The protective effects of sulforaphane on high-fat diet-induced metabolic associated fatty liver disease in mice <i>via</i> mediating the FXR/LXRα pathway

Ma, Shaotong; Pang, Xinyi; Tian, Shuhua; Sun, Jing; Hu, Qiaobin; Li, Xiangfei; Lu, Yingjian

doi:10.1039/d2fo02341e

Cited by 6 publications

(3 citation statements)

References 56 publications

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“…122 The genes FXR, SHP, LXRα, and SREBP-1C are all associated with bile acid synthesis and metabolism. 123 Ma et al 124 conducted extensive research and discovered that SFN regulates bile acid synthesis and metabolism by upregulating the expression of genes such as FXR, SHP, and CYP7A1, while downregulating the expression of genes like LXRα and SREBP-1C. Additionally, Cardenia et al 125 fed mice with broccoli extract abundant in sulforaphane (BE) and found that BE inhibited cholesterol oxidation in the liver cells.…”

Section: ■ Potential Adverse Health Effects Of Copsmentioning

confidence: 99%

Cholesterol Oxidation Products: Potential Adverse Effect and Prevention of Their Production in Foods

Deng,

Li,

Liu

et al. 2023

J. Agric. Food Chem.

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Section: ■ Potential Adverse Health Effects Of Copsmentioning

confidence: 99%

Cholesterol Oxidation Products: Potential Adverse Effect and Prevention of Their Production in Foods

Deng,

Li,

Liu

et al. 2023

J. Agric. Food Chem.

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“…Apart from activation of Nrf2, SFN was also shown to prevent high-fat diet (HFD)-induced NAFLD in mice by inhibiting NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in liver through AMP-activated protein kinase (AMPK)-autophagy axis when administered with a daily dose of 30 mg/kg for 9 weeks along with HFD ( Yang et al, 2016 ). In recent years, the number of new mechanisms and molecular targets of SFN in the treatment of fatty liver reported by experimental studies has increased rapidly ( Figure 1 ), such as inhibition of lipogenic enzymes via ER stress-dependent decrease of X-box binding protein 1 (XBP1) expression and ER stress-independent blocking of sterol regulatory element binding protein-1c (SREBP1c) pathways ( Tian et al, 2018a ), alleviated ER stress through the upregulation of AMPK and peroxisome proliferators-activated receptor α (PPARα) ( Mansour et al, 2022 ), enhanced mitochondrial function via Nrf2 activation or promotion of mitochondrial biogenesis by peroxisome proliferator-activated receptor alpha co-activator pathway ( Lei et al, 2019 ), and regulation of FXR-mediated bile acid metabolism and LXRα-mediated fatty acid synthesis pathways ( Ma et al, 2022 ). SFN was also found to alleviate HFD-induced lipid deposition and suppress apoptosis by regulating the AMPK/SREBP1c/FAS signaling pathway both in vitro and in vivo ( Li et al, 2021 ).…”

Section: The Efficacy Of Sfn In the Treatment Of Liver Diseasesmentioning

confidence: 99%

Therapeutic potential of sulforaphane in liver diseases: a review

Yan,

Yan

2023

Front. Pharmacol.

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The burden of liver diseases such as metabolic-associated fatty liver diseases and hepatocellular carcinoma has increased rapidly worldwide over the past decades. However, pharmacological therapies for these liver diseases are insufficient. Sulforaphane (SFN), an isothiocyanate that is mainly found in cruciferous vegetables, has been found to have a broad spectrum of activities like antioxidation, anti-inflammation, anti-diabetic, and anticancer effects. Recently, a growing number of studies have reported that SFN could significantly ameliorate hepatic steatosis and prevent the development of fatty liver, improve insulin sensitivity, attenuate oxidative damage and liver injury, induce apoptosis, and inhibit the proliferation of hepatoma cells through multiple signaling pathways. Moreover, many clinical studies have demonstrated that SFN is harmless to the human body and well-tolerated by individuals. This emerging evidence suggests SFN to be a promising drug candidate in the treatment of liver diseases. Nevertheless, limitations exist in the development of SFN as a hepatoprotective drug due to its special properties, including instability, water insolubility, and high inter-individual variation of bioavailability when used from broccoli sprout extracts. Herein, we comprehensively review the recent progress of SFN in the treatment of common liver diseases and the underlying mechanisms, with the aim to provide a better understanding of the therapeutic potential of SFN in liver diseases.

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“…BAs are important in lipid metabolism because they emulsify lipids, increase their interaction with lipase, and regulate the activity of pancreatic lipase and lipoprotein esterase. Consequently, BA enhances lipid hydrolysis metabolism in vivo [ 9 ]. BA produced by cholesterol catabolism facilitates the digestion and absorption of dietary lipids and actively participates in the regulation of lipid metabolism [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Involvement of Bile Acid Metabolism and Gut Microbiota in the Amelioration of Experimental Metabolism-Associated Fatty Liver Disease by Nobiletin

Xu,

Yuan,

Niu

et al. 2024

Molecules

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Metabolism-associated fatty liver disease (MAFLD), a growing health problem worldwide, is one of the major risks for the development of cirrhosis and liver cancer. Oral administration of nobiletin (NOB), a natural citrus flavonoid, modulates the gut microbes and their metabolites in mice. In the present study, we established a mouse model of MAFLD by subjecting mice to a high-fat diet (HFD) for 12 weeks. Throughout this timeframe, NOB was administered to investigate its potential benefits on gut microbial balance and bile acid (BA) metabolism using various techniques, including 16S rRNA sequencing, targeted metabolomics of BA, and biological assays. NOB effectively slowed the progression of MAFLD by reducing serum lipid levels, blood glucose levels, LPS levels, and hepatic IL-1β and TNF-α levels. Furthermore, NOB reinstated diversity within the gut microbial community, increasing the population of bacteria that produce bile salt hydrolase (BSH) to enhance BA excretion. By exploring further, we found NOB downregulated hepatic expression of the farnesoid X receptor (FXR) and its associated small heterodimer partner (SHP), and it increased the expression of downstream enzymes, including cholesterol 7α-hydroxylase (CYP7A1) and cytochrome P450 27A1 (CYP27A1). This acceleration in cholesterol conversion within the liver contributes to mitigating MAFLD. The present findings underscore the significant role of NOB in regulating gut microbial balance and BA metabolism, revealing that long-term intake of NOB plays beneficial roles in the prevention or intervention of MAFLD.

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The protective effects of sulforaphane on high-fat diet-induced metabolic associated fatty liver disease in mice via mediating the FXR/LXRα pathway

Abstract: Metabolic associated fatty liver disease (MAFLD) is becoming the key factor in causing chronic liver disease over the world. Sulforaphane (SFN) has been proved to be effective in alleviating many...

Cited by 6 publications

References 56 publications

Cholesterol Oxidation Products: Potential Adverse Effect and Prevention of Their Production in Foods

Cholesterol Oxidation Products: Potential Adverse Effect and Prevention of Their Production in Foods

Therapeutic potential of sulforaphane in liver diseases: a review

Involvement of Bile Acid Metabolism and Gut Microbiota in the Amelioration of Experimental Metabolism-Associated Fatty Liver Disease by Nobiletin

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