The Protective Effect of α-Tocopherol and GdCl3 Against Hepatic Ischemia/Reperfusion Injury

Giakoustidis, Dimitrios; Παπαγεωργίου, Γεώργιος; Iliadis, Stavros; Giakoustidis, Alexandros; Kostopoulou, Evanthia; Kontos, Nickolas; Botsoglou, Evropi; Tsantilas, Dimitrios; Papanikolaou, Vasilios; Takoudas, D

doi:10.1007/s00595-005-3162-9

Cited by 39 publications

(27 citation statements)

References 38 publications

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“…The role of ROS in I/R injury is supported by previous studies which have shown increased PMNLs around the I/R injured areas which release ROS (Yamaguchi et al 1997) and reduced I/R injury secondary to the use of antioxidants such as melatonin, quercetin, ascorbic acid, L-carnitine, n-asetyl cystein, L-arginine and α -tocopherol (Ustundag et al 2000;Mojzis et al 2001;Giakoustidis et al 2006;Chen et al 2007;Dokmeci et al 2007;Higa et al 2007;Sayan et al 2008).…”

supporting

confidence: 57%

Resveratrol, a Natural Antioxidant, Attenuates Intestinal Ischemia/Reperfusion Injury in Rats

Özkan

Yüzbaşıoğlu

Çıralık

et al. 2009

Tohoku J. Exp. Med.

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supporting

confidence: 57%

Resveratrol, a Natural Antioxidant, Attenuates Intestinal Ischemia/Reperfusion Injury in Rats

Özkan

Yüzbaşıoğlu

Çıralık

et al. 2009

Tohoku J. Exp. Med.

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“…In liver ischemia-reperfusion injury, this mechanism is exacerbated. The consequent damage to liver cells by reperfusion results in mitochondrial dysfunction and it can also induce microcirculatory disturbances 8 .…”

Section: Discussionmentioning

confidence: 99%

Postconditioning ameliorates lipid peroxidation in liver ischemia-reperfusion injury in rats

et al. 2009

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Purpose: Liver ischemia-reperfusion injury is a phenomenon presents in events like liver resections and transplantation. The restoration of blood flow may leads to local and systemic injury. Several techniques have been developed in order to avoid or ameliorate ischemia-reperfusion injury in clinical situations. The application of a sttuter reperfusion after the ischemic event (postconditioning) could alters the hydrodynamics and stimulates endogenous mechanisms that attenuate the reperfusion injury. The present study was designed to evaluate the potential protective effect of postconditioning in a model of ischemia-reperfusion in rats. Methods: Hepatic anterior pedicle of median and left anterolateral segments were exposed and clamped for 1 hour. Two hours later, clamp was released in two different ways: Control Group (n=7): clamp was release straightforward; Postconditioning Group (n=7): clamp was released intermittently. Lipid peroxidation (malondialdehyde) and expression of the glutathione-s-transferase--3 gene were studied. Results: Lipid peroxidation was significantly decreased in ischemic and non-ischemic liver by postconditioning. GST-3 gene was overexpressed in postconditioned group, but not significantly. Conclusion: Postconditioning induced hepatoprotection by reducing lipid peroxidation in the ischemic and non-ischemic liver. Key words: Liver. Ischemia. Reperfusion. Lipid Peroxidation. Rats. RESUMOObjetivo: A lesão de isquemia-reperfusão hepática é um fenômeno presente em eventos tais como ressecções hepáticas e transplante de fígado. A restauração do fluxo sangüíneo após a isquemia gera lesões locais e sistêmicas. Várias técnicas foram desenvolvidas com o objetivo de evitar ou diminuir a lesão de isquemia-reperfusão hepática em situações clínicas. A utilização da reperfusão intermitente após o evento isquêmico (pós-condicionamento) pode alterar a hidrodinâmica e estimular mecanismos endógenos que atenuam o dano da reperfusão. O presente estudo foi realizado para avaliar o potencial efeito protetor do pós-condicionamento em um modelo de isquemia-reperfusão em ratos. Métodos: O pedículo dos lobos mediano e ântero-lateral foi isolado e clampeado por 1 hora. Após 2 horas, o pedículo foi liberado de duas maneiras diferentes: Grupo Controle (n=7): clampe liberado de uma só vez; Grupo Pós-condicionamento (n=7): clampe liberado de maneira intermitente. Malondialdeído (MDA) e expressão do gene GST-3 foram estudadas nos grupos. Resultados: A peroxidação lipídica foi significativamente diminuída no fígado isquêmico e no fígado não isquêmico pelo pós-condicionamento. A expressão do gene GST-3 aumentou, porém não significativamente, no grupo pós-condicionamento. Conclusão: O pós-condicionamento induziu hepatoproteção pela redução da peroxidação lipídica nos fígados isquêmico e não isquêmico. Descritores: Fígado. Isquemia. Reperfusão. Peroxidação de Lipídeos. Ratos.

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“…The present myocardial I/R rat model demonstrated a lower extent of myocardial injury with decreased infarction size and reduced levels of myocardial injury markers (eg, CK-MB, cTnI, and LDH) in GdCl 3 (10 mg/kg) and nifedipine groups compared with the I/R group (Figure 4). The dose of GdCl 3 used in the current study was the same as that used in other studies [20,34] . The increased infarction area of the heart after reperfusion is most likely the result of cell apoptosis [35,36] .…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with low-dose gadolinium chloride attenuates myocardial ischemia/reperfusion injury in rats

et al. 2016

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Aim:We have shown that low-dose gadolinium chloride (GdCl 3 ) abolishes arachidonic acid (AA)-induced increase of cytoplasmic Ca 2+ , which is known to play a crucial role in myocardial ischemia/reperfusion (I/R) injury. The present study sought to determine whether low-dose GdCl 3 pretreatment protected rat myocardium against I/R injury in vitro and in vivo. Methods: Cultured neonatal rat ventricular myocytes (NRVMs) were treated with GdCl 3 or nifedipine, followed by exposure to anoxia/ reoxygenation (A/R). Cell apoptosis was detected; the levels of related signaling molecules were assessed. SD rats were intravenously injected with GdCl 3 or nifedipine. Thirty min after the administration the rats were subjected to LAD coronary artery ligation followed by reperfusion. Infarction size, the release of serum myocardial injury markers and AA were measured; cell apoptosis and related molecules were assessed. Results: In A/R-treated NRVMs, pretreatment with GdCl 3 (2.5, 5, 10 μmol/L) dose-dependently inhibited caspase-3 activation, death receptor-related molecules DR5/Fas/FADD/caspase-8 expression, cytochrome c release, AA release and sustained cytoplasmic Ca 2+ increases induced by exogenous AA. In I/R-treated rats, pre-administration of GdCl 3 (10 mg/kg) significantly reduced the infarct size, and the serum levels of CK-MB, cardiac troponin-I, LDH and AA. Pre-administration of GdCl 3 also significantly decreased the number of apoptotic cells, caspase-3 activity, death receptor-related molecules (DR5/Fas/FADD) expression and cytochrome c release in heart tissues. The positive control drug nifedipine produced comparable cardioprotective effects in vitro and in vivo. Conclusion: Pretreatment with low-dose GdCl 3 significantly attenuates I/R-induced myocardial apoptosis in rats by suppressing activation of both death receptor and mitochondria-mediated pathways.

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The Protective Effect of α-Tocopherol and GdCl3 Against Hepatic Ischemia/Reperfusion Injury

Abstract: The administration of GdCl3 and alpha-tocopherol is likely to protect the liver against lipid peroxidation by suppressing Kupffer cell and polymorphonuclear leukocyte activation and enhancing endogenous antioxidant activity.

Cited by 39 publications

References 38 publications

Resveratrol, a Natural Antioxidant, Attenuates Intestinal Ischemia/Reperfusion Injury in Rats

Resveratrol, a Natural Antioxidant, Attenuates Intestinal Ischemia/Reperfusion Injury in Rats

Postconditioning ameliorates lipid peroxidation in liver ischemia-reperfusion injury in rats

Pretreatment with low-dose gadolinium chloride attenuates myocardial ischemia/reperfusion injury in rats

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