Non-Alcoholic Fatty Liver Disease (NAFLD) Pathogenesis and Natural Products for Prevention and Treatment

Guo, Xiangyu; Yin, Xinghui; Liu, Zuojia; Wang, Jin

doi:10.3390/ijms232415489

Cited by 68 publications

(50 citation statements)

References 124 publications

(159 reference statements)

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“…HepG2 cells are widely used in in vitro NAFLD models because they have the characteristics of hepatocytes that accumulates intracellular lipids by FFA treatments such as oleic acid and/or palmitic acid [ 9 , 34 , 35 ]. Many studies have reported that the exposure of HepG2 cells to 0.5–1 mM of FFA for 24 h results in significant lipid accumulation [ 16 , 36 , 37 ].…”

Section: Resultsmentioning

confidence: 99%

“…In addition, polyphenol compounds have been shown to inhibit lipogenic enzyme activity and control new lipid synthesis [ 7 , 8 ]. Given that inflammation and oxidative stress are primary risk factors involved in the development of NAFLD [ 9 ], recent studies have reported that consuming a polyphenol-rich diet could help prevent and treat NAFLD [ 10 ]. Accordingly, considerable efforts have been made to assess the effectiveness of polyphenols on insulin resistance and metabolic pathologies in NAFLD.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells

et al. 2023

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Liver metabolic disorders and oxidative stress are crucial factors in the development of nonalcoholic fatty liver disease (NAFLD); however, treatment strategies to combat NAFLD remain poorly established, presenting an important challenge that needs to be addressed. Herein, we aimed to examine the effect of isoquercitrin on lipid accumulation induced by exogenous free fatty acids (FFA) using HepG2 cells and elucidate the underlying molecular mechanism. The cells were exposed to 0.5 mM FFA to induce intracellular lipid accumulation, followed by co-treatment with isoquercitrin to confirm the potential inhibitory effect on FFA-induced lipid production. HepG2 cells exposed to FFA alone exhibited intracellular lipid accumulation, compromised endoplasmic reticulum (ER) stress, and enhanced expression of proteins and genes involved in lipid synthesis; however, co-treatment with isoquercitrin decreased the expression of these molecules in a dose-dependent manner. Furthermore, isoquercitrin could activate AMP-activated protein kinase (AMPK), a key regulatory protein of hepatic fatty acid oxidation, suppressing new lipid production by phosphorylating acetyl-CoA carboxylase (ACC) and inhibiting sterol regulatory element-binding transcription factor 1 (SREBP-1)/fatty acid synthase (FAS) signals. Overall, these findings suggest that isoquercitrin can be employed as a therapeutic agent to improve NAFLD via the regulation of lipid metabolism by targeting the AMPK/ACC and SREBP1/FAS pathways.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells

et al. 2023

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“…NASH is considered the progressive form of NAFLD and is characterized by liver steatosis, inflammation, hepatocellular injury and different degrees of fibrosis ( Schuster et al, 2018 ). Accumulating studies demonstrated that a pivotal issue relates to the identification of those factors that trigger inflammation, thus fuelling the transition from NAFLD to NASH ( Guo et al, 2022 ; An et al, 2023 ). These triggers of inflammtion in liver might be associated with their origins outside the liver as well as inside the organ, both of which accelerate to NASH development ( Han et al, 2022 ).…”

Section: Extrahepatic Factors In Nashmentioning

confidence: 99%

Recent evaluation about inflammatory mechanisms in nonalcoholic fatty liver disease

Long

Huang

2023

Front. Pharmacol.

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Non-alcoholic fatty liver disease (NAFLD) is common chronic metabolic liver disorder which is associated with fat accumulation in the liver. It causes a wide range of pathological effects such as insulin resistance, obesity, hypertension, diabetes, non-alcoholic steatohepatitis (NASH) and cirrhosis, cardiovascular diseases. The molecular mechanisms that cause the initiation and progression of NAFLD remain fully unclear. Inflammation is regarded as a significant mechanism which could result in cell death and tissue injury. Accumulation of leukocytes and hepatic inflammation are important contributors in NAFLD. Excessive inflammatory response can deteriorate the tissue injury in NAFLD. Thus, inhibition of inflammation improves NAFLD by reducing intrahepatic fat content, increasing β-oxidation of fatty acids, inducing hepato-protective autophagy, overexpressing peroxisome proliferator-activated receptor- γ (PPAR-γ), as well as attenuating hepatocyte apoptosis and increasing insulin sensitivity. Therefore, understanding the molecules and signaling pathways suggests us valuable information about NAFLD progression. This review aimed to evaluate the inflammation in NAFLD and the molecular mechanism on NAFLD.

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“…10,12 Because of their low side effects and high safety, natural products have recently become a research hotspot for human health-related issues. 13 Lycium barbarum , a traditional Chinese edible and medicinal plant, 14 is also known as Goji berry and Chinese wolfberry. 15 According to related studies, the main active components of the plant are polyphenols, pigments, polysaccharides, flavonoids, amino acids, alkaloids, vitamins, and trace minerals.…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of Lycium barbarum Betaine and Effervescent Tablet Against Carbon Tetrachloride-Induced Acute Liver Injury in Rats

Zhai

Tang

Zhang

et al. 2023

Natural Product Communications

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The liver is essential for animals and humans. Because of their low side effects and high safety, natural products have recently become a research hotspot for human health-related issues that can damage the liver. In this study, we investigated the protective effects in rats of Lycium barbarum betaine (LBB) and Lycium barbarum betaine Effervescent Tablet (LBBET) against liver injury caused by carbon tetrachloride (CCl4). The results showed that LBB and LBBET pretreatment significantly reduced the serum levels of alanine aminotransferase, aspartate transaminase (AST), and alkaline phosphatase, as well as the liver tissue levels of malondialdehyde. Meanwhile, glutathione peroxidase, and superoxide dismutase levels were significantly increased in liver tissues. In addition, LBB and LBBET may effectively alleviate CCl4-induced liver injury by a mechanism related to the activation of the Nrf2 signaling pathway. In conclusion, LBB and LBBET may serve as potential mitigators of CCl4-induced liver injury. Effervescent Tablet can be used as either a new formulation or practical product for patients who have difficulty swallowing regular tablets or capsules. This study provides a basis and new ideas for the development of functional foods or drugs related to the field of liver protection.

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Non-Alcoholic Fatty Liver Disease (NAFLD) Pathogenesis and Natural Products for Prevention and Treatment

Cited by 68 publications

References 124 publications

Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells

Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells

Recent evaluation about inflammatory mechanisms in nonalcoholic fatty liver disease

The Protective Effect of Lycium barbarum Betaine and Effervescent Tablet Against Carbon Tetrachloride-Induced Acute Liver Injury in Rats

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