Protective effect of post-ischemic treatment with trans-resveratrol on cytokine production and neutrophil recruitment by rat liver

Hassan-Khabbar, Sahar; Vamy, Michel; Cottart, Charles‐Henry; Wendum, Dominique; Vibert, Françoise; Savouret, Jean‐François; Thérond, Patrice; Clot, Jean-Pierre; Waligora, Anne-Judith; Nivet-Antoine, Valérie

doi:10.1016/j.biochi.2009.12.009

Cited by 33 publications

(27 citation statements)

References 34 publications

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“…Liver injury following I/R has a biphasic pattern [12]. In the initial phase, 0.5–2 h after the onset of reperfusion, reactive oxygen species (ROS) are released and Kupffer cells and hepatocytes are activated.…”

Section: Introductionmentioning

confidence: 99%

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

et al. 2011

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Introduction and AimMangafodipir is a contrast agent used in magnetic resonance imaging that concentrates in the liver and displays pleiotropic antioxidant properties. Since reactive oxygen species are involved in ischemia-reperfusion damages, we hypothesized that the use of mangafodipir could prevent liver lesions in a mouse model of hepatic ischemia reperfusion injury. Mangafodipir (MnDPDP) was compared to ischemic preconditioning and intermittent inflow occlusion for the prevention of hepatic ischemia-reperfusion injury in the mouse.MethodsMice were subjected to 70% hepatic ischemia (continuous ischemia) for 90 min. Thirty minutes before the ischemic period, either mangafodipir (10 mg/kg) or saline was injected intraperitoneally. Those experimental groups were compared with one group of mice preconditioned by 10 minutes' ischemia followed by 15 minutes' reperfusion, and one group with intermittent inflow occlusion. Hepatic ischemia-reperfusion injury was evaluated by measurement of serum levels of aspartate aminotransferase (ASAT) activity, histologic analysis of the livers, and determination of hepatocyte apoptosis (cytochrome c release, caspase 3 activity). The effect of mangafodipir on the survival rate of mice was studied in a model of total hepatic ischemia.ResultsMangafodipir prevented experimental hepatic ischemia-reperfusion injuries in the mouse as indicated by a reduction in serum ASAT activity (P<0.01), in liver tissue damages, in markers of apoptosis (P<0.01), and by higher rates of survival in treated than in untreated animals (P<0.001). The level of protection by mangafodipir was similar to that observed following intermittent inflow occlusion and higher than after ischemic preconditioning.ConclusionsMangafodipir is a potential new preventive treatment for hepatic ischemia-reperfusion injury.

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Section: Introductionmentioning

confidence: 99%

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

et al. 2011

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“…These results suggest that intraperitoneally administered resveratrol exerts a preventive effect on ANIT-induced liver injury in rats by inhibiting neutrophil infiltration into the liver tissue. Moreover, resveratrol is known to protect against ischemia/ reperfusion-induced liver injury in rats by inhibiting neutrophil infiltration and release of cytokines such as TNF-α, IL-1β, and IL-6 [32] . We observed a suppression of liver TNF-α and IL-6 levels in the present study, suggesting that resveratrol decreases the early release of cytokines and neutrophil recruitment, leading to a reduction in late inflammatory processes and an improvement in liver injury after ANIT intoxication.…”

Section: Wwwchinapharcom Wang T Et Almentioning

confidence: 99%

Resveratrol effectively attenuates α-naphthyl-isothiocyanate-induced acute cholestasis and liver injury through choleretic and anti-inflammatory mechanisms

et al. 2014

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Aim: α-Naphthylisothiocyanate (ANIT) is a well-characterized cholestatic agent for rats. The aim of this study was to examine whether resveratrol could attenuate ANIT-induced acute cholestasis and liver injury in rats. Methods: SD rats were treated with resveratrol (15 or 30 mg/kg, ip) or a positive control drug ursodeoxycholic acid (100 mg/kg, po) for 5 consecutive days followed by a single dose of ANIT (60 mg/kg, po). Bile flow, and serum biochemical markers and bile constituents were measured 48 h after ANIT administration. Hepatic levels of oxidative repair enzymes (glutathione peroxidase, catalase and MnSOD), myeloperoxidase activity, TNF-α, IL-6, and ATP content, as well as the expression of liver transporter genes and proteins were assayed. Results: ANIT exposure resulted in serious cholestasis and liver injury, as shown by marked neutrophil infiltration in liver, dramatically increased serum levels of ALT, AST, GGT, ALP, TBA, TBIL, IBIL, and DBIL, and significantly decreased bile excretion and biliary output of GSH and HCO 3 -. ANIT significantly increased TNF-α and IL-6 release and myeloperoxidase activity, decreased mitochondrial biogenesis in liver, but had little effect on hepatic oxidative repair enzymes and ATP content. Furthermore, ANIT significantly decreased the expression of Mrp2, FXR, and Cyp7a1, markedly increased Mrp3 expression in liver. Pretreatment with resveratrol attenuated ANITinduced acute cholestasis and liver injury, and other pathological changes. Pretreatment with ursodeoxycholic acid was less effective. Conclusion: Resveratrol effectively attenuates ANIT-induced acute cholestasis and liver injury in rats, possibly through suppression of neutrophil infiltration, as well as upregulation of expression of hepatic transporters and enzymes, thus decreasing accumulation of bile acids.

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“…Among these products, resveratrol (RSV), a natural polyphenolic compound primarily found in the skin of grapes, is particularly well-studied (Bishayee et al, 2010). It has been shown to protect against liver damage caused by hepatic ischemia-reperfusion (Hassan-Khabbar et al, 2008; 2010; Plin et al, 2005), ethanol toxicity (Ajmo et al, 2008; Min et al, 2008), high fat diet (Ahn et al, 2008) and hepatotoxic agents such as APAP (Masubuchi et al, 2009; Sener et al, 2006) and carbon tetrachloride (Rivera et al, 2008). The mechanisms that have been proposed to explain this protection include antioxidant effects, up-regulation of anti-oxidant enzymes, modulation of inflammatory responses, and induction of mitochondrial biogenesis (Lagouge et al, 2006; Baur et al, 2006; Sener et al, 2006; Masubuchi et al, 2009; Bishayee et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol prevents protein nitration and release of endonucleases from mitochondria during acetaminophen hepatotoxicity

McGill

Xie

et al. 2015

Food and Chemical Toxicology

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Overdose of acetaminophen (APAP) is a common cause of acute liver injury and liver failure. The mechanism involves formation of a reactive metabolite, protein binding, oxidative stress and activation of c-Jun N-terminal kinase (JNK), mitochondrial dysfunction, and nuclear DNA fragmentation caused by endonucleases released from damaged mitochondria. Previous work has shown that the natural product resveratrol (RSV) can protect against APAP hepatotoxicity in mice through prevention of lipid peroxidation and anti-inflammatory effects. However, these earlier studies did not take into consideration several fundamental aspects of the pathophysiology. To address this, we treated C57Bl/6 mice with 300 mg/kg APAP followed by 50 mg/kg RSV 1.5h later. Our results confirmed that RSV reduced liver injury after APAP overdose in mice. Importantly, RSV did not inhibit reactive metabolite formation and protein bindings, nor did it reduce activation of JNK. However, RSV decreased protein nitration after APAP treatment, possibly through direct scavenging of peroxynitrite. Interestingly, RSV also inhibited release of apoptosis-inducing factor and endonuclease G from mitochondria independent of Bax pore formation and prevented the downstream nuclear DNA fragmentation. Our data show that RSV protects against APAP hepatotoxicity both through antioxidant effects and by preventing mitochondrial release of endonucleases and nuclear DNA damage.

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Protective effect of post-ischemic treatment with trans-resveratrol on cytokine production and neutrophil recruitment by rat liver

Cited by 33 publications

References 34 publications

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

Resveratrol effectively attenuates α-naphthyl-isothiocyanate-induced acute cholestasis and liver injury through choleretic and anti-inflammatory mechanisms

Resveratrol prevents protein nitration and release of endonucleases from mitochondria during acetaminophen hepatotoxicity

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