Abstract:MAFLD stands for metabolic-related fatty liver disease, which is a prevalent liver disease affecting one-third of adults worldwide, and is strongly associated with obesity, hyperlipidemia, and type 2 diabetes. It encompasses a broad spectrum of conditions ranging from simple liver fat accumulation to advanced stages like chronic inflammation, tissue damage, fibrosis, cirrhosis, and even hepatocellular carcinoma. With limited approved drugs for MAFLD, identifying promising drug targets and developing effective … Show more
“…At present, increasing evidence has shown that alcohol-induced abnormity can be regulated by autophagy ( Li, Ouyang & Zhu, 2023 ). Autophagy is a critical self-protection and survival mechanism of eukaryotic cells that exerts a protective role in ALD by scavenging damaged mitochondria ( Thomes et al, 2015 ), accumulated LDs ( Lin et al, 2013 ; Schulze et al, 2017 ), and protein polymers ( Bonilla et al, 2013 ).…”
Alcohol-related liver disease (ALD) is chronic liver damage caused by long-term heavy drinking with, extremely complicated pathogenesis. The current studies speculated that excessive alcohol and its metabolites are the major causes of liver cell toxicity. Autophagy is evolutionarily conserved in eukaryotes and aggravates alcoholic liver damage, through various mechanisms, such as cellular oxidative stress, inflammation, mitochondrial damage and lipid metabolism disorders. Therefore, autophagy plays an critical role in the occurrence and development of ALD. Some studies have shown that traditional Chinese medicine extracts improve the histological characteristics of ALD, as reflected in the improvement of oxidative stress and lipid droplet clearance, which might be achieved by inducing autophagy. This article reviews the mechanisms of quercetin, baicalin, glycycoumarin, salvianolic acid A, resveratrol, ginsenoside rg1, and dihydromyricetin inducing autophagy and their participation in the inhibition of ALD. The regulation of autophagy in ALD by these traditional Chinese medicine extracts provides novel ideas for the treatment of the disease; however, its molecular mechanism needs to be elucidated further.
“…At present, increasing evidence has shown that alcohol-induced abnormity can be regulated by autophagy ( Li, Ouyang & Zhu, 2023 ). Autophagy is a critical self-protection and survival mechanism of eukaryotic cells that exerts a protective role in ALD by scavenging damaged mitochondria ( Thomes et al, 2015 ), accumulated LDs ( Lin et al, 2013 ; Schulze et al, 2017 ), and protein polymers ( Bonilla et al, 2013 ).…”
Alcohol-related liver disease (ALD) is chronic liver damage caused by long-term heavy drinking with, extremely complicated pathogenesis. The current studies speculated that excessive alcohol and its metabolites are the major causes of liver cell toxicity. Autophagy is evolutionarily conserved in eukaryotes and aggravates alcoholic liver damage, through various mechanisms, such as cellular oxidative stress, inflammation, mitochondrial damage and lipid metabolism disorders. Therefore, autophagy plays an critical role in the occurrence and development of ALD. Some studies have shown that traditional Chinese medicine extracts improve the histological characteristics of ALD, as reflected in the improvement of oxidative stress and lipid droplet clearance, which might be achieved by inducing autophagy. This article reviews the mechanisms of quercetin, baicalin, glycycoumarin, salvianolic acid A, resveratrol, ginsenoside rg1, and dihydromyricetin inducing autophagy and their participation in the inhibition of ALD. The regulation of autophagy in ALD by these traditional Chinese medicine extracts provides novel ideas for the treatment of the disease; however, its molecular mechanism needs to be elucidated further.
“…Multiple factors, such as oxidative stress-induced lipotoxicity and cellular senescence, contribute to the pathogenesis and progression of MAFLD ( 12 ). Additionally, inflammatory responses accelerate the development of MAFLD ( 13 ). A study reported that several components of traditional Chinese herbal medicine could inhibit liver inflammation and alleviate liver damage ( 13 ).…”
Section: Introductionmentioning
confidence: 99%
“…Additionally, inflammatory responses accelerate the development of MAFLD ( 13 ). A study reported that several components of traditional Chinese herbal medicine could inhibit liver inflammation and alleviate liver damage ( 13 ). Therefore, supplementing the antioxidant or anti-inflammatory nutrients might have similar effects.…”
BackgroundDespite the rapid increase in the global prevalence of Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD), there are no approved therapeutic drugs for MAFLD yet. Nutrient supplementation might mitigate the risk of MAFLD. It is more typical for individuals to consume multiple nutrients simultaneously. However, the studies exploring the combined effects of multiple nutrients on MAFLD are limited. This study aimed to investigate the relationship between both individual nutrients and their combined influence on the risk of MAFLD.MethodsData were obtained from National Health and Nutrition Examination Survey (NHANES), and 18 types of nutrients were considered in this study. Logistic regression analysis was performed to evaluate the correlation between single nutrients and the risk of MAFLD. The Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis was performed to pinpoint the most relevant nutrient associated with the risk of MAFLD. Subsequently, both Weighted Quantile Sum (WQS) regression and Quantile g-computation (Qgcomp) were used to assess the combined effects of multiple nutrients on the risk of MAFLD.ResultsA total of 3,069 participants were included in this study. LASSO regression analysis showed that Se, α-tocopherol, and γ-tocopherol exhibited a positive association with the risk of MAFLD. In contrast, the serum levels of Co, P, α-cryptoxanthin, LZ, and trans-β-carotene were inversely associated with the prevalence of MAFLD. When Se and two types of vitamin E were excluded, the WQS index showed a significant inverse relationship between the remaining 15 nutrients and the risk of MAFLD; α-cryptoxanthin showed the most substantial contribution. Similarly, Qgcomp suggested that the combined effects of these 15 nutrients were associated with a lower risk of MAFLD, with α-cryptoxanthin possessing the most significant negative weights.ConclusionThis study suggested that the complex nutrients with either a low proportion of Se, α-tocopherol, and γ-tocopherol or without them should be recommended for patients with MAFLD to reduce its risk.
Introduction:
The incidence of non-alcoholic fatty liver disease (NAFLD) has increased in recent
years. Hepatic fibrosis (HF) is an important step in the progression of NAFLD to cirrhosis and even carcinoma
and is also recognized as a possible reversal phase.
Aims:
We previously found that the aqueous extract of Sedum Lineare Thunb. has hepatoprotective effects.
This study investigated the hepatoprotective effect and mechanism of the Sedum Lineare Thunb. n-butanol
phase (SLNP) on HF in rats.
Methods:
Animals were intraperitoneally injected with thioacetamide solution twice a week for 8 weeks to prepare
an HF model and were administered the corresponding drugs or an equal volume of normal saline by intragastric
administration once a day for 8 weeks. Liver function, hydroxyproline and malondialdehyde (MDA)
content, superoxide dismutase (SOD), Na+-K+-ATPase, and Ca2+-Mg2+-ATPase were analyzed using colorimetric
methods. Moreover, mRNA expression and protein levels in the liver tissue were detected via quantitative
polymerase chain reaction and western blotting, respectively.
Results:
The results showed that SLNP could effectively improve the liver function of rats with HF and significantly
reduce the content of hydroxyproline; the mRNA expression and protein levels of alpha-smooth muscle
actin (α-SMA), collagen I, III, and IV, transforming growth factor beta 1 (TGF-β1), Smad2/3, and Smad4
were also significantly reduced. Simultaneously, SLNP significantly increased the activities of SOD, Na+-K+-
ATPase, and Ca2+-Mg2+-ATPase in the rat liver tissues, whereas it reduced the levels of MDA and SOD in the
serum and liver tissues.
Conclusion:
This study revealed that SLNP elicits an anti-fibrotic effect by inhibiting oxidative stress and stellate
cell activation, thereby reducing the formation and deposition of the extracellular matrix. The TGF-β1/Smads
signaling pathway may be involved in this process
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