Corilagin Alleviates Nonalcoholic Fatty Liver Disease in High-Fat Diet-Induced C57BL/6 Mice by Ameliorating Oxidative Stress and Restoring Autophagic Flux

Zhang, Rong; Chu, K. C.; Zhao, Nengjiang; Wu, Jingjing; Ma, Lifeng; Zhu, Chenfang; Xia, Chen; Wei, Gang; Liao, Min

doi:10.3389/fphar.2019.01693

Cited by 43 publications

(22 citation statements)

References 49 publications

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“…The artificial uncoupler 2,4-dinitrophenol has toxic effects [347]. Further studies need to assess the ultimate role of this therapeutic strategy, especially in NAFLD [348]. Controlled-release mitochondrial protonophore (CRMP) is a controlled-release oral formulation of DNP that produces mild hepatic mitochondrial uncoupling.…”

Section: Antioxidant Agentsmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease (NAFLD). Mitochondria as Players and Targets of Therapies?

Ciaula

Passarella

Shanmugam

et al. 2021

IJMS

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Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and represents the hepatic expression of several metabolic abnormalities of high epidemiologic relevance. Fat accumulation in the hepatocytes results in cellular fragility and risk of progression toward necroinflammation, i.e., nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually hepatocellular carcinoma. Several pathways contribute to fat accumulation and damage in the liver and can also involve the mitochondria, whose functional integrity is essential to maintain liver bioenergetics. In NAFLD/NASH, both structural and functional mitochondrial abnormalities occur and can involve mitochondrial electron transport chain, decreased mitochondrial β-oxidation of free fatty acids, excessive generation of reactive oxygen species, and lipid peroxidation. NASH is a major target of therapy, but there is no established single or combined treatment so far. Notably, translational and clinical studies point to mitochondria as future therapeutic targets in NAFLD since the prevention of mitochondrial damage could improve liver bioenergetics.

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Section: Antioxidant Agentsmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease (NAFLD). Mitochondria as Players and Targets of Therapies?

Ciaula

Passarella

Shanmugam

et al. 2021

IJMS

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“…16,17 OA and PA are the main fatty acids in the high fat foods that induce steatosis, which correlates to a high fat diet-fed mice model. 18 This model demonstrated the formation of lipid vacuoles in the mouse livers, which was relieved by myricetin. Hence, myricetin might present an effective NAFLD treatment.…”

Section: Pa-induced Nafld In Hepg2 Cellsmentioning

confidence: 88%

Hesperidin and Myricetin Attenuated Non-Alcoholic Fatty Liver Disease (NAFLD) in HepG2 Cells

2020

TJNPR

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fruits, berries, teas, and vegetables, has anti-oxidation, antiinflammation, anti-tumour, and anti-diabetic activities. 7 Hesperidin, a flavanone β-7-rutinoside of hesperetin present in citrus fruits such as lemon, orange, and grapefruit, has anti-oxidant, anti-inflammatory, and anti-carcinogenic properties. 8 Silymarin, a flavonol derived from thistle milk (Silybum marianum), has demonstrated antioxidant, antifibrotic, and antiviral properties. 9 The multifarious actions of flavonoids may suit the treatment of NAFLD. Currently, the multi-hit hypothesis is used to explain the pathogenesis of NAFLD. It states that there are multiple hits involving insulin resistance, mitochondrial dysfunction, endoplasmic reticulum stress, adipose tissue dysfunction, and dietary factors that lead to lipid accumulation in the liver and the advancement and progression of NAFLD. 4 The most common hits that cause NAFLD are insulin resistance and mitochondrial dysfunction. Altered expression of PPAR-α and PPAR-γ, SREBP-1a and SREBP-1c, acetyl-CoA carboxylase (ACC), acyl-CoA oxidase (ACOX), and fatty acid synthase (FAS) metabolic genes are indicators of these two hits. 10 Altered expressions of these genes directly affect liver function and hepatic histomorphology. Hence, this study aimed at developing therapeutics from flavonoids. In addition, three subclasses of flavonoids (flavones, flavanones, and flavonols) were evaluated for their effects on hepatic cell histomorphology and the expression of PPAR-α/γ, SREBP-1a/1c, ACC, ACOX, and FAS in OA or PAinduced NAFLD using HepG2 cells.

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“…Lipid peroxidation converts ROS into active chemicals, which amplifies ROS’ effect by chain or chain branching reaction. Simultaneously, due to the accumulation of ROS, the consumption of antioxidants in liver tissue increases, and the expression of SOD, CAT, GSH-Px, and GSH decreases ( Zhang R. et al, 2019b ). We evaluated the role of TUG1 in LPS-induced hepatocyte inflammation by detecting oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Silencing lncRNA TUG1 Alleviates LPS-Induced Mouse Hepatocyte Inflammation by Targeting miR-140/TNF

Liu

et al. 2021

Front. Cell Dev. Biol.

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Hepatitis is a major public health problem that increases the risk of liver cirrhosis and liver cancer. Numerous studies have revealed that long non-coding RNAs (lncRNAs) exert essential function in the inflammatory response of multiple organs. Herein, we aimed to explore the effect of lncRNA TUG1 in LPS-induced hepatocyte inflammation response and further illuminate the underlying mechanisms. Mice were intraperitoneally injected with LPS, and the liver inflammation was evaluated. Microarray showed that lncRNA TUG1 was upregulated in LPS-induced hepatocyte inflammation. qRT-PCR and immunofluorescence assay indicated a significant increase of TUG1 in mice with LPS injection. Functional analysis showed that si-TUG1 inhibited LPS-induced inflammation response in mice liver, inhibited apoptosis level, and protected liver function. Then, we knock down TUG1 in normal human hepatocyte AML12. Consistent with in vivo results, si-TUG1 removed the injury of LPS on AML12 cells. Furthermore, TUG1 acted as a sponge of miR-140, and miR-140 directly targeted TNFα (TNF). MiR-140 or si-TNF remitted the beneficial effects of TUG1 on LPS-induced hepatocyte inflammation response both in vitro and in vivo. Our data revealed that deletion of TUG1 protected against LPS-induced hepatocyte inflammation via regulating miR-140/TNF, which might provide new insight for hepatitis treatment.

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Corilagin Alleviates Nonalcoholic Fatty Liver Disease in High-Fat Diet-Induced C57BL/6 Mice by Ameliorating Oxidative Stress and Restoring Autophagic Flux

Cited by 43 publications

References 49 publications

Nonalcoholic Fatty Liver Disease (NAFLD). Mitochondria as Players and Targets of Therapies?

Nonalcoholic Fatty Liver Disease (NAFLD). Mitochondria as Players and Targets of Therapies?

Hesperidin and Myricetin Attenuated Non-Alcoholic Fatty Liver Disease (NAFLD) in HepG2 Cells

Silencing lncRNA TUG1 Alleviates LPS-Induced Mouse Hepatocyte Inflammation by Targeting miR-140/TNF

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