time quantitative polymerase chain reaction analysis to assess acute kidney injury markers, cytokines, and microRNA-21. RESULTS: Forty-five minutes of unilateral ischemia-reperfusion injury caused marked changes in histology at 48 hours, characterized by endothelial loss, tubulointerstitial damage (inflammation, cast formation), tubular cell necrosis, and glomerular capsule thickening. The ischemia-reperfusion injury and ischemic preconditioning/ischemia-reperfusion injury groups showed no measurable differences in histology. Expression of the acute kidney injury markers was significantly increased in the ischemia-reperfusion injury versus Sham group; however, no difference was found between the ischemia reperfusion injury and ischemic preconditioning/ischemia-reperfusion injury groups. Similarly, expression of interleukin 17, interleukin 18, and tumor necrosis factor ? was significantly increased in the ischemia-reperfusion injury versus Sham group. No significant difference was found between the ischemia-reperfusion injury and ischemic preconditioning/ischemia-reperfusion injury groups for interleukin 17 and interleukin 18; however, tumor necrosis factor ? expression was significantly increased in the ischemic preconditioning/ischemia-reperfusion injury versus ischemia-reperfusion injury group. CONCLUSIONS: In our ischemic preconditioning model, tumor necrosis factor α expression was increased without altering the sequelae of ischemia-reperfusion injury. The long-term consequences of this augmented early inflammatory response and whether these consequences are altered by variations in ischemic preconditioning or a subsequent injury require further study.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Publisher: Baskent University
ISSN: 1304-0855
Last Modified: 01 Nov 2022 10:16
URI: https://orca.cardiff.ac.uk/id/eprint/90860

Citation Data

Cited 9 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item