Effet du pré-conditionnement ischémique et de la vitamine C sur la reprise fonctionnelle des reins ischémiques

Mahfoudh-Boussaid, Asma; Badet, Lionel; Zaouali, A.; Saidane-Mosbahi, Dalila; Miled, Abdelhédi; Abdennebi, Hassen Ben

doi:10.1016/s1166-7087(07)92303-9

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…For example, the functional parameters of rat kidneys were improved by preconditioning with two successive cycles of ischemia/reperfusion (10). Pretreatment with vitamin D3 resulted in a protective effect against subsequent ischemia/reperfusion injury of the rat (11). Preconditioning can also induce crossover protection from another injury.…”

Section: Introductionmentioning

confidence: 99%

Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

Pessoa

Convento

Silva

et al. 2009

Braz J Med Biol Res

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Nephrotoxicity is the main side effect of antibiotics such as gentamicin. Preconditioning has been reported to protect against injuries as ischemia/reperfusion. The objective of the present study was to determine the effect of preconditioning with gentamicin on LLC-PK1 cells. Preconditioning was induced in LLC-PK1 cells by 24-h exposure to 2.0 mM gentamicin (G/IU). After 4 or 15 days of preconditioning, cells were again exposed to gentamicin (2.0 mM) and compared to untreated control or G/ IU cells. Necrosis and apoptosis were assessed by acridine orange and HOESCHT 33346. Nitric oxide (NO) and endothelin-1 were assessed by the Griess method and available kit. Heat shock proteins were analyzed by Western blotting. After 15 days of preconditioning, LLC-PK1 cells exhibited a significant decrease in necrosis (23.5 ± 4.3 to 6.5 ± 0.3%) and apoptosis (23.5 ± 4.3 to 6.5 ± 2.1%) and an increase in cell proliferation compared to G/IU. NO (0.177 ± 0.05 to 0.368 ± 0.073 μg/mg protein) and endothelin-1 (1.88 ± 0.47 to 2.75 ± 0.53 pg/mL) production significantly increased after 15 days of preconditioning compared to G/IU. No difference in inducible HSP 70, constitutive HSC 70 or HSP 90 synthesis in tubular cells was observed after preconditioning with gentamicin. The present data suggest that preconditioning with gentamicin has protective effects on proximal tubular cells, that involved NO synthesis but not reduction of endothelin-1 or production of HSP 70, HSC 70, or HSP 90. We conclude that preconditioning could be a useful tool to prevent the nephrotoxicity induced by gentamicin.

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Section: Introductionmentioning

confidence: 99%

Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

Pessoa

Convento

Silva

et al. 2009

Braz J Med Biol Res

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“…HS and subsequent resuscitation is regarded as a systemic I/R process that causes oxidative injuries of multiple vulnerable organs including the liver [ 32 ], lung [ 33 ] and kidney [ 34 ]. Pre-exposure of these organs to temporal sublethal stress, known as “organ preconditioning”, has been shown to increase the tolerance of the organ to I/R injuries.…”

Section: Discussionmentioning

confidence: 99%

Vitamin C treatment attenuates hemorrhagic shock related multi-organ injuries through the induction of heme oxygenase-1

Zhao

Fei

Chen

et al. 2014

BMC Complement Altern Med

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BackgroundVitamin C (VitC) has recently been shown to exert beneficial effects, including protecting organ function and inhibiting inflammation, in various critical care conditions, but the specific mechanism remains unclear. Induction of heme oxygenase (HO)-1, a heat shock protein, has been shown to prevent organ injuries in hemorrhagic shock (HS) but the relationship between VitC and HO-1 are still ill-defined so far. Here we conducted a systemic in vivo study to investigate if VitC promoted HO-1 expression in multiple organs, and then tested if the HO-1 induction property of VitC was related to its organ protection and anti-inflammatory effect.MethodsFirstly, to determine the HO-1 induction property of VitC, the HO-1 level were measured in tissues including kidney, liver and lung of the normal and HS model of Sprague–Dawley (SD) rats after VitC treatment (100 mg/kg body weight). Secondly, to testify if VitC prevented HS related organ injuries via inducing HO-1, the HS model of rats were separately pre- and post-treated with VitC, and some of them also received Zinc protoporphyrin (Znpp), a specific HO-1 inhibitor. The HO-1 activity in tissues was tested; the organ injuries (as judged by histological changes in tissues and the biochemical indicators level in serum) and inflammatory response in tissues (as judged by the level of pro-inflammatory cytokines Tumor necrosis factor-α and Interleukin-6 ) were analyzed.ResultsThe HO-1 mRNA and protein level in kidney, liver, and lung were highly induced by VitC treatement under normal and HS conditions. The HO-1 activity in tissues was enhanced by both VitC pre- and post-treatment, which was shown to improve the organ injuries and inhibit the inflammatory response in the HS model of rats. Of note, the beneficial effects of VitC were abolished after HO-1 activity was blocked by Znpp.ConclusionsVitC led to a profound induction of HO-1 in multiple organs including the kidney, liver and lung, and this property might be responsible for the organ protection and inflammation inhibitory effects of both pre- and post-treatment with VitC in HS.

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“…ROS are capable of reacting with proteins, lipids, and nucleic acids leading to protein denaturation, lipid peroxidation, and DNA damage (Bidmon et al, 2012;Wang et al, 2012a). Many antioxidants have been the focus of studies for developing strategies for use in I/R therapy (Mahfoudh Boussaid et al, 2007;Wang et al, 2012a;Aydogan et al, 2013). Along with others, we have shown that the antioxidant molecule, melatonin, has a significant protective action against renal damage that occurs during I/R injury (Aktoz et al, 2007;Ersoz et al, 2009;Hadj Ayed Tka et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Involvement of AMP-activated protein kinase in the protective effectof melatonin against renal ischemia reperfusion injury

Tka¹,

Boussaid²,

Kessabi³

et al. 2016

Turk J Biol

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We investigated the implication of AMP-activated protein kinase (AMPK) in melatonin-induced protection in a renal ischemia/reperfusion (I/R) model. Animals were divided into four groups: rats of the sham group were not subjected to renal I/R. Rats in the I/R group received the vehicle 30 min before renal ischemia for 1 h followed by reperfusion for 6 h. Rats in the Mel+I/R group received melatonin (10 mg/kg) 30 min before the onset of I/R. Rats in the Mel+I/R+araA group received araA (AMPK inhibitor, 100 µg/kg per min for 10 min) just before melatonin administration. The results showed that melatonin treatment induced a significant improvement in renal function, morphology, and antioxidant status, as well as Akt pathway activation. It also decreased cytolysis and endoplasmic reticulum stress. Inhibition of AMPK by araA administration completely abolished the effects of melatonin in regard to the above parameters except for Akt and some of its downstream target molecules. These results demonstrate that the effects of melatonin on renal I/R are, for the most part, linked to AMPK activation, with the exception of the Akt pathway, which seems to be independent of AMPK.

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Effet du pré-conditionnement ischémique et de la vitamine C sur la reprise fonctionnelle des reins ischémiques

Cited by 6 publications

References 19 publications

Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

Vitamin C treatment attenuates hemorrhagic shock related multi-organ injuries through the induction of heme oxygenase-1

Involvement of AMP-activated protein kinase in the protective effectof melatonin against renal ischemia reperfusion injury

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