scholarly journals Auricularia auricula Melanin Protects against Alcoholic Liver Injury and Modulates Intestinal Microbiota Composition in Mice Exposed to Alcohol Intake

Foods ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2436
Author(s):  
Yichen Lin ◽  
Hua Chen ◽  
Yingjia Cao ◽  
Yuanhui Zhang ◽  
Wenfeng Li ◽  
...  

The potential effects of Auricularia auricula melanin (AAM) on the intestinal flora and liver metabolome in mice exposed to alcohol intake were investigated for the first time. The results showed that oral administration of AAM significantly reduced the abnormal elevation of serum total triglyceride (TG), cholesterol (TC), low density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and significantly inhibited hepatic lipid accumulation and steatosis in mice exposed to alcohol intake. Besides, the abnormally high levels of bile acids (BAs) and lactate dehydrogenase (LDH) in the liver of mice with alcohol intake were significantly decreased by AAM intervention, while the hepatic levels of glutathione (GSH) and superoxide dismutase (SOD) were appreciably increased. Compared with the model group, AAM supplementation significantly changed the composition of intestinal flora and up-regulated the levels of Akkermansia, Bifidobacterium, Romboutsia, Muribaculaceae, Lachnospiraceae_NK4A136_group, etc. Furthermore, liver metabolomics demonstrated that AAM had a significant regulatory effect on the composition of liver metabolites in mice with alcohol intake, especially the metabolites involved in phosphatidylinositol signaling system, ascorbate and aldarate metabolism, starch and sucrose metabolism, galactose metabolism, alpha-linolenic acid metabolism, glycolysis/gluconeogenesis, and biosynthesis of unsaturated fatty acids. At the gene level, AAM treatment regulated the mRNA levels of lipid metabolism and inflammatory response related genes in liver, including ACC-1, FASn, CPT-1, CD36, IFN-γ, LDLr and TNF-α. Conclusively, these findings suggest that AAM has potential beneficial effects on alleviating alcohol-induced liver injury and is expected to become a new functional food ingredient.

2022 ◽  
Vol 2022 ◽  
pp. 1-12
Author(s):  
Jingxuan Zhou ◽  
Nanhai Zhang ◽  
Liang Zhao ◽  
Mohamed Mohamed Soliman ◽  
Wei Wu ◽  
...  

Honey-processed Astragalus (HPA) is a mixture of Astragalus and honey, which is a processed product of Chinese medicine. It has the active ingredients of Astragalus and the unique effects of honey. However, the mechanism of HPA for improving alcoholic liver disease (ALD) is not clear. The purpose of this study is to explore the ameliorating effect and mechanism of HPA (4 and 8 g/kg bw) on alcoholic liver injury. Two doses of HPA were orally administered to alcohol-treated mice for four weeks. The results showed that HPA could effectively reduce triglycerides (TG) by 59% and free fat acid (FFA) and total cholesterol (TC) in serum and hepatic were reduced by least 25.9%. HPA could cause a decrease in serum low-density lipoprotein cholesterol (LDL-C) from 0.145 mM to 0.117 mM, and the serum high-density lipoprotein cholesterol (HDL-C) was increased. After alcohol-treated mice were supplemented with HPA, antioxidant markers (superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and Glutathione peroxidase (GSH-Px)), liver function index (alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP)), proinflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)), and liver tissue were all significantly improved. This is related to the fact that HPA can promote the expression of oxidative stress-related genes and inhibit the expression of inflammation-related genes. In addition, HPA could also regulate the disturbance of the intestinal microflora. In general, HPA could significantly improve the accumulation of serum and liver lipids caused by alcohol and the imbalance of intestinal flora in mice. It could also improve liver function, oxidative stress, and inflammation.


2021 ◽  
Author(s):  
Yanna Fan ◽  
Lu Yan ◽  
Mengyao Li ◽  
Zhiyu Pu ◽  
Yannan Zhang ◽  
...  

Abstract Previous studies had indicated that the gut microbiota was a main internal factor leading to obesity through energy storage and metabolic disorders. Lycium Barbarum Polysaccharides (LBP) have been discovered with a more protective effect on intestinal flora. But it is unclear whether LBP could regulate the gut microbiota to modulate metabolites, finally relieving obesity. A related study of high-throughput 16S rRNA sequencing and serum metabolomics profiling in LBP intervention on high fat diet-induced obese rats then explored the beneficial effects of LBP and the underlying mechanism. LBP affected lipid parameters such as total cholesterol, Triglyceride, and High-density lipoprotein. The gut microbiota result detected 16 types of the phylum of bacteria in total, while four of them (Bacteroidetes, Firmicutes, Proteobacteria, Deferribacteres) were significantly different. LBP upregulated the level of Firmicutes of obese rats. LBP might associate with the gut microbiota that participates in the membrane transport and metabolism of amino acid, carbohydrate, energy, and lipid. The serum metabolomics profiling of high-fat diet-induced obesity rats found over 30 differential metabolites between model and intervention groups. Primary metabolites include cortisol, glycohyocholic acid, homo-L-arginine, ursodeoxycholic acid, isoursodeoxycholic acid, glycoursocholic acid, 4-ethylphenylsulfate, deoxycholic acid, 7-hydroxy-3-oxocholanoic acid isomers, gly-phe, pipecolic acid, proline betaine, and pyrocatechol sulfate. Pathway analysis in serum found four disorder pathways: glycerophospholipid metabolism, glycine-serine-threonine metabolism, biosynthesis of unsaturated fatty acids, and linoleic acid metabolism. The studies revealed that LBP treatment increased the diversity of fecal microorganisms and reduced metabolic disorders in obese rats. LBP ameliorated metabolic disorders and rebalanced the gut microbiome.


2019 ◽  
Vol 20 (5) ◽  
pp. 422-432 ◽  
Author(s):  
Yu-lin Tan ◽  
Han-xiao Ou ◽  
Min Zhang ◽  
Duo Gong ◽  
Zhen-wang Zhao ◽  
...  

Background: Tanshinone IIA (Tan IIA) and Omentin-1 have a protective role in the cardiovascular system. However, if and how Tan IIA and Omentin-1 regulate cholesterol metabolism in macrophages has not been fully elucidated. Objective: To investigate the possible mechanisms of Tan IIA and Omentin-1 on preventing macrophage cholesterol accumulation and atherosclerosis development. Methods: The effect of Tan IIA on the protein and mRNA levels of Omentin-1 and ATP-binding cassette transporter A1 (ABCA1) in macrophages was examined by Western blot and qRT-PCR assay, respectively. Cholesterol efflux was assessed by liquid scintillation counting (LSC). Cellular lipid droplet was measured by Oil Red O staining, and intracellular lipid content was detected by high performance liquid chromatography (HPLC). In addition, the serum lipid profile of apoE−/− mice was measured by enzymatic method. The size of atherosclerotic lesion areas and content of lipids and collagen in the aortic of apoE−/− mice were examined by Sudan IV, Oil-red O, and Masson staining, respectively. Results: Tan IIA up-regulated expression of Omentin-1 and ABCA1 in THP-1 macrophages, promoting ABCA1-mediated cholesterol efflux and consequently decreasing cellular lipid content. Consistently, Tan IIA increased reverse cholesterol transport in apoE−/− mice. Plasma levels of high-density lipoprotein cholesterol (HDL-C), ABCA1 expression and atherosclerotic plaque collagen content were increased while plasma levels of low-density lipoprotein cholesterol (LDL-C) and atherosclerotic plaque sizes were reduced in Tan IIA-treated apoE−/− mice. These beneficial effects were, however, essentially blocked by knockdown of Omentin-1. Conclusion: Our results revealed that Tan IIA promotes cholesterol efflux and ameliorates lipid accumulation in macrophages most likely via the Omentin-1/ABCA1 pathway, reducing the development of aortic atherosclerosis.


2021 ◽  
Vol 11 (1) ◽  
pp. 390
Author(s):  
Beom-Rak Choi ◽  
Il-Je Cho ◽  
Su-Jin Jung ◽  
Jae-Kwang Kim ◽  
Dae-Geon Lee ◽  
...  

Lemon balm and dandelion are commonly used medicinal herbs exhibiting numerous pharmacological activities that are beneficial for human health. In this study, we explored the protective effects of a 2:1 (w/w) mixture of lemon balm and dandelion extracts (MLD) on carbon tetrachloride (CCl4)-induced acute liver injury in mice. CCl4 (0.5 mL/kg; i.p.) injection inhibited body weight gain and increased relative liver weight. Pre-administration of MLD (50–200 mg/kg) for 7 days prevented these CCl4-mediated changes. In addition, histopathological analysis revealed that MLD synergistically alleviated CCl4-mediated hepatocyte degeneration and infiltration of inflammatory cells. MLD decreased serum aspartate aminotransferase and alanine transferase activities and reduced the number of liver cells that stained positive for cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase, suggesting that MLD protects against CCl4-induced hepatic damage via the inhibition of apoptosis. Moreover, MLD attenuated CCl4-mediated lipid peroxidation and protein nitrosylation by restoring impaired hepatic nuclear factor erythroid 2-related factor 2 mRNA levels and its dependent antioxidant activities. Furthermore, MLD synergistically decreased mRNA and protein levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the liver. Together, these results suggest that MLD has potential for preventing acute liver injury by inhibiting apoptosis, oxidative stress, and inflammation.


Author(s):  
Sihoon Park ◽  
Jae-Joon Lee ◽  
Hye-Won Shin ◽  
Sunyoon Jung ◽  
Jung-Heun Ha

Soybean koji refers to steamed soybeans inoculated with microbial species. Soybean fermentation improves the health benefits of soybeans. Obesity is a serious health concern owing to its increasing incidence rate and high association with other metabolic diseases. Therefore, we investigated the effects of soybean and soybean koji on high-fat diet-induced obesity in rats. Five-week-old male Sprague-Dawley rats were randomly divided into four groups (n = 8/group) as follows: (1) regular diet (RD), (2) high-fat diet (HFD), (3) HFD + steamed soybean (HFD+SS), and (4) HFD + soybean koji (HFD+SK). SK contained more free amino acids and unsaturated fatty acids than SS. In a rat model of obesity, SK consumption significantly alleviated the increase in weight of white adipose tissue and mRNA expression of lipogenic genes, whereas SS consumption did not. Both SS and SK reduced serum triglyceride, total cholesterol, and low-density lipoprotein cholesterol levels, and increased high-density lipoprotein cholesterol levels. SS and SK also inhibited lipid accumulation in the liver and white adipose tissue and reduced adipocyte size. Although both SS and SK could alleviate HFD-induced dyslipidemia, SK has better anti-obesity effects than SS by regulating lipogenesis. Overall, SK is an excellent functional food that may prevent obesity.


2008 ◽  
Vol 295 (1) ◽  
pp. G45-G53 ◽  
Author(s):  
Bin Hu ◽  
Lisa M. Colletti

Stem cell factor (SCF) and its receptor c-kit are important in hematopoiesis and cellular proliferation. c-kit has also been identified as a cell surface marker for progenitor cells. We have previously shown that there is a large reservoir of hepatic SCF, and this molecule plays a significant role in liver regeneration after 70% hepatectomy. In the current study, we further examined the expression of SCF and c-kit in acetaminophen (APAP)-induced liver injury in C57BL/6J mice or SCF-deficient sl-sld mice and their appropriate wild-type controls. Following APAP-induced liver injury, c-kit mRNA expression increased, with peak levels detected 48 h postinjury. Hepatic SCF mRNA levels after APAP injury were also increased, with peak levels seen 16 h post-APAP. The mortality rate in SCF-deficient mice treated with APAP was significantly higher than that of wild-type mice; furthermore, administration of exogenous SCF significantly reduced the mortality of APAP-treated wild-type mice. Bromodeoxyuridine incorporation experiments showed that SCF significantly increased hepatocyte proliferation at 48 and 72 h in APAP-treated mice. SCF inhibited APAP-induced hepatocyte apoptosis and increased Bcl-2 and Bcl-xL expression, suggesting that this decrease in hepatocyte apoptosis is mediated through Bcl-2 and Bcl-xL. In summary, SCF and c-kit expression was increased after APAP-induced liver injury. Administration of exogenous SCF reduces mortality in APAP-treated mice, increases hepatocyte proliferation, and prevents hepatocyte apoptosis induced by APAP, suggesting that these molecules are important in the liver's recovery from these injuries.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Linton R Harriss ◽  
Dallas R English ◽  
Rory Wolfe ◽  
Andrew M Tonkin ◽  
Kerin O’Dea ◽  
...  

Introduction: Alcohol intake is positively associated with high-density lipoprotein (HDL) cholesterol, however no studies have investigated the association with lipoprotein sub-classes using nuclear magnetic resonance spectroscopy (NMR). Hypothesis: We assessed the hypothesis that usual daily alcohol intake (volume), beverage type and drinking frequency influence plasma HDL sub-class concentrations as determined by NMR. Methods: Six hundred and ninety volunteers (389 women) aged 40 – 69 years at baseline (1990 –1994) participated in a cross-sectional study using the Melbourne Collaborative Cohort Study, Australia. Measures included self-reported alcohol intake using beverage-specific quantity-frequency questions (volume) and a drinking diary for previous week (frequency). Results: Median alcohol intake was 15.2 g/d (2.7, 32.0) for men and 1.0 g/d (0, 9.6) for women. Alcohol volume was positively associated with total HDL particle concentration in men and women. For men, a 10 g/d increment in alcohol intake increased total HDL particle concentration by 0.62 μmol/L (95% CI: 0.27, 0.98) and small HDL particle concentration by 0.34 μmol/L (0.01, 0.68). For women, total HDL particle concentration increased 1.06 μmol/L (0.60, 1.53) for every 10 g/d increment in alcohol intake. Alcohol volume was positively associated with large HDL particle concentration in premenopausal women [0.67 μmol/L (0.19, 1.15)] and small HDL particle concentration in postmenopausal women [0.82 μmol/L (0.14, 1.51)]. Beer, wine and spirits were all positively associated with total HDL concentration for men. Beer and wine were both positively associated with total HDL concentration for women. Drinking frequency was not associated with total HDL particle concentration or any of its’ sub-classes. Conclusions: Alcohol volume (and not drinking frequency) was positively associated with NMR-determined plasma total HDL particle concentration for men and women. These associations appeared to be regardless of beverage type, although comparison of beverage types was not possible for women. These results suggest that for any given weekly volume of alcohol, the number of drinking days does not influence HDL particle concentration.


2001 ◽  
Vol 281 (6) ◽  
pp. G1348-G1356 ◽  
Author(s):  
Amin A. Nanji ◽  
Kalle Jokelainen ◽  
Maryam Fotouhinia ◽  
Amir Rahemtulla ◽  
Peter Thomas ◽  
...  

Alcoholic liver injury is more severe and rapidly developing in women than men. To evaluate the reason(s) for these gender-related differences, we determined whether pathogenic mechanisms important in alcoholic liver injury in male rats were further upregulated in female rats. Male and age-matched female rats (7/group) were fed ethanol and a diet containing fish oil for 4 wk by intragastric infusion. Dextrose isocalorically replaced ethanol in control rats. We analyzed liver histopathology, lipid peroxidation, cytochrome P-450 (CYP)2E1 activity, nonheme iron, endotoxin, nuclear factor-κB (NF-κB) activation, and mRNA levels of cyclooxygenase-1 (COX-1) and COX-2, tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-2 (MIP-2). Alcohol-induced liver injury was more severe in female vs. male rats. Female rats had higher endotoxin, lipid peroxidation, and nonheme iron levels and increased NF-κB activation and upregulation of the chemokines MCP-1 and MIP-2. CYP2E1 activity and TNF-α and COX-2 levels were similar in male and female rats. Remarkably, female rats fed fish oil and dextrose also showed necrosis and inflammation. Our findings in ethanol-fed rats suggest that increased endotoxemia and lipid peroxidation in females stimulate NF-κB activation and chemokine production, enhancing liver injury. TNF-α and COX-2 upregulation are probably important in causing liver injury but do not explain gender-related differences.


Genes ◽  
2018 ◽  
Vol 9 (8) ◽  
pp. 410 ◽  
Author(s):  
Daniel Castellano-Castillo ◽  
Isabel Moreno-Indias ◽  
Jose Carlos Fernandez-Garcia ◽  
Mercedes Clemente-Postigo ◽  
Manuel Castro-Cabezas ◽  
...  

Epigenetic marks, and especially DNA methylation, are becoming an important factor in obesity, which could help to explain its etiology and associated comorbidities. Adipose tissue, now considered as an important endocrine organ, produces complement system factors. Complement component 3 (C3) turns out to be an important protein in metabolic disorders, via either inflammation or the C3 subproduct acylation stimulating protein (ASP) which directly stimulates lipid storage. In this study, we analyze C3 DNA methylation in adipose tissue from subjects with a different grade of obesity. Adipose tissue samples were collected from subjects with a different degree of obesity determined by their body mass index (BMI) as: Overweight subjects (BMI ≥ 25 and <30), obese class 1/2 subjects (BMI ≥ 30 and <40) and obese class 3 subjects (BMI ≥ 40). C3 DNA methylation was measured for 7 CpGs by pyrosequencition using the Pyromark technology (Qiagen, Madrid Spain). C3 messenger RNA (mRNA) levels were analyzed by pre-designed Taqman assays (Applied biosystems, Foster City, CA, USA) and ASP/C3a was measured using a ELISA kit. The data were analyzed using the statistic package SPSS. C3 DNA methylation levels were lower in the morbid obese group. Accordingly, C3 methylation correlated negatively with BMI and leptin. However, C3 mRNA levels were more associated with insulin resistance, and positive correlations with insulin, glucose and homeostasis model assessment-estimated insulin resistance (HOMA-IR) existed. ASP correlated negatively with high density lipoprotein (HDL) cholesterol. C3 methylation levels were associated to adiposity variables, such as BMI and leptin, while the C3 mRNA levels were associated to glucose metabolism.


1995 ◽  
Vol 311 (1) ◽  
pp. 167-173 ◽  
Author(s):  
A J Bennett ◽  
M A Billett ◽  
A M Salter ◽  
E H Mangiapane ◽  
J S Bruce ◽  
...  

Different dietary fatty acids exert specific effects on plasma lipids but the mechanism by which this occurs is unknown. Hamsters were fed on low-cholesterol diets containing triacylglycerols enriched in specific saturated fatty acids, and effects on plasma lipids and the expression of genes involved in hepatic lipoprotein metabolism were measured. Trimyristin and tripalmitin caused significant rises in low-density lipoprotein (LDL) cholesterol which were accompanied by significant reductions in hepatic LDL receptor mRNA levels. Tripalmitin also increased hepatic expression of the apolipoprotein B gene, implying an increased production of LDL via very-low-density lipoprotein (VLDL) and decreased removal of LDL in animals fed this fat. Hepatic levels of 3-hydroxy-3-methylglutaryl-CoA reductase mRNA did not vary significantly between the groups. Compared with triolein, tristearin had little effect on hepatic gene expression or total plasma cholesterol. However, it caused a marked decrease in VLDL cholesterol and a rise in LDL cholesterol such that overall it appeared to be neutral. Lipid analysis suggested a rapid desaturation of much of the dietary stearate. The differential changes in plasma lipids and hepatic mRNA levels induced by specific dietary fats suggests a role for fatty acids or a metabolite thereof in the regulation of the expression of genes involved in lipoprotein metabolism.


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