Apigenin protects against alcohol-induced liver injury in mice by regulating hepatic CYP2E1-mediated oxidative stress and PPARα-mediated lipogenic gene expression

Wang, Feng; Liu, Jincheng; Zhou, Ruijun; Zhao, Xi; Liu, Mei; Ye, Hua; Xie, Ming

doi:10.1016/j.cbi.2017.08.006

Cited by 88 publications

(76 citation statements)

References 37 publications

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“…As shown in previous evidence, it can be up-regulated by highly expressed TNF-a, further inducing necrobiosis lipoidica. 6,49 Alcohol consumption can stimulate Kupffer cells to generate ROS and subsequently activate NF-kB pathway, bringing on a high expression of TNF-a. 50,51 Therefore, once TNF-a is inhibited, it could completely block the development of ethanol-induced hepatotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…3,4 The interplay between oxidative stress and steatosis in ethanol-induced liver failure has been discussed by multiple researchers. 5,6 Alcohol intake activates the activity of hepatic cytochrome P450 2E1(CYP2E1) that accelerates the alcohol oxidation and acetaldehyde accumulation. 7 The interaction between acetaldehyde, proteins and lipids can lead to massive reactive oxygen species (ROS) formation and severe cell damage, and cause hepatic oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

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Patchouli oil isolated from the leaves of Pogostemon cablin ameliorates ethanol-induced acute liver injury in rats via inhibition of oxidative stress and lipid accumulation

Huang

Chen

et al. 2018

RSC Adv.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Patchouli oil isolated from the leaves of Pogostemon cablin ameliorates ethanol-induced acute liver injury in rats via inhibition of oxidative stress and lipid accumulation

Huang

Chen

et al. 2018

RSC Adv.

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“…Apigenin is distributed ubiquitously in a wide range of vegetables, fruits and medicinal plants as well as dietary and herbal supplements [37,40]. Recently, apigenin has drawn much attention for its powerful medicinal properties, including anti-tumor, anti-virus, anti- Fig.…”

Section: Discussionmentioning

confidence: 99%

“…-/-mice Apigenin has been found to effectively improve alcohol-induced liver injury in mice without obvious toxicity [37]. As increased cellular cholesterol efflux and decreased levels of pro-inflammatory cytokines can impede atherogenesis, we determined the effects of apigenin on atherosclerotic lesion sizes and plaque composition in apoE -/-mice.…”

Section: Apigenin Decreases Atherosclerotic Lesions and The Contents mentioning

confidence: 99%

Apigenin Retards Atherogenesis by Promoting ABCA1-Mediated Cholesterol Efflux and Suppressing Inflammation

Ren

Jiang

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: The development of atherosclerosis is accompanied by escalating inflammation and lipid accumulation within blood vessel walls. ABCA1 plays a crucial role in mediating cholesterol efflux from macrophages, which protects against atherogenesis. This research was designed to explore the effects and underlying mechanisms of apigenin (4’, 5, 7-trihydroxyflavone) on ABCA1-mediated cellular cholesterol efflux and LPS-stimulated inflammation in RAW264.7 macrophages and apoE^-/- mice. Methods: Expression of genes or proteins was examined by RT-PCR or western blot analysis. Liquid scintillation counting was used to detect percent cholesterol efflux. Cellular cholesterol content was measured using HPLC assay. The secretion levels of pro-inflammatory cytokines were quantified by ELISA assay. Atherosclerotic lesion sizes were determined with Oil Red O staining. The contents of macrophages and smooth muscle cells in atherosclerotic lesion were evaluated using immunohistochemistry. Plasma TC, TG, HDL-C and LDL-C levels in apoE^-/- mice were evaluated using commercial test kits. Results: Apigenin potently increased ABCA1 expression through miR-33 repression in a dose- and time-dependent manner. Treatment with apigenin significantly increased ABCA1-mediated cholesterol efflux, and reduced TC, FC and CE levels in macrophage-derived foam cells. In LPS-treated macrophages, the expression levels of TLR-4, MyD88 and p-IκB-α as well as nuclear NF-κB p65 were decreased by the addition of apigenin. Moreover, apigenin markedly decreased secretion levels of several pro-inflammatory cytokines. Lastly, in LPS-challenged apoE^-/- mice, apigenin administration augmented ABCA1 expression, decreased the contents of macrophages and smooth muscle cells in atherosclerotic lesion, reduced miR-33, TLR-4, and NF-κB p65 levels, improved plasma lipid profile and relieved inflammation, which results in less atherosclerotic lesion size. Conclusions: Taken together, these results suggest that apigenin may attenuate atherogenesis through up-regulating ABCA1-mediated cholesterol efflux and inhibiting inflammation.

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“…Lately, apigenin was shown to be protective against alcohol‐induced liver injury in mice (Wang et al, ). Apigenin treatment results in decreased expression of CYP2E1, as well as upregulated levels of hepatic reduced GSH‐Px and GST, indicating its antioxidant ability.…”

Section: Natural Compounds Beneficial For Ald Treatmentmentioning

confidence: 99%

Natural compounds in the chemoprevention of alcoholic liver disease

Zhu

Wang

et al. 2019

Phytotherapy Research

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Alcoholic liver disease (ALD), caused by excessive consumption of alcohol, is a major cause of chronic liver disease worldwide. Much effort has been expended to explore the pathogenesis of ALD. Hepatic cell injury, oxidative stress, inflammation, regeneration, and bacterial translocation are all involved in the pathogenesis of ALD. Immediate abstinence is the most important therapeutic treatment for affected individuals. However, the medical treatment for ALD had not advanced in a long period. Intriguingly, an increasing body of research indicates the potential of natural compounds in the targeted therapy of ALD. A plethora of dietary natural products such as flavonoids, resveratrol, saponins, and β‐carotene are found to exert protective effects on ALD. This occurs through various mechanisms composed of antioxidative, anti‐inflammatory, iron chelation, pro‐apoptosis, and/or antiproliferation of hepatic stellate cells and hepatocellular carcinoma cells. In this review, we will summarize current knowledge about the pathogenesis and treatments of ALD and focus on the potential of natural compounds in ALD therapies and underlying mechanisms.

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Apigenin protects against alcohol-induced liver injury in mice by regulating hepatic CYP2E1-mediated oxidative stress and PPARα-mediated lipogenic gene expression

Cited by 88 publications

References 37 publications

Patchouli oil isolated from the leaves of Pogostemon cablin ameliorates ethanol-induced acute liver injury in rats via inhibition of oxidative stress and lipid accumulation

Patchouli oil isolated from the leaves of Pogostemon cablin ameliorates ethanol-induced acute liver injury in rats via inhibition of oxidative stress and lipid accumulation

Apigenin Retards Atherogenesis by Promoting ABCA1-Mediated Cholesterol Efflux and Suppressing Inflammation

Natural compounds in the chemoprevention of alcoholic liver disease

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