scholarly journals Synbiotics Alleviate Hepatic Damage, Intestinal Injury and Muscular Beclin-1 Elevation in Rats after Chronic Ethanol Administration

2021 ◽  
Vol 22 (22) ◽  
pp. 12547
Author(s):  
Yi-Hsiu Chen ◽  
Wan-Chun Chiu ◽  
Qian Xiao ◽  
Ya-Ling Chen ◽  
Hitoshi Shirakawa ◽  
...  
Keyword(s):  
Liver Damage ◽  
Muscle Protein ◽  
Liquid Diet ◽  
Beclin 1 ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Control Group ◽  
Beneficial Effects ◽  
Ethanol Feeding ◽  
Cyp2e1 Expression

The purpose of this study was to investigate the beneficial effects of synbiotics on liver damage, intestinal health, and muscle loss, and their relevance in rats with chronic ethanol feeding. Thirty Wistar rats fed with a control liquid diet were divided into control and synbiotics groups, which were respectively provided with water or synbiotics solution (1.5 g/kg body weight/day) for 2 weeks. From the 3rd to 8th week, the control group was divided into a C group (control liquid diet + water) and an E group (ethanol liquid diet + water). The synbiotics group was separated in to three groups, SC, ASE, and PSE. The SC group was given a control liquid diet with synbiotics solution; the ASE group was given ethanol liquid diet with synbiotics solution, and the PSE group was given ethanol liquid diet and water. As the results, the E group exhibited liver damage, including increased AST and ALT activities, hepatic fatty changes, and higher CYP2E1 expression. Intestinal mRNA expressions of occludin and claudin-1 were significantly decreased and the plasma endotoxin level was significantly higher in the E group. In muscles, beclin-1 was significantly increased in the E group. Compared to the E group, the PSE and ASE groups had lower plasma ALT activities, hepatic fatty changes, and CYP2E1 expression. The PSE and ASE groups had significantly higher intestinal occludin and claudin-1 mRNA expressions and lower muscular beclin-1 expression when compared to the E group. In conclusion, synbiotics supplementation might reduce protein expression of muscle protein degradation biomarkers such as beclin-1 in rats with chronic ethanol feeding, which is speculated to be linked to the improvement of intestinal tight junction and the reduction of liver damage.

Acute and chronic ethanol on hepatic oxygen ethanol and lactate metabolism in cats

1990 ◽  
Vol 258 (3) ◽  
pp. G411-G418 ◽  
Author(s):  
C. V. Greenway ◽  
W. W. Lautt
Keyword(s):  
Venous Blood ◽  
Chronic Administration ◽  
Chronic Ethanol ◽  
Ethanol Metabolism ◽  
Ethanol Administration ◽  
Control Group ◽  
Base Line ◽  
Acute Administration ◽  
Lactate Metabolism ◽  
O2 Uptake

The effects of increasing blood ethanol levels on hepatic hemodynamics and O2, ethanol, and lactate metabolism were studied in two groups of anesthetized cats: a control group and a group whose prior fluid intake contained 2, 4, then 8% ethanol for 24 days. Within each group, responses were compared in cats with acutely denervated and innervated livers. A hepatic venous long-circuit technique with an extracorporeal reservoir was used to allow hemodynamic measurements and repeated sampling of arterial, portal, and hepatic venous blood without depletion of the cats' blood volume. Vmax for ethanol was 105 +/- 9 and 91 +/- 6 mumol.min-1 g liver-1 and Km was 136 +/- 18 and 168 +/- 24 microM for control and chronic alcohol groups, respectively. There was no stimulation of ethanol metabolism after chronic administration. O2 uptake by the liver was not altered during acute ethanol administration in any group and base-line O2 uptakes before acute administration of ethanol were not different between normal and chronic ethanol groups. No evidence for a hypermetabolic state induced by chronic ethanol administration was seen in innervated or acutely denervated livers. Oxidation of ethanol required 40-45% of normal O2 uptake; thus other oxidative processes must have been suppressed during ethanol metabolism. Hepatic lactate uptake remained unaltered when ethanol metabolism was less than 0.5 Vmax, but was suppressed on an equimolar basis with ethanol metabolism when ethanol metabolism rose to greater than 0.5 Vmax. Thus lactate metabolism is one process that can be suppressed to allow ethanol metabolism without additional O2 uptake by the liver.

scholarly journals Mate Tea Prevents Oxidative Stress in the Blood and Hippocampus of Rats with Acute or Chronic Ethanol Administration

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Bianca Scolaro ◽  
Daniela Delwing-de Lima ◽  
José Geraldo Pereira da Cruz ◽  
Débora Delwing-Dal Magro
Keyword(s):  
Oxidative Stress ◽  
Chronic Administration ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Chronic Ethanol Administration ◽  
Mate Tea

Objective. The aim of this study was to evaluate the influence of acute and chronic intake of mate tea on the effects elicited by acute and chronic administration of ethanol.Methods. Oxidative stress was evaluated by measuring thiobarbituric acid-reactive substances (TBARS), as well as the activities of the antioxidant enzymes, catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the hippocampus and blood of rats. Male Wistar rats were randomly assigned to four groups, for both acute and chronic treatment: (1) control group, (2) treated group, (3) intoxicated group, (4) and intoxicated group treated with mate tea.Results. Both ethanol administrations significantly increased TBARS in plasma and hippocampus of rats and altered antioxidant enzyme activities, changes which were reverted by mate tea administration.Conclusions. Data indicate that acute and chronic ethanol administration induced oxidative stress in hippocampus and blood and that mate tea treatment was able to prevent this situation.

Chronic Alcoholism Decreases Polyunsaturated Fatty Acid Levels in Human Plasma, Erythrocytes, and Platelets – Influence of Chronic Liver Disease

1997 ◽  
Vol 78 (02) ◽  
pp. 808-812 ◽  
Author(s):  
María-Luisa Pita ◽  
José-María Rubio ◽  
María-Luisa Murillo ◽  
Olimpia Carreras ◽  
Mariá-José Delgado
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Alcoholism ◽  
Chronic Liver ◽  
Chronic Ethanol ◽  
Ethanol Ingestion ◽  
Control Group ◽  
Docosatetraenoic Acid ◽  
Long Chain

SummaryThe effect of chronic ethanol ingestion on fatty acid composition of plasma, erythrocyte and platelet phospholipids and on plasma 6-keto-PGF1α was studied. Two groups of alcoholic subjects, one of them with chronic liver disease, were studied and compared to a control group of healthy subjects. Linoleic acid was not affected by alcoholism but its larger metabolites arachidonic acid (20:4n6) and docosatetraenoic acid (22: 4n6) tended to be lower in erythrocytes and platelets of both groups of alcoholic patients; the decrease was more marked in the presence of chronic liver disease. Docosahexaenoic acid (22:6n3) was markedly decreased in plasma, erythrocytes and platelets obtained from alcoholic patients with chronic liver disease. Plasma levels of 6-keto-PGF1α, a metabolite of prostacyclin (PGI2), remained unchanged. We conclude that chronic ethanol ingestion induces important changes in long-chain polyunsaturated fatty acids, mainly in platelets, and that these changes are exacerbated when patients suffer from chronic liver disease.

Dietary Quercetin Alleviated DSS-induced Colitis in Mice Through Several Possible Pathways by Transcriptome Analysis

2020 ◽  
Vol 21 (15) ◽  
pp. 1666-1673 ◽  
Author(s):  
Yuanyang Dong ◽  
Jiaqi Lei ◽  
Bingkun Zhang
Keyword(s):  
Antioxidant Capacity ◽  
Underlying Mechanism ◽  
Control Group ◽  
Sequencing Analysis ◽  
Colon Tissue ◽  
Beneficial Effects ◽  
Intestinal Integrity ◽  
Inflammatory Bowel ◽  
Vegetables And Fruits ◽  
Key Pathways

Background: The prevalence of inflammatory bowel disease is rapidly increasing around the world. Quercetin is a flavonoid commonly found in vegetables and fruits and has been reported to exert numerous pharmacological activities such as enhancing antioxidant capacity or suppressing inflammation. Objective: We aimed to explore whether quercetin was effective for IBD and the underlying mechanism of quercetin for the ameliorative effects on the DSS-induced colitis in mice. Methods: Thirty-six mice were randomly assigned to three treatments, including the control group (Ctr), DSS-induced colitis group (DSS) and DSS-induced colitis supplemented with 500 ppm quercetin (DQ500). Colitis was induced by DSS intake, and body weight was recorded every day. After six days administration of DSS, intestinal permeability was measured, and the liver was taken for antioxidant enzyme tests. Colonic tissue was taken for the histopathlogical score and RNA-sequencing analysis. Results: In this experiment, dietary quercetin for 500ppm alleviated the DSS-induced colitis, possibly by strengthening intestinal integrity, liver antioxidant capacity. Based on the results of the transcriptome of colon tissue, several key genes were modulated by quercetin. ERK1/2-FKBP pathway and RXR-STAT3 pathway were involved in the development of IBD, furthermore, in the down-regulation of S100a8/9, FBN2 contributed to lowering the risk of colongenesis. Conclusion: We demonstrated that dietary quercetin alleviated the DSS-induced colitis in mice. This is most likely due to its beneficial effects on intestinal integrity and modulation of several key pathways. Based on our research, quercetin was a promising candidate for IBD and its pharmaceutical effects on both IBD and colongenesis need further research.

Lentiviral-Mediated Beclin-1 Overexpression Inhibits Cell Proliferation and Induces Autophagy of Human Esophageal Carcinoma Eca109 Cell Xenograft in Nude Mice

2020 ◽  
Vol 15 (1) ◽  
pp. 70-77
Author(s):  
Junhe Zhang ◽  
Weihua Dong
Keyword(s):  
Growth Rate ◽  
Cell Proliferation ◽  
Esophageal Carcinoma ◽  
Nude Mice ◽  
Beclin 1 ◽  
Control Group ◽  
Vector Group ◽  
Empty Vector ◽  
Empty Vector Group

Background: Esophageal carcinoma is one of the common malignant tumors in digestive tract. BECLIN-1 is a key gene that regulates autophagy, and its abnormal expression may be related with many human tumors. However, the mechanism of BECLIN-1 in esophageal carcinoma remains unknown. Objective: In this study, we explored the effect of BECLIN-1 overexpression on tumor growth in mice with esophageal carcinoma and its mechanism. Methods: Recombined lentiviral vector containing BECLIN-1 was used to transfect human esophageal carcinoma Eca109 cells and establish stable cell line. qRT-PCR was used to detect BECLIN-1 mRNA level in the transfected Eca109 cells, CCK-8 assay was used to detect cell proliferation. Beclin-1, P62 and LC3-II protein expression levels in Eca109 cells were detected using Western blot analysis. Subcutaneous xenograft nude mice model of human esophageal carcinoma was established, and the tumor growths in Beclin-1 group, control group and empty vector group were monitored. Beclin-1 protein expression in vivo was detected by immunohistochemistry. Results: Beclin-1 mRNA and protein were overexpressed in Eca109 cells. Compared with empty vector group, the growth rate of cells transfected with BECLIN-1 decreased significantly. Compared with the control group and empty vector group, the expression level of P62 protein in beclin-1 group was significantly decreased, while the expression level of LC3-II protein was significantly increased. The tumor growth rate in nude mice of Beclin-1 group was significantly lower than that of the control group and empty vector group, and Beclin-1 protein was mainly expressed in Beclin-1 group in vivo. Conclusion: BECLIN-1 can induce autophagy in esophageal carcinoma Eca109 cells, and it can significantly inhibit the growth of esophageal carcinoma.

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