Apigenin ameliorates HFD-induced NAFLD through regulation of the XO/NLRP3 pathways

Lv, Yanan; Gao, Xiaona; Luo, Yan; Fan, Wentao; Shen, Tao; Ding, Chenchen; Yao, Mingde; Song, Suquan; Yan, Liping

doi:10.1016/j.jnutbio.2019.05.015

Cited by 83 publications

(57 citation statements)

References 57 publications

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“…The activation of NLRP3 inflammasome causes the activation of caspase‐1 enzyme and the release of pro‐inflammatory cytokines (Wree et al, 2014). Apigenin is another flavonoid found in propolis which its application in high‐fat diet mice results in the blockade of macrophage migration and NLRP3 activation and consequently NAFLD prevention (Lv et al, 2019). Pinocembrin (PIN; another flavonoid found in propolis) has down‐regulated the expression of TNF‐α, IL‐1β, and IL‐6 genes.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of propolis on hepatic steatosis and fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) evaluated by real‐time two‐dimensional shear wave elastography: A randomized clinical trial

Soleimani

Rezaie

Rajabzadeh

et al. 2020

Phytotherapy Research

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Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, while no drugs have been approved for its treatment. The pieces of evidence indicate that propolis as a novel anti-inflammatory agent might be a promising candidate to treat NAFLD. We aimed to evaluate the efficacy of propolis on hepatic steatosis and fibrosis in patients with NAFLD. This randomized clinical trial was conducted on 54 patients with NAFLD. Patients were randomly assigned to receive propolis tablets at a dose of 250 mg twice daily for 4 months or placebo. The improvement in hepatic steatosis and fibrosis was evaluated using two-dimensional shear wave elastography. Improvement in the hepatic steatosis was significantly higher in the propolis group than the placebo group, even after adjustment for baseline value and changes in weight, energy intake, and physical activity (odds ratio [OR]: 5.67; 95% confidence intervals [CI]: 1.41-22.8; p = .014). A significant reduction was observed on the liver stiffness in the propolis group (−0.65 ± 0.56 kPa; p = .001), whereas it increased in the placebo group (0.27 ± 0.59 kPa; p = .037). Also, the intake of propolis significantly decreased high-sensitivity C-reactive protein (hs-CRP) levels compared with the placebo group (−0.371; 95%CI: −0.582 to −0.16 mg/L; p = .01). Changes in serum levels of fasting blood sugar, alanine aminotransferase, aspartate aminotransferase,

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Section: Discussionmentioning

confidence: 99%

Protective effects of propolis on hepatic steatosis and fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) evaluated by real‐time two‐dimensional shear wave elastography: A randomized clinical trial

Soleimani

Rezaie

Rajabzadeh

et al. 2020

Phytotherapy Research

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“…Apigenin treatment downregulated the expression of genes related to lipid droplet formation ( Cidea, Plin2, fat storage inducing transmembrane protein 1 and 2 and) as well as genes involved in FA uptake ( Fabp1 and Lpl ), FAO ( Cpt1a, Pdk4, Acox1, Acaa2 ) and lipogenesis (Fasn, Scd11, Acaca) [ 341 ]. On the other side, apigenin may act as a PPARγ modulator in a mouse model of obesity where it activated the p65/PPARγ complex translocation into the nucleus, thereby decreasing the NF-κB activation and favoring the M2 macrophage polarization [ 356 ] or blocking NLRP3 inflammasome assembly and the ROS production [ 357 ]. The capacity of flavones to modulate PPARγ activity and induce macrophage polarization to M2 phenotype has also been described for Chrysin in a HFD-fed mice model [ 358 ].…”

Section: Flavonesmentioning

confidence: 99%

Metabolic Impact of Flavonoids Consumption in Obesity: From Central to Peripheral

et al. 2020

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The prevention and treatment of obesity is primary based on the follow-up of a healthy lifestyle, which includes a healthy diet with an important presence of bioactive compounds such as polyphenols. For many years, the health benefits of polyphenols have been attributed to their anti-oxidant capacity as free radical scavengers. More recently it has been described that polyphenols activate other cell-signaling pathways that are not related to ROS production but rather involved in metabolic regulation. In this review, we have summarized the current knowledge in this field by focusing on the metabolic effects of flavonoids. Flavonoids are widely distributed in the plant kingdom where they are used for growing and defensing. They are structurally characterized by two benzene rings and a heterocyclic pyrone ring and based on the oxidation and saturation status of the heterocyclic ring flavonoids are grouped in seven different subclasses. The present work is focused on describing the molecular mechanisms underlying the metabolic impact of flavonoids in obesity and obesity-related diseases. We described the effects of each group of flavonoids in liver, white and brown adipose tissue and central nervous system and the metabolic and signaling pathways involved on them.

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“…In order to elucidate the pathogenesis of NAFLD and find out the effective treatment strategies, a high-fat diet (HFD) is widely used to induce NAFLD in experimental animals [5,6]. Previous studies demonstrated that HFD induced hepatic fat accumulation by accelerating lipogenesis and depressing fatty acid oxidation [5,7]. A transcriptome analysis demonstrated that HFD upregulated pro-inflammatory genes and downregulated the genes related to antioxidative capacity [8].…”

Section: Introductionmentioning

confidence: 99%

Chitosan Oligosaccharide Attenuates Nonalcoholic Fatty Liver Disease Induced by High Fat Diet through Reducing Lipid Accumulation, Inflammation and Oxidative Stress in C57BL/6 Mice

et al. 2019

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Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease closely associated with metabolic syndrome, but there are no validated pharmacological therapies. The aim of this study was to investigate the effect of chitosan oligosaccharide (COS) on NAFLD. Mice were fed either a control diet or a high-fat diet (HFD) with or without COS (200 or 400 mg/kg body weight (BW)) by oral gavage for seven weeks. Administration with COS significantly lowered serum lipid levels in the HFD-fed mice. The hepatic lipid accumulation was significantly decreased by COS, which was attributed to decreased expressions of lipogenic genes and increased expressions of fatty β-oxidation-related genes. Moreover, pro-inflammatory cytokines, neutrophils infiltration, and macrophage polarization were decreased by COS in the liver. Furthermore, COS ameliorated hepatic oxidative stress by activating the nuclear factor E2-related factor 2 (Nrf2) pathway and upregulating gene expressions of antioxidant enzymes. These beneficial effects were mediated by the activation of the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. Therefore, COS might be a potent dietary supplement to ameliorate NAFLD.

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Apigenin ameliorates HFD-induced NAFLD through regulation of the XO/NLRP3 pathways

Cited by 83 publications

References 57 publications

Protective effects of propolis on hepatic steatosis and fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) evaluated by real‐time two‐dimensional shear wave elastography: A randomized clinical trial

Protective effects of propolis on hepatic steatosis and fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) evaluated by real‐time two‐dimensional shear wave elastography: A randomized clinical trial

Metabolic Impact of Flavonoids Consumption in Obesity: From Central to Peripheral

Chitosan Oligosaccharide Attenuates Nonalcoholic Fatty Liver Disease Induced by High Fat Diet through Reducing Lipid Accumulation, Inflammation and Oxidative Stress in C57BL/6 Mice

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