A Corn Oil–Based Diet Protects Against Combined Ethanol and Iron‐Induced Liver Injury in a Mouse Model of Hemochromatosis

Tan, Terrence; Crawford, Darrell H. G.; Jaskowski, L.; Murphy, Tamara C.; Santrampurwala, Nishreen; Crane, Denis I.; Clouston, Andrew D.; Subramaniam, V. Nathan; Anderson, Gregory J.; Fletcher, Linda M.

doi:10.1111/acer.12155

Cited by 8 publications

(10 citation statements)

References 49 publications

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“…Supporting this notion it has been reported that mice fed with corn oil-based diet for 8 weeks displayed hepatoprotection against ethanol and iron-induced liver injury. This could be attributed to attenuation of hepatic oxidative stress and steatosis, preservation of the enzymatic antioxidant defence system (CAT, GPx), modulation of the inflammatory cascade and fibrogenic pathways, protecting against liver fibrosis (Tan et al 2013). However, we did not observe such improvement in liver functions and structure in the BPA group although it was dissolved in the same dose of corn oil as in the vehicle control group.…”

Section: Discussionmentioning

confidence: 99%

“…This could be attributed to attenuation of hepatic oxidative stress and steatosis, preservation of the enzymatic antioxidant defence system (CAT, GPx), modulation of the inflammatory cascade and fibrogenic pathways, protecting against liver fibrosis (Tan et al 2013). Supporting this notion it has International Journal of Experimental Pathology, 2016, 97, 369-379 been reported that mice fed with corn oil-based diet for 8 weeks displayed hepatoprotection against ethanol and iron-induced liver injury.…”

Section: Inflammatory Markersmentioning

confidence: 99%

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Inflammation, oxidative stress and apoptosis cascade implications in bisphenol A‐induced liver fibrosis in male rats

Elswefy

Abdallah

Atteia

et al. 2016

Int J Experimental Path

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Bisphenol A (BPA) is a key monomer in the production of plastics. It has been shown to be hepatotoxic. Inflammation and oxidative stress are closely linked with liver fibrosis, the major contributing factor to hepatic failure. Therefore, the aim of this study was to evaluate the impact of chronic exposure to BPA on the development of hepatic fibrosis in male rats and to determine the cross-talk between the hepatic cytokine network, oxidative stress and apoptosis. For this purpose, 30 male Wistar albino rats were divided into three equal groups as follows: the first group was given no treatment (normal control group); the second group was given corn oil once daily by oral gavage for 8 weeks (vehicle control group); and the third group received BPA (50 mg/kg body weight/day, p.o.) for 8 weeks. BPA administration induced liver fibrosis as reflected in an increase in serum hepatic enzymes activities, hepatic hydroxyproline content and histopathological changes particularly increased collagen fibre deposition around the portal tract. In addition, there was inflammation (as reflected in increase in interleukin-1beta 'IL-1β', decrease in interleukin-10 'IL-10' serum levels and increase in IL-1β/IL-10 ratio), oxidative stress (as reflected in increase in malondialdehyde (MDA) level, reduction in reduced glutathione (GSH) content and inhibition of catalase (CAT) activity) and apoptosis [as reflected in an increase in caspase-3 level and a decrease in numbers of B-cell lymphoma 2 (BCL2)-immunopositive hepatocytes]. Interestingly, BPA had an upregulating effect on an extracellular matrix turnover gene [as reflected in matrix metalloproteinase-9 (MMP-9)] and a downregulating effect on its inhibitor gene [as reflected in tissue inhibitor of matrix metalloproteinase-2 (TIMP-2)] expression. Thus, the mechanism by which BPA induced liver fibrosis seems to be related to stimulation of the inflammatory response, along with oxidative stress, the apoptotic pathway and activation of extracellular matrix turnover.

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Section: Discussionmentioning

confidence: 99%

Section: Inflammatory Markersmentioning

confidence: 99%

Inflammation, oxidative stress and apoptosis cascade implications in bisphenol A‐induced liver fibrosis in male rats

Elswefy

Abdallah

Atteia

et al. 2016

Int J Experimental Path

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“…A corn oil–based diet protects against combined alcohol- and iron-induced mild steatohepatitis and portal–portal tract linkage fibrosis and increases the levels of AMPK, which is low in mice hepatic fibrosis models. This suggests that AMPK has a preventative role in fibrosis arising from alcoholic steatohepatitis [ 71 ]. Moderate obesity plus alcohol intake cause pericellular fibrosis and synergistic steatohepatitis in an alcohol dose-dependent manner whereas adiponectin increases the levels of AMPK and reverses these effects [ 72 ].…”

Section: Protection Of Ampk Against Hepatic Fibrosis By Various Causementioning

confidence: 99%

“…CCl 4 , also known as tetrachloromethane, is an organic compound that induces hepatic fibrosis in experimental animals. In the CCl 4 mouse model, AMPK suppresses the expression of Nox4, TGF-β, and α-SMA and restrains the proliferation of HSC in a dose- and time-dependent manner [ 71 ]. ADP355 can attenuate CCl 4 -induced hepatic fibrosis via AMPK signaling.…”

Section: Protection Of Ampk Against Hepatic Fibrosis By Various Causementioning

confidence: 99%

AMPK: a novel target for treating hepatic fibrosis

Liang

Jiang

et al. 2017

Oncotarget

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Fibrosis is a common process of excessive extracellular matrix (ECM) accumulation following inflammatory injury. Fibrosis is involved in the pathogenesis of almost all liver diseases for which there is no effective treatment. 5'-AMP-activated protein kinase (AMPK) is a cellular energy sensor that can ameliorate the process of hepatic fibrogenesis. Given the existing evidence, we first introduce the basic background of AMPK and hepatic fibrosis and the actions of AMPK in hepatic fibrosis. Second, we discuss the three phases of hepatic fibrosis and potential drugs that target AMPK. Third, we analyze possible anti-fibrosis mechanisms and other benefits of AMPK on the liver. Finally, we summarize and briefly explain the current objections to targeting AMPK. This review may aid clinical and basic research on AMPK, which may be a novel drug candidate for hepatic fibrosis.

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“…For instance, ethanol enhances fatty acid synthesis in hepatocytes through the upregulation of sterol regulatory element binding protein 1c (SREBP-1c) protein expression, which induces a battery of lipogenic enzymes [ 4 ]. In addition, alcohol promotes lipid accumulation by inhibiting peroxisome proliferator-activated receptor- α (PPAR- α ) and adenosine monophosphate-activated protein kinase (AMPK), which have been investigated to control the transcription of a range of genes involved in free fatty acid transport and oxidation [ 5 , 6 ]. Moreover, Gao reported that adiponectin and tumor necrosis factor- α (TNF- α ) suppress mutual gene expression and antagonize their biological effects in the liver tissues [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Herbal SGR Formula Prevents Acute Ethanol-Induced Liver Steatosis via Inhibition of Lipogenesis and Enhancement Fatty Acid Oxidation in Mice

Qiu

Kong

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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Our previous study indicated that herbal SGR formula partially attenuates ethanol-induced fatty liver, but the underlying mechanisms remain unclear. In the present study, mice were pretreated with SGR (100 and 200 mg/kg/d bw) for 30 d before being exposed to ethanol (4.8 g/kg bw). The biochemical indices and histopathological changes were examined to evaluate the protective effects and to explore potential mechanisms by investigating the adiponectin, tumor necrosis factor-α (TNF-α), peroxisome proliferators-activated receptor-α (PPAR-α), sterol regulatory element binding protein-1c (SREBP-1c), adenosine monophosphate-activated protein kinase (AMPK), and so forth. Results showed that SGR pretreatment markedly inhibited acute ethanol-induced liver steatosis, significantly reduced serum and hepatic triglyceride (TG) level, and improved classic histopathological changes. SGR suppressed the protein expression of hepatic SREBP-1c and TNF-α and increased adiponectin, PPAR-α, and AMPK phosphorylation in the liver. Meanwhile, acute toxicity tests showed that no death or toxic side effects within 14 days were observed upon oral administration of the extracts at a dose of 16 g/kg body wt. These results demonstrate that SGR could protect against acute alcohol-induced liver steatosis without any toxic side effects. Therefore, our studies provide novel molecular insights into the hepatoprotective effect of SGR formula, which may be exploited as a therapeutic agent for ethanol-induced hepatosteatosis.

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A Corn Oil–Based Diet Protects Against Combined Ethanol and Iron‐Induced Liver Injury in a Mouse Model of Hemochromatosis

Abstract: A CO-based diet is protective against combined EtOH- and iron-induced liver toxicity, likely via attenuation of hepatic steatosis and oxidative stress and may have a role in the prevention of fibrosis development in chronic liver disease.

Cited by 8 publications

References 49 publications

Inflammation, oxidative stress and apoptosis cascade implications in bisphenol A‐induced liver fibrosis in male rats

Inflammation, oxidative stress and apoptosis cascade implications in bisphenol A‐induced liver fibrosis in male rats

AMPK: a novel target for treating hepatic fibrosis

Herbal SGR Formula Prevents Acute Ethanol-Induced Liver Steatosis via Inhibition of Lipogenesis and Enhancement Fatty Acid Oxidation in Mice

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