2009
DOI: 10.1016/j.transproceed.2009.06.060
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Effect of Preconditioning With Triiodothyronine on Renal Ischemia/Reperfusion Injury and Poly(ADP-Ribose) Polymerase Expression in Rats

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Cited by 14 publications
(11 citation statements)
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“…This suggests that under conditions of demand ischemia, the ApoE−/−- mice had decreased acute stress response. Since the basal levels of PARP were increased in the ApoE mice, and demand ischemia subsequently reduced PAR activity, the reduced PAR activity could be due to preconditioning which has been described in other systems(28, 29). …”
Section: Resultsmentioning
confidence: 73%
“…This suggests that under conditions of demand ischemia, the ApoE−/−- mice had decreased acute stress response. Since the basal levels of PARP were increased in the ApoE mice, and demand ischemia subsequently reduced PAR activity, the reduced PAR activity could be due to preconditioning which has been described in other systems(28, 29). …”
Section: Resultsmentioning
confidence: 73%
“…Furthermore, T 3 induces microRNAs 30a and 29 having antiapoptotic and antifibrotic actions, respectively [65], an aspect that requires further investigation under IR conditions. Redox signaling by TH also operates in kidney PC against IR injury as it improves renal function by increasing inulin clearance [66] and diminishing serum creatinine and urea levels [67] and proteinuria [68].…”
Section: T H Y R O I D H O R M O N E -D E P E N D E N T Protection Ofmentioning
confidence: 99%
“…Redox-dependent mechanisms such as oxidative stress suppression [67][68][69] and HO-1 induction [67] (Figure 1) are accompanied by improvement in renal ATP levels [66] and anti-inflammatory responses [67]. Besides heart and kidney PC by THs, T 4 administration to rats significantly diminished brain injury caused by middle cerebral artery occlusion, which was associated with downregulation of the expression of the inflammatoryrelated pro-oxidant enzymes inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2), while restoring that of neurotrophins [70].…”
Section: T H Y R O I D H O R M O N E -D E P E N D E N T Protection Ofmentioning
confidence: 99%
“…This effect was mediated by a T3 transient oxidative stress, and thus, it was abrogated by the administration of antioxidant N-acetyl-cysteine [23]. Thyroxine was cytoprotective in toxic and ischemic injury in kidney [24, 26]. Thus, T3 administration 24 h prior to renal ischemia could precondition against ischemia-reperfusion (I/R) injury.…”
Section: Thyroid Hormone: the “Black Box Of Repair?”mentioning
confidence: 99%
“…This was evident by a marked decrease in I/R-induced proteinuria. T3 treatment also improved lipid peroxidation biomarkers and increased antioxidant enzymes [24]. In another study, T4 administration immediately or 24 h after ischemia resulted in higher Inulin clearance and preserved cellular integrity [26].…”
Section: Thyroid Hormone: the “Black Box Of Repair?”mentioning
confidence: 99%