Ischemic Preconditioning-Like Effect of Polyunsaturated Fatty Acid-Rich Diet on Hepatic Ischemia/Reperfusion Injury

Coelho, Ana Maria M.; Machado, Marcel Cerqueira César; Takahashi, Hilton Kenji; Sampietre, Sandra N.; Stefano, José Tadeu; Lamothe, André; Curi, Rui; D’Albuquerque, Luiz Augusto Carneiro

doi:10.1007/s11605-011-1648-x

Cited by 8 publications

(6 citation statements)

References 44 publications

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“…In general, these COX and LOX metabolites are pro-inflammatory and have been implicated in several pathological conditions, including liver fibrosis [38]. Our result runs counter to liver damage and tumorigenesis studies in which dietary supplementation with DHA or mixtures of ω-3 fatty acids results in a lowering of these COX and LOX metabolites [39, 40], although a recent study has reported that in humans, dietary supplementation with DHA resulted in variation in prostaglandin levels between individuals, with some individuals displaying no decrease or a slight increase in certain COX and LOX metabolites [41]. Before interpreting these results, a number of differences between previous studies and the present study must be taken into account.…”

Section: Discussionmentioning

confidence: 85%

An ω-3-enriched diet alone does not attenuate CCl 4 -induced hepatic fibrosis

Harris

Kodani

Yang

et al. 2016

The Journal of Nutritional Biochemistry

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Exposure to the halogenated hydrocarbon carbon tetrachloride (CCl4) leads to hepatic lipid peroxidation, inflammation, and fibrosis. Dietary supplementation of ω-3 fatty acids has been increasingly advocated as being generally anti-inflammatory, though its effect in models of liver fibrosis is mixed. This raises the question of whether diets high in ω-3 fatty acids will result in a greater sensitivity or resistance to liver fibrosis as a result of environmental toxicants like CCl4. In this study we fed CCl4-treated mice a high ω-3 diet (using a mix of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) ethyl esters). We also co-administered an inhibitor of soluble epoxide hydrolase, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), which has been shown to boost anti-inflammatory epoxy fatty acids that are produced from both ω-3 and ω-6 dietary lipids. In this study, we showed that soluble epoxide inhibitors reduced CCl4-induced liver fibrosis. Three major results were obtained. First, the ω-3 enriched diet did not attenuate CCl4-induced liver fibrosis as judged by collagen deposition and collagen mRNA expression. Second, the ω-3 enriched diet raised hepatic tissue levels of several inflammatory lipoxygenase metabolites and prostaglandins, including PGE2. Third, treatment with TPPU in drinking water in conjunction with the ω-3 enriched diet resulted in a reduction in liver fibrosis compared to all other groups. Taken together, these results indicate that dietary ω-3 supplementation alone did not attenuate CCl4-induced liver fibrosis. Additionally, oxylipin signaling molecules may play role in the CCl4-induced liver fibrosis in the high ω-3 diet groups.

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Section: Discussionmentioning

confidence: 85%

An ω-3-enriched diet alone does not attenuate CCl 4 -induced hepatic fibrosis

Harris

Kodani

Yang

et al. 2016

The Journal of Nutritional Biochemistry

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“…Further study is needed to clarify the clinical factors that would negatively influence the protective effect of IP. [42] 2004 10I+10R maintenance of hemodynamic stability Li et al [43] 2004 5I+5R improvement of liver function Nuzzo et al [44] 2004 10I+10R reduction of IR injury Choukèr et al [45] 2005 10I+10R reduction of IR injury Heizmann et al [46] 2008 10I+10R reduction of IR injury Azoulay et al [47] 2006 10I+10R no improvement of liver function Domart et al [48] 2009 10I+10R increased in necrotic changes [71] demonstrated that n-3 PUFA administration relieved IR stress on mitochondria. They showed that the respiratory control ratio as well as the ADP/O ratio were well preserved after IR in rats fed with n-3 PUFA, whereas those parameters were significantly worsened in the control rats who showed uncoupling of mitochondrial respiration.…”

Section: Ischemic Preconditioningmentioning

confidence: 99%

Optimizing the Liver for Resection in Patients Undergoing Extended Hepatectomy or Receiving Chemotherapy

Uchinami¹,

Yamamoto²

2012

Viszeralmedizin

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In the era of effective chemotherapy for colorectal liver metastasis, indications for liver resection are expanding. However, liver resection for initially unresectable tumors has 2 distinctive features: One is that it often necessitates extended hepatectomy, and the other that the liver is often damaged by chemotherapy. To overcome these factors, strategies to optimize the livers for resection are significant. In this article, we review the current status of portal vein embolization for enlarging the future remnant liver, the clinical and experimental knowledge of preconditioning for ameliorating ischemia/reperfusion injury of the liver, and the possible strategies for the yellow (steatohepatitis) and blue livers (sinusoidal injury) after chemotherapy with the FOLFIRI and FOLFOX regimen, respectively. Arguments regarding the clinical strategy and clinical perspectives of experimental knowledge are discussed.

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“…Experimental studies have been performed on rats for the investigation of the prevention of hepatic IR injury by administering an n-3 PUFA-rich diet ( 11 , 12 ). It was shown that n-3 PUFA treatment effectively reduced hepatic steatosis and consequently attenuated hepatic IR injury in rats ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

“…It was shown that n-3 PUFA treatment effectively reduced hepatic steatosis and consequently attenuated hepatic IR injury in rats ( 11 ). A diet enriched with n-3 has also been shown to have a pre-conditioning effect to reduce liver IR injury in rats ( 12 ). Liver pre-conditioning against IR injury by n-3 PUFA supplementation has been reported to be mediated by the antagonistic effect of peroxisome proliferator-activated receptor alfa with the nuclear factor-kappa-B-controlled transcription of pro-inflammatory mediators ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

Analysis of polyunsaturated fatty acids and the omega-6 inflammatory pathway in hepatic ischemia/re-perfusion injury

Kıraç

Özcan

Tuzcu

et al. 2015

Molecular Medicine Reports

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The aim of the present study was to assess omega-3 (n-3) and omega-6 (n-6) polyunsaturated fatty acids (PUFAs) in liver tissue and evaluate changes in the n-6-associated inflammatory pathway following liver ischemia/re-perfusion (IR) injury. Male Wistar rats which were allowed free access to standard rat chow were included in the study. Blood vessels supplying the median and left lateral hepatic lobes were occluded with an arterial clamp for 60 min, followed by 60 min of re-perfusion. Levels of arachidonic acid (AA, C20:4n-6), dihomo-gamma-linolenic acid (DGLA, C20:3n-6), eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C22:6n-3) in liver tissue were determined by an optimized multiple reaction monitoring method using ultra fast-liquid chromatography coupled with tandem mass spectrometry. Phospholipase A2 (PLA2), cyclooxygenase (COX) and prostaglandin E2 (PGE2) were measured in tissue samples to evaluate changes in the n-6 inflammatory pathway. Total histopathological score of cellular damage were significantly increased following hepatic IR injury. n-3 and n-6 PUFA levels were significantly increased in post-ischemic liver tissue compared to those in non-ischemic controls. No significant difference was observed in the AA/DHA and AA/EPA ratio in post-ischemic liver tissues compared with that in the control. Tissue activity of PLA2 and COX as well as PGE2 levels were significantly increased in post-ischemic liver tissues compared to those in non-ischemic controls. The results of the present study suggested that increased hydrolysis of fatty acids via PLA2 triggers the activity of COX and leads to increased PGE2 levels. Future studies evaluating agents which block the formation of eicosanoids derived from n-6 PUFAs may facilitate the development and application of treatment strategies in liver injury following IR.

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Ischemic Preconditioning-Like Effect of Polyunsaturated Fatty Acid-Rich Diet on Hepatic Ischemia/Reperfusion Injury

Abstract: In this experimental model in the rat, PRD has a preconditioning effect protecting the liver from I/R injury and should be object of future clinical studies.

Cited by 8 publications

References 44 publications

An ω-3-enriched diet alone does not attenuate CCl 4 -induced hepatic fibrosis

An ω-3-enriched diet alone does not attenuate CCl 4 -induced hepatic fibrosis

Optimizing the Liver for Resection in Patients Undergoing Extended Hepatectomy or Receiving Chemotherapy

Analysis of polyunsaturated fatty acids and the omega-6 inflammatory pathway in hepatic ischemia/re-perfusion injury

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