Effect of trimetazidine on the nucleotide profile in rat kidney with ischemia–reperfusion injury

Domański, Leszek; Sulikowski, Tadeusz; Safranow, Krzysztof; Pawlik, Andrzej; Olszewska, Maria; Chlubek, Dariusz; Urasińska, Elżbieta; Ciechanowski, Kazimierz

doi:10.1016/j.ejps.2005.10.012

Cited by 35 publications

(19 citation statements)

References 39 publications

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“…In our study, the protective effect of TMZ in renal tissue of pretreated groups was correlated with an earlier and higher expression of stathmin than in renal tissue without TMZ treatment. This effect on stathmin, which is involved in the regulation of mitosis and proposed to be a relay integrating diverse intracellular signaling pathways controlling cell proliferation, differentiation, and functions, could be related to a recently suggested effect against dephosphorylation of nucleotides during ischemia (8). In addition, these results suggest that stathmin is a critical protein in the regulation of cell mitosis in damaged tissue.…”

Section: Discussionsupporting

confidence: 54%

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Jayle¹,

Favreau²,

Zhang³

et al. 2007

American Journal of Physiology-Renal Physiology

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Acute renal failure (ARF) is often the consequence of an ischemia-reperfusion injury (IRI) and associated with high mortality. Warm ischemia (WI) is a crucial factor of tissue damage, and tissue destruction led by ischemia-reperfusion (I/R) can impact the early and long-term functional outcome. Trimetazidine (TMZ) is an anti-ischemic drug. Previously, we already verified its protective effect on a cold-ischemic pig kidney model by directly adding TMZ into the preservation solution (Faure JP, Baumert H, Han Z, Goujon JM, Favreau F, Dutheil D, Petit I, Barriere M, Tallineau C, Tillement JP, Carretier M, Mauco G, Papadopoulos V, Hauet T. Biochem Pharmacol 66: 2241–2250, 2003; Faure JP, Petit I, Zhang K, Dutheil D, Doucet C, Favreau F, Eugene M, Goujon JM, Tillement JP, Mauco G, Vandewalle A, Hauet T. Am J Transplant 4: 495–504, 2004). In this study, we aimed to study the potential effect of TMZ pretreatment (5 mg/kg iv 24 h before WI) on the injury caused by WI for 45, 60, and 90 min and reperfusion in a WI pig kidney model. Compared with sham-operated (control) and uninephrectomized animals (UNX), TMZ pretreatment significantly reduced deleterious effects after 45 min, and particularly 60 and 90 min, of WI by improving the recovery of renal function and minimizing the inflammatory response commonly prevalent in ischemic kidney injury. Compared with controls (control group and UNX group), it was observed that 1) hypoxia-inducible factor-1 (HIF-1α) expression occurred earlier and with a higher intensity in the TMZ-treated groups; 2) the reduction of IRI during the first week following reperfusion was correlated with an earlier and greater expression of stathmin, which is involved in the process of tubular repair; and 3) the tubulointerstitial fibrosis was reduced, particularly after 60 and 90 min of WI. In conclusion, TMZ made the warm-ischemic kidneys more resistant to the deleterious impact of a single episode of I/R and reduced early and long-term subsequent damage.

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Section: Discussionsupporting

confidence: 54%

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Jayle¹,

Favreau²,

Zhang³

et al. 2007

American Journal of Physiology-Renal Physiology

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show abstract

“…Trimetazidine is an antioxidant agent used to protect kidney grafts from ischemia-reperfusion injury; tissue concentrations of ATP and ADP were significantly increased in kidneys from rats treated with trimetazidine, and it was suggested that this drug protects against dephosphorylation of nucleotides and ischemic damage (Domanski et al, 2006). In an in vitro model of ischemic injury involving severe depletion of intracellular ATP in rabbit cultured proximal tubule cells, P2Y receptor agonists were shown to be protective, and the mechanism involved reduced activation of NF-kB, an inducible transcription factor associated with inhibitory proteins (Lee and Han, 2005).…”

Section: Ischemiamentioning

confidence: 99%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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“…[11] Trimetazidine is another antioxidant agent used to protect rat kidney from I/R injury. [12] It has been suggested that the use of quercetin and naringin as antioxidants can protect kidneys against I/R injury. [3,14] Additionally, N-acetylcysteine, α-tocopherol, and melatonin administered to rats following I/R decrease the ROS levels providing kidney damage protection.…”

Section: Introductionmentioning

confidence: 99%

The Protective Effects of Ascorbic Acid against Renal Ischemia-Reperfusion Injury in Male Rats

Korkmaz

Kolankaya

2009

Renal Failure

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Effect of trimetazidine on the nucleotide profile in rat kidney with ischemia–reperfusion injury

Cited by 35 publications

References 39 publications

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Purinergic Signaling and Blood Vessels in Health and Disease

The Protective Effects of Ascorbic Acid against Renal Ischemia-Reperfusion Injury in Male Rats

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