Effects of post ischemia-reperfusion treatment with trimetazidine on renal injury in rats: Insights on delayed renal fibrosis progression

Jin Ha Park, Ji Hae Jun, Jae Kwang Shim, Eun Jung Shin, Eunah Shin, Younglan Kwak

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Even after recovery from acute kidney injury, glomeruli remain vulnerable to further injury by way of interstitial fibrosis. This study is aimed at elucidating the effects of post ischemia-reperfusion (I/R) treatment with trimetazidine on the progression to renal fibrosis as well as short- and intermediate-term aspects. Trimetazidine 3 mg/kg or 0.9% saline was given intraperitoneally once upon reperfusion or daily thereafter for 5 d or 8 w. Renal histologic changes and related signaling proteins were assessed. After 24 h, post I/R treatment with trimetazidine significantly reduced serum blood urea nitrogen and creatinine levels and tubular injury accompanied with upregulation of hypoxia-inducible factor- (HIF-) 1α, vascular endothelial growth factor (VEGF), and Bcl-2 expression. After 5 d, post I/R treatment with trimetazidine reduced renal tubular cell necrosis and apoptosis with upregulation of HIF-1α-VEGF and tissue inhibitors of metalloproteinase activities, attenuation of matrix metalloproteinase activities, and alteration of the ratio of Bax to Bcl-2 levels. After 8 w, however, post I/R treatment with trimetazidine did not modify the progression of renal fibrosis. In conclusion, post I/R treatment with trimetazidine allows ischemic kidneys to regain renal function and structure more rapidly compared to nontreated kidneys, but not enough to resolute renal fibrosis in long-term aspect.

Original languageEnglish
Article number1072805
JournalOxidative medicine and cellular longevity
Volume2018
DOIs
Publication statusPublished - 2018 Jan 1

Fingerprint

Trimetazidine
Reperfusion
Rats
Fibrosis
Ischemia
Kidney
Wounds and Injuries
Hypoxia-Inducible Factor 1
Vascular Endothelial Growth Factor A
Tissue Inhibitor of Metalloproteinases
Regain
Up-Regulation
Kidney Glomerulus
Matrix Metalloproteinases
Urea
Blood Urea Nitrogen
Creatinine
Blood
Nitrogen
Acute Kidney Injury

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Ageing
  • Cell Biology

Cite this

@article{874d225b080a4ffeaab816a1aae94ad7,
title = "Effects of post ischemia-reperfusion treatment with trimetazidine on renal injury in rats: Insights on delayed renal fibrosis progression",
abstract = "Even after recovery from acute kidney injury, glomeruli remain vulnerable to further injury by way of interstitial fibrosis. This study is aimed at elucidating the effects of post ischemia-reperfusion (I/R) treatment with trimetazidine on the progression to renal fibrosis as well as short- and intermediate-term aspects. Trimetazidine 3 mg/kg or 0.9{\%} saline was given intraperitoneally once upon reperfusion or daily thereafter for 5 d or 8 w. Renal histologic changes and related signaling proteins were assessed. After 24 h, post I/R treatment with trimetazidine significantly reduced serum blood urea nitrogen and creatinine levels and tubular injury accompanied with upregulation of hypoxia-inducible factor- (HIF-) 1α, vascular endothelial growth factor (VEGF), and Bcl-2 expression. After 5 d, post I/R treatment with trimetazidine reduced renal tubular cell necrosis and apoptosis with upregulation of HIF-1α-VEGF and tissue inhibitors of metalloproteinase activities, attenuation of matrix metalloproteinase activities, and alteration of the ratio of Bax to Bcl-2 levels. After 8 w, however, post I/R treatment with trimetazidine did not modify the progression of renal fibrosis. In conclusion, post I/R treatment with trimetazidine allows ischemic kidneys to regain renal function and structure more rapidly compared to nontreated kidneys, but not enough to resolute renal fibrosis in long-term aspect.",
author = "Park, {Jin Ha} and Jun, {Ji Hae} and Shim, {Jae Kwang} and Shin, {Eun Jung} and Eunah Shin and Younglan Kwak",
year = "2018",
month = "1",
day = "1",
doi = "10.1155/2018/1072805",
language = "English",
volume = "2018",
journal = "Oxidative Medicine and Cellular Longevity",
issn = "1942-0900",
publisher = "Hindawi Publishing Corporation",

}

Effects of post ischemia-reperfusion treatment with trimetazidine on renal injury in rats : Insights on delayed renal fibrosis progression. / Park, Jin Ha; Jun, Ji Hae; Shim, Jae Kwang; Shin, Eun Jung; Shin, Eunah; Kwak, Younglan.

In: Oxidative medicine and cellular longevity, Vol. 2018, 1072805, 01.01.2018.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of post ischemia-reperfusion treatment with trimetazidine on renal injury in rats

T2 - Insights on delayed renal fibrosis progression

AU - Park, Jin Ha

AU - Jun, Ji Hae

AU - Shim, Jae Kwang

AU - Shin, Eun Jung

AU - Shin, Eunah

AU - Kwak, Younglan

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Even after recovery from acute kidney injury, glomeruli remain vulnerable to further injury by way of interstitial fibrosis. This study is aimed at elucidating the effects of post ischemia-reperfusion (I/R) treatment with trimetazidine on the progression to renal fibrosis as well as short- and intermediate-term aspects. Trimetazidine 3 mg/kg or 0.9% saline was given intraperitoneally once upon reperfusion or daily thereafter for 5 d or 8 w. Renal histologic changes and related signaling proteins were assessed. After 24 h, post I/R treatment with trimetazidine significantly reduced serum blood urea nitrogen and creatinine levels and tubular injury accompanied with upregulation of hypoxia-inducible factor- (HIF-) 1α, vascular endothelial growth factor (VEGF), and Bcl-2 expression. After 5 d, post I/R treatment with trimetazidine reduced renal tubular cell necrosis and apoptosis with upregulation of HIF-1α-VEGF and tissue inhibitors of metalloproteinase activities, attenuation of matrix metalloproteinase activities, and alteration of the ratio of Bax to Bcl-2 levels. After 8 w, however, post I/R treatment with trimetazidine did not modify the progression of renal fibrosis. In conclusion, post I/R treatment with trimetazidine allows ischemic kidneys to regain renal function and structure more rapidly compared to nontreated kidneys, but not enough to resolute renal fibrosis in long-term aspect.

AB - Even after recovery from acute kidney injury, glomeruli remain vulnerable to further injury by way of interstitial fibrosis. This study is aimed at elucidating the effects of post ischemia-reperfusion (I/R) treatment with trimetazidine on the progression to renal fibrosis as well as short- and intermediate-term aspects. Trimetazidine 3 mg/kg or 0.9% saline was given intraperitoneally once upon reperfusion or daily thereafter for 5 d or 8 w. Renal histologic changes and related signaling proteins were assessed. After 24 h, post I/R treatment with trimetazidine significantly reduced serum blood urea nitrogen and creatinine levels and tubular injury accompanied with upregulation of hypoxia-inducible factor- (HIF-) 1α, vascular endothelial growth factor (VEGF), and Bcl-2 expression. After 5 d, post I/R treatment with trimetazidine reduced renal tubular cell necrosis and apoptosis with upregulation of HIF-1α-VEGF and tissue inhibitors of metalloproteinase activities, attenuation of matrix metalloproteinase activities, and alteration of the ratio of Bax to Bcl-2 levels. After 8 w, however, post I/R treatment with trimetazidine did not modify the progression of renal fibrosis. In conclusion, post I/R treatment with trimetazidine allows ischemic kidneys to regain renal function and structure more rapidly compared to nontreated kidneys, but not enough to resolute renal fibrosis in long-term aspect.

UR - http://www.scopus.com/inward/record.url?scp=85055203730&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85055203730&partnerID=8YFLogxK

U2 - 10.1155/2018/1072805

DO - 10.1155/2018/1072805

M3 - Article

C2 - 30057668

AN - SCOPUS:85055203730

VL - 2018

JO - Oxidative Medicine and Cellular Longevity

JF - Oxidative Medicine and Cellular Longevity

SN - 1942-0900

M1 - 1072805

ER -