Theaflavin attenuates ischemia–reperfusion injury in a mouse fatty liver model

Luo, Xiaoyu; Takahara, Taro; Hou, Junyi; Kawai, Kengo; Sugiyama, Toshiro; Tsukada, Kazuhiro; Takemoto, Masumi; Takeuchi, Masao; Liu, Zhong; Li, Xiaokang

doi:10.1016/j.bbrc.2011.11.102

Cited by 37 publications

(33 citation statements)

References 29 publications

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“…Twenty-seven studies utilizing the thiobarbituric acid reactive substances assay showed significantly increased levels of MDA in steatotic livers post-IRI [20,21,23,25,28,32,34,38,40,44,46,48,52,54,55,57,[61][62][63]69,[71][72][73][75][76][77][78] while Nakano and colleagues [17] reported similar levels of perfusate MDA to that seen from lean livers. Serviddio et al [47] also reported a significant increase in mitochondrial 4-hydroxy-2-nonenal-protein adducts post-IRI in steatotic livers.…”

Section: Lipid Peroxidationmentioning

confidence: 95%

“…QUORUM Diagram. [18]; b, [19]; c, [20]; d, [21]; e, [22]; f, [23], g, [24]; h, [25]; i, [26]; j, [27]; k, [28]; l, [29]; m, [30]; n, [17]; o, [31]; p, [32]; q, [33]; r, [34]; s, [35]; t, [36]; u, [37] [38]; b, [39]; c, [40]; d, [41]; e, [42]; f, [43]; g, [44]; h, [45]; i, [46]; j, [47]; k, [48]; l, [49]; m, [50]; n, [51]; o, [52] [62]; c, [63]; d, [64]; e, [65]; f, [66]; g, [67]; h, [68]; i, [69]; j, [70]; k, [71]; l, [17]; m, [60]; n, [72]; o, [73]<...>…”

Section: Papers Identified From Reference Lists N=19mentioning

confidence: 99%

“…The flow of protons through the F 1 /F 0 ATP-synthase back into the matrix then couples the ETS to ATP synthesis. Appropriate mito- [37]; n, [46]; o, [19] chondrial function is critical for proper cellular function, and mitochondrial dysfunction has wide metabolic consequences for the cell and survival.…”

Section: Bioenergetics Mitochondrial Function (Table 6)mentioning

confidence: 99%

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Effect of Hepatic Steatosis on Bioenergetic Function During Hepatic Ischemia-reperfusion: A Systematic Review

Chu¹

2013

TOTRANSJ

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Abstract:Background: The impact of hepatic steatosis on bioenergetics following hepatic ischemia-reperfusion injury (IRI) remains controversial and is associated with variable reports on its outcome. Large numbers of studies have been published examining the relationship between hepatic steatosis and cellular bioenergetics following hepatic IRI. This systematic review evaluates these studies.Methods: An electronic search of the Medline and Embase databases (January 1946 to June 2012) was performed to select studies that reported relevant outcomes in animal models or patients with hepatic steatosis subjected to IRI.Results: A total of 489 articles were identified, of which 63 animal studies met the predefined criteria and were included in the study. There was large variation in the type of animal model, duration and type of IRI utilized and histological description of hepatic steatosis. Bioenergetic impairments appear to increase the susceptibility of steatotic livers to IRI. The most common impairment was decreased adenosine triphosphate recovery with increased oxidative stress following IRI. Impaired mitochondrial function play a key role in the susceptibility of steatotic livers to IRI.Conclusions: Animals with >30% hepatic steatosis have been shown to have poor outcome following IRI. Despite limitations of different experimental models and inconsistency in histological description, impaired mitochondrial function and bioenergetics appear to be important mediators in the decreased tolerance of steatotic livers to IRI. Future studies need to be consistent and clinically relevant to further improve our understanding of this issue.

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Section: Lipid Peroxidationmentioning

confidence: 95%

Section: Papers Identified From Reference Lists N=19mentioning

confidence: 99%

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Effect of Hepatic Steatosis on Bioenergetic Function During Hepatic Ischemia-reperfusion: A Systematic Review

Chu¹

2013

TOTRANSJ

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“…Particular experimental pharmacological strategies to rescue steatotic livers consisted of the improvement of hepatic microcirculation (Hakamada et al, 1997;Caraceni et al, 1999), inhibition of oxygen-free radical-mediated injury (Nakano et al, 1997;Pesonen et al, 1998;Luo et al, 2012), and inhibition of the proteasome system with bortezomib (Ramachandran et al, 2012;Zaouali et al, 2013). In clinical practice, only a few pharmacological protective strategies, consisting of bezafibrate, an activator of peroxisome proliferator-activated receptor alpha and -b/d, were used to treat human living donors for liver transplantation (Nakamuta et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Acetazolamide Protects Steatotic Liver Grafts against Cold Ischemia Reperfusion Injury

Béjaoui

Pantazi

Luca

et al. 2015

J Pharmacol Exp Ther

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Ischemia reperfusion injury (IRI) is a primary concern in liver transplantation, especially when steatosis is present. Acetazolamide (AZ), a specific carbonic anhydrase (CA) inhibitor, has been suggested to protect against hypoxia. Here, we hypothesized that AZ administration could be efficient to protect fatty livers against cold IRI. Obese Zucker rat livers were preserved in Institut Georges Lopez-1 storage solution for 24 hours at 4°C and ex vivo perfused for 2 hours at 37°C. Alternatively, rats were also treated with intravenous injection of AZ (30 mg/kg) before liver recovery. Liver injury, hepatic function, and vascular resistance were determined. CA II protein levels and CA hydratase activity were assessed as well as other parameters involved in IRI (endothelial nitric oxide synthase, mitogen activated protein kinase family, hypoxic inducible factor 1 alpha, and erythropoietin). We demonstrated that AZ administration efficiently protects the steatotic liver against cold IRI. AZ protection was associated with better function, decreased vascular resistance, and activation of endothelial nitric oxide synthase. This was consistent with an effective mitogen activated protein kinase inactivation. Finally, no effect on the hypoxic inductible factor 1 alpha/erythropoietin pathway was observed. The present study demonstrated that AZ administration is a suitable pharmacological strategy for preserving fatty liver grafts against cold IRI.

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“…Its use in a mouse model of fatty liver resulted in a decrease of hepatic steatosis, oxidative stress, inflammation and apoptosis, contributing to its protective effect against ischemia-reperfusion injury [115]. Green tea contents a high amount of catechins as EGCG, whose beneficial properties on NAFLD have been summarized herein.…”

Section: Fig (2)mentioning

confidence: 99%

Flavonoids and Related Compounds in Non-Alcoholic Fatty Liver Disease Therapy

Pisonero-Vaquero¹,

González‐Gallego²,

Sánchez-Campos³

et al. 2015

CMC

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Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, is one of the most common chronic liver diseases, which may progress to fibrosis, cirrhosis and hepatocellular carcinoma. NAFLD is characterized by the accumulation of lipids in the liver arising from multiple factors: increased fatty acid uptake, increased de novo lipogenesis, reduced fatty acid oxidation and very low density lipoproteins (VLDL) secretion. Most therapeutic approaches for this disease are often directed at reducing body mass index and improving insulin resistance through lifestyle modifications, bariatric surgery and pharmacological treatments. Nevertheless, there is increasing evidence that the use of natural compounds, as polyphenols, exert multiple benefits on the disorders associated with NAFLD. These molecules seem to be able to regulate the expression of genes mainly involved in de novo lipogenesis and fatty acid oxidation, which contributes to their lipid-lowering effect in the liver. Their antioxidant, anti-inflammatory, antifibrogenic and antilipogenic properties seem to confer on them a great potential as strategy for preventing NAFLD progression. In this review, we summarized the effects of these compounds, especially flavonoids, and their mechanisms of action, that have been reported in several studies carried out in in vitro and in vivo models of NAFLD.

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Theaflavin attenuates ischemia–reperfusion injury in a mouse fatty liver model

Cited by 37 publications

References 29 publications

Effect of Hepatic Steatosis on Bioenergetic Function During Hepatic Ischemia-reperfusion: A Systematic Review

Effect of Hepatic Steatosis on Bioenergetic Function During Hepatic Ischemia-reperfusion: A Systematic Review

Acetazolamide Protects Steatotic Liver Grafts against Cold Ischemia Reperfusion Injury

Flavonoids and Related Compounds in Non-Alcoholic Fatty Liver Disease Therapy

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