High density lipoprotein (HDL) reduces renal ischemia/reperfusion injury.

C. Thiemermann, N. Patel, E. O. Kvale, G. W. Cockerill, Paul Anthony James Brown, Keith Nicol Stewart, S. Cuzzocrea, D. Britti, H. Mota-Filipe, P. K. Chatterjee

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

High-density lipoproteins (HDL) have been shown to reduce organ injury and mortality in animal models of shock via modulation of the expression of adhesion molecules and pro-inflammatory enzymes. As renal inflammation plays an important role in the development of ischemia/reperfusion (I/R) injury of the kidney, the aim of this study was to investigate the ability of HDL to alleviate renal dysfunction and injury in a rat model of renal I/R. HDL (80 mg/kg, intravenous) was administered to male Wistar rats 30 min before bilateral renal ischemia for 45 min followed by reperfusion for up to 48 h. After 6-h reperfusion, HDL significantly reduced (1) renal and tubular dysfunction, (2) tubular and reperfusion-injury, and (3) histologic evidence of renal injury. HDL also improved renal function (after 24-h and 48-h reperfusion) and reduced histologic signs of renal injury (after 48-h reperfusion). Administration of HDL significantly reduced the numbers of polymorphonuclear leukocytes (PMN) infiltrating into renal tissues during reperfusion, which was reflected by an attenuation of the increase in renal myeloperoxidase activity caused by I/R. Furthermore, HDL markedly reduced expression of the adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), and P-selectin during reperfusion. The increase in renal malondialdehyde levels caused by renal I/R was also significantly reduced by HDL, suggesting attenuation of lipid peroxidation subsequent to oxidative stress. These results demonstrate that HDL significantly reduces renal I/R injury and severity of ischemic acute renal failure. It is proposed that the mechanism of protection involves reduction of the expression of adhesion molecules, resulting in reduction of PMN infiltration and oxidative stress.

Original languageEnglish
Pages (from-to)1833-1843
Number of pages10
JournalJournal of the American Society of Nephrology
Volume14
Issue number7
DOIs
Publication statusPublished - 2003

Keywords

  • ISCHEMIA-REPERFUSION INJURY
  • CYTOKINE-INDUCED EXPRESSION
  • CELL-ADHESION MOLECULES
  • APOLIPOPROTEIN-A-I
  • CARDIOVASCULAR-DISEASE
  • RAT-KIDNEY
  • E-SELECTIN
  • FAILURE
  • INHIBITION
  • VIVO

Cite this

Thiemermann, C., Patel, N., Kvale, E. O., Cockerill, G. W., Brown, P. A. J., Stewart, K. N., ... Chatterjee, P. K. (2003). High density lipoprotein (HDL) reduces renal ischemia/reperfusion injury. Journal of the American Society of Nephrology, 14(7), 1833-1843. https://doi.org/10.1097/01.ASN.0000075552.97794.8C

High density lipoprotein (HDL) reduces renal ischemia/reperfusion injury. / Thiemermann, C.; Patel, N.; Kvale, E. O.; Cockerill, G. W.; Brown, Paul Anthony James; Stewart, Keith Nicol; Cuzzocrea, S.; Britti, D.; Mota-Filipe, H.; Chatterjee, P. K.

In: Journal of the American Society of Nephrology, Vol. 14, No. 7, 2003, p. 1833-1843.

Research output: Contribution to journalArticle

Thiemermann, C, Patel, N, Kvale, EO, Cockerill, GW, Brown, PAJ, Stewart, KN, Cuzzocrea, S, Britti, D, Mota-Filipe, H & Chatterjee, PK 2003, 'High density lipoprotein (HDL) reduces renal ischemia/reperfusion injury.' Journal of the American Society of Nephrology, vol. 14, no. 7, pp. 1833-1843. https://doi.org/10.1097/01.ASN.0000075552.97794.8C
Thiemermann, C. ; Patel, N. ; Kvale, E. O. ; Cockerill, G. W. ; Brown, Paul Anthony James ; Stewart, Keith Nicol ; Cuzzocrea, S. ; Britti, D. ; Mota-Filipe, H. ; Chatterjee, P. K. / High density lipoprotein (HDL) reduces renal ischemia/reperfusion injury. In: Journal of the American Society of Nephrology. 2003 ; Vol. 14, No. 7. pp. 1833-1843.
@article{056da5e3c983414394b0c7ed99bdd084,
title = "High density lipoprotein (HDL) reduces renal ischemia/reperfusion injury.",
abstract = "High-density lipoproteins (HDL) have been shown to reduce organ injury and mortality in animal models of shock via modulation of the expression of adhesion molecules and pro-inflammatory enzymes. As renal inflammation plays an important role in the development of ischemia/reperfusion (I/R) injury of the kidney, the aim of this study was to investigate the ability of HDL to alleviate renal dysfunction and injury in a rat model of renal I/R. HDL (80 mg/kg, intravenous) was administered to male Wistar rats 30 min before bilateral renal ischemia for 45 min followed by reperfusion for up to 48 h. After 6-h reperfusion, HDL significantly reduced (1) renal and tubular dysfunction, (2) tubular and reperfusion-injury, and (3) histologic evidence of renal injury. HDL also improved renal function (after 24-h and 48-h reperfusion) and reduced histologic signs of renal injury (after 48-h reperfusion). Administration of HDL significantly reduced the numbers of polymorphonuclear leukocytes (PMN) infiltrating into renal tissues during reperfusion, which was reflected by an attenuation of the increase in renal myeloperoxidase activity caused by I/R. Furthermore, HDL markedly reduced expression of the adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), and P-selectin during reperfusion. The increase in renal malondialdehyde levels caused by renal I/R was also significantly reduced by HDL, suggesting attenuation of lipid peroxidation subsequent to oxidative stress. These results demonstrate that HDL significantly reduces renal I/R injury and severity of ischemic acute renal failure. It is proposed that the mechanism of protection involves reduction of the expression of adhesion molecules, resulting in reduction of PMN infiltration and oxidative stress.",
keywords = "ISCHEMIA-REPERFUSION INJURY, CYTOKINE-INDUCED EXPRESSION, CELL-ADHESION MOLECULES, APOLIPOPROTEIN-A-I, CARDIOVASCULAR-DISEASE, RAT-KIDNEY, E-SELECTIN, FAILURE, INHIBITION, VIVO",
author = "C. Thiemermann and N. Patel and Kvale, {E. O.} and Cockerill, {G. W.} and Brown, {Paul Anthony James} and Stewart, {Keith Nicol} and S. Cuzzocrea and D. Britti and H. Mota-Filipe and Chatterjee, {P. K.}",
year = "2003",
doi = "10.1097/01.ASN.0000075552.97794.8C",
language = "English",
volume = "14",
pages = "1833--1843",
journal = "Journal of the American Society of Nephrology",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "7",

}

TY - JOUR

T1 - High density lipoprotein (HDL) reduces renal ischemia/reperfusion injury.

AU - Thiemermann, C.

AU - Patel, N.

AU - Kvale, E. O.

AU - Cockerill, G. W.

AU - Brown, Paul Anthony James

AU - Stewart, Keith Nicol

AU - Cuzzocrea, S.

AU - Britti, D.

AU - Mota-Filipe, H.

AU - Chatterjee, P. K.

PY - 2003

Y1 - 2003

N2 - High-density lipoproteins (HDL) have been shown to reduce organ injury and mortality in animal models of shock via modulation of the expression of adhesion molecules and pro-inflammatory enzymes. As renal inflammation plays an important role in the development of ischemia/reperfusion (I/R) injury of the kidney, the aim of this study was to investigate the ability of HDL to alleviate renal dysfunction and injury in a rat model of renal I/R. HDL (80 mg/kg, intravenous) was administered to male Wistar rats 30 min before bilateral renal ischemia for 45 min followed by reperfusion for up to 48 h. After 6-h reperfusion, HDL significantly reduced (1) renal and tubular dysfunction, (2) tubular and reperfusion-injury, and (3) histologic evidence of renal injury. HDL also improved renal function (after 24-h and 48-h reperfusion) and reduced histologic signs of renal injury (after 48-h reperfusion). Administration of HDL significantly reduced the numbers of polymorphonuclear leukocytes (PMN) infiltrating into renal tissues during reperfusion, which was reflected by an attenuation of the increase in renal myeloperoxidase activity caused by I/R. Furthermore, HDL markedly reduced expression of the adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), and P-selectin during reperfusion. The increase in renal malondialdehyde levels caused by renal I/R was also significantly reduced by HDL, suggesting attenuation of lipid peroxidation subsequent to oxidative stress. These results demonstrate that HDL significantly reduces renal I/R injury and severity of ischemic acute renal failure. It is proposed that the mechanism of protection involves reduction of the expression of adhesion molecules, resulting in reduction of PMN infiltration and oxidative stress.

AB - High-density lipoproteins (HDL) have been shown to reduce organ injury and mortality in animal models of shock via modulation of the expression of adhesion molecules and pro-inflammatory enzymes. As renal inflammation plays an important role in the development of ischemia/reperfusion (I/R) injury of the kidney, the aim of this study was to investigate the ability of HDL to alleviate renal dysfunction and injury in a rat model of renal I/R. HDL (80 mg/kg, intravenous) was administered to male Wistar rats 30 min before bilateral renal ischemia for 45 min followed by reperfusion for up to 48 h. After 6-h reperfusion, HDL significantly reduced (1) renal and tubular dysfunction, (2) tubular and reperfusion-injury, and (3) histologic evidence of renal injury. HDL also improved renal function (after 24-h and 48-h reperfusion) and reduced histologic signs of renal injury (after 48-h reperfusion). Administration of HDL significantly reduced the numbers of polymorphonuclear leukocytes (PMN) infiltrating into renal tissues during reperfusion, which was reflected by an attenuation of the increase in renal myeloperoxidase activity caused by I/R. Furthermore, HDL markedly reduced expression of the adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), and P-selectin during reperfusion. The increase in renal malondialdehyde levels caused by renal I/R was also significantly reduced by HDL, suggesting attenuation of lipid peroxidation subsequent to oxidative stress. These results demonstrate that HDL significantly reduces renal I/R injury and severity of ischemic acute renal failure. It is proposed that the mechanism of protection involves reduction of the expression of adhesion molecules, resulting in reduction of PMN infiltration and oxidative stress.

KW - ISCHEMIA-REPERFUSION INJURY

KW - CYTOKINE-INDUCED EXPRESSION

KW - CELL-ADHESION MOLECULES

KW - APOLIPOPROTEIN-A-I

KW - CARDIOVASCULAR-DISEASE

KW - RAT-KIDNEY

KW - E-SELECTIN

KW - FAILURE

KW - INHIBITION

KW - VIVO

U2 - 10.1097/01.ASN.0000075552.97794.8C

DO - 10.1097/01.ASN.0000075552.97794.8C

M3 - Article

VL - 14

SP - 1833

EP - 1843

JO - Journal of the American Society of Nephrology

JF - Journal of the American Society of Nephrology

SN - 1046-6673

IS - 7

ER -