scholarly journals Camel milk ameliorates inflammatory mechanisms in an alcohol-induced liver injury mouse model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liang Ming ◽  
Bule Qi ◽  
Shiqi Hao ◽  
Rimutu Ji
Keyword(s):  
Liver Injury ◽  
Liver Tissue ◽  
Chronic Alcoholism ◽  
Camel Milk ◽  
Inflammatory Factors ◽  
Control Group ◽  
Chronic Alcoholic ◽  
Inflammatory Mechanism ◽  
Proteomic Analyses ◽  
Gut Microbial Community

AbstractCamel milk (CM) is considered to protect the liver in the practice of traditional medicine in nomadic areas. The purpose of the present study was to investigate the effects of CM on the hepatic biochemical and multiple omics alterations induced by chronic alcoholic liver disease (ALD). An intragastric gavage mice Lieber DeCarli + Gao binge model (NIAAA model) was employed to investigate the inflammatory mechanism of camel milk on the liver tissue of mice. A gut microbiota of the feces of mice and transcriptomic and proteomic analyses of the liver of mice were performed. Analysis of serum and liver biochemical indexes revealed that camel milk not only prevents alcohol-induced colonic dysfunction and lipid accumulation, but also regulates oxidative stress and inflammatory cytokine production to protect against chronic ALD in mouse. The gut microbial community of mice treated with camel milk was more similar to the untreated control group than to the model group, indicating that the intake of camel milk pre- and post-alcohol gavage effectively prevents and alleviates the intestinal microbial disorder caused by chronic alcoholism in mice. Furthermore, the results of the transcriptomic and proteomic analyses of the liver tissue showed that camel milk can improve alcoholic liver injury in mice by regulating inflammatory factors and immune system disruptions. This study provides insights into the molecular mechanism by which camel milk can be developed as a potential functional food with no side effects and against liver injury.

scholarly journals A Preliminary Study on the Effect of Hydrogen Gas on Alleviating Early CCl4-Induced Chronic Liver Injury in Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1933
Author(s):  
Jianwei Wang ◽  
Quancheng Cheng ◽  
Jinyu Fang ◽  
Huiru Ding ◽  
Huaicun Liu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Tissue ◽  
Uncoupling Protein ◽  
Liver Cells ◽  
Hydrogen Gas ◽  
Chronic Liver ◽  
Control Group ◽  
Protective Mechanism ◽  
Chronic Liver Injury ◽  
Ucp2 Expression

As a small-molecule reductant substance, hydrogen gas has an obvious antioxidant function. It can selectively neutralize hydroxyl radicals (•OH) and peroxynitrite (ONOO•) in cells, reducing oxidative stress damage. The purpose of this study was to investigate the effect of hydrogen gas (3%) on early chronic liver injury (CLI) induced by CCl4 and to preliminarily explore the protective mechanism of hydrogen gas on hepatocytes by observing the expression of uncoupling protein 2 (UCP2) in liver tissue. Here, 32 rats were divided into four groups: the control group, CCl4 group, H2 (hydrogen gas) group, and CCl4 + H2 group. The effect of hydrogen gas on early CLI was observed by serological tests, ELISA, hematoxylin and eosin staining, and oil red O staining. Immunohistochemical staining and Western blotting were used to observe the expression of UCP2 in liver tissues. We found that CCl4 can induce significant steatosis in hepatocytes. When the hydrogen gas was inhaled, hepatocyte steatosis was reduced, and the UCP2 expression level in liver tissue was increased. These results suggest that hydrogen gas might upregulate UCP2 expression levels, reduce the generation of intracellular oxygen free radicals, affect lipid metabolism in liver cells, and play a protective role in liver cells.

Anti-Inflammatory and Hepatoprotective Effects of Ganoderma lucidum Polysaccharides against Carbon Tetrachloride-Induced Liver Injury in Kunming Mice

Pharmacology ◽  
2019 ◽  
Vol 103 (3-4) ◽  
pp. 143-150 ◽  
Author(s):  
Yu-Sheng Chen ◽  
Quan-Zhan Chen ◽  
Zhen-Jiong Wang ◽  
Chun Hua
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Liver Tissue ◽  
Ganoderma Lucidum ◽  
Acute Liver Injury ◽  
Liver Weight ◽  
Inflammatory Factors ◽  
Ganoderma Lucidum Polysaccharides ◽  
Hepatoprotective Effects ◽  
Anti Inflammatory

Background: Ganoderma lucidum Polysaccharides (GLPS) were found to possess various pharmacological properties including anti-inflammatory and hepatoprotective activities. However, the effect and possible mechanism of GLPS treatment on liver injury have not yet been reported. Therefore, this study aimed to explore the potential anti-inflammatory and hepatoprotective effects and possible mechanism of GLPS in carbon tetrachloride (CCl4)-induced acute liver injury mice. Summary: GLPS significantly reduced the activation of NLRP3 inflammasome and improved liver function in liver injury mice. It significantly inhibited CCl4-induced changes of alanine aminotransferase and aspartate aminotransferase activities in serum, as well as nitric oxide synthase (NOS) and cytochrome P450 2E1 (CYP2E1) activities in liver tissue; it also remarkably decreased levels of liver weight and index, total bilirubin, interleukin (IL)-1β, IL-18, IL-6 and tumor necrosis factor-α in serum, as well as malondialdehyde and IL-1β in liver tissue. Protein expression levels of liver NLRP3, ASC, and Caspase-1 were also downregulated, while the glutathione level in liver tissue was remarkably enhanced in GLPS groups compared to that of the model group. Key Message: These results suggested that GLPS may be a potential for the prevention and treatment of acute liver injury with liver inflammation. The possible mechanism may be related to the inhibition of free radical lipid peroxidation, NOS, and CYP2E1 activities and activation of liver inflammatory factors.

scholarly journals UMBI UBI JALAR UNGU BALI (Ipomoea batatas) DI TRANSAMINASE SERUM, MALONDIALDEHIDE HEPAR DAN ALKOHOL KRONIS

2018 ◽  
Vol 17 (3) ◽  
pp. 151
Author(s):  
I Wayan Putu Sutirta-Yasa ◽  
I Made Jawi ◽  
Ida Bagus Ngurah ◽  
Anak Agung Ngurah Subawa
Keyword(s):  
Sweet Potato ◽  
Liver Tissue ◽  
Ipomoea Batatas ◽  
Ethanol Extract ◽  
Antioxidant Effect ◽  
Control Group ◽  
Chronic Alcoholic ◽  
Purple Sweet Potato ◽  
Group Post ◽  
Alcoholic Intake

Oxidative stress as a consequence of chronic alcoholic intake causes lesions of liver tissue. The objective of this study was to identifythe antioxidant effect of ethanol extract derived from Balinese purple sweet potato on the liver tissue in mice after chronic consumptionof alcohol. Subjects of this study were 32 adults male Swiss mice (12–14 weeks) divided into 4 groups with control group post-testonly design. Post-treatment of blood and liver samples were collected from each group of 8 mice. The MDA liver was quantified withthiobarbituric acid reactive substances (TBARS) method. Samples were collected from control group of 8 mice without sweet potatoextract and alcohol, 8 mice with 1 mg extract of Balinese purple sweet potato, 8 mice with 0.8 gram alcohol, and 8 mice with combineof alcohol and extract of Balinese purple sweet potato, each treatment was carried out every day for 4 weeks. The results showed asignificant increase of serum SGOT, SGPT and liver MDA level, after chronic consumption of alcohol (p = 0.00). The decrease of serumSGOT, SGPT and liver level MDA was significant in the group with extract of Balinese purple sweet potato (p = 0.00). The researchersconcluded that the extract of Balinese purple sweet potato had an antioxidant effect in mice which consumed alcohol chronically. Basedon this study it is concluded that extract of Balinese purple sweet potato has a protective effect on the liver cell in mice which consumedalcohol chronically.

scholarly journals Study on the Mechanism of Salvia Miltiorrhiza Polysaccharides in Relieving Liver Injury of Broilers Induced by Fluorophenicol

2021 ◽  
Author(s):  
Yumeng Geng ◽  
Chunyu Lu ◽  
Guozhong Jin ◽  
Shuying Li ◽  
Yuqing Cui ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Liver Tissue ◽  
Tap Water ◽  
Salvia Miltiorrhiza ◽  
Serum Levels ◽  
Mapk Signaling ◽  
Liver Cells ◽  
Control Group ◽  
Daily Gain

Abstract In order to explore the transcriptomics and proteomics targets and pathways of Salvia miltiorrhiza polysaccharides (SMPs) alleviating florfenicol (FFC)-induced liver injury in broilers,60 1-day-old broilers were randomly divided into 3 groups: control group ( GP1) was fed tap water, FFC model (GP2) was given tap water containing FFC 0.15 g/L, and SMPs treatment group (GP3) was given tap water containing FFC 0.15 g/L and SMPs 5 g/L.Starting from 1 day of age, the drug was administered continuously for 5 days. On the 6th day, blood was collected from the heart and the liver was taken. Then 3 chickens were randomly taken from each group, and their liver tissues were aseptically removed and placed in an enzyme-free tube. Using high-throughput mRNA sequencing and TMT-labeled quantitative proteomics technology, the transcriptome and proteome of the three groups of broiler liver were analyzed respectively. The results of the study showed that the liver tissue morphology of the chicks in the GP1 and GP3 groups was complete, and there were no obvious necrotic cells in the liver cells. The liver tissue cells in the GP2 group showed obvious damage, the intercellular space increased, and the liver cells showed extensive vacuolation and steatosis. Compared with the GP1 group, the daily gain of chicks in the GP2 group was significantly reduced (P < 0.0 5 or P < 0.01). Compared with the GP2 group, the GP3 group significantly increased the daily gain of chicks (P <0.0 5 or P <0.01). Compared with the GP1 group, the serum levels of ALT, AST, liver LPO, ROS and IL-6 in the GP2 group were significantly increased (P < 0.0 5 or P < 0.01), and the contents of T-AOC, GSH-PX, IL-4 and IL-10 in the liver were significantly decreased (P < 0.0 5 o r P < 0.01). After SMPs treatment, the serum levels of ALT, AST, liver LPO, ROS and IL-6 were significantly reduced (P < 0.0 5 or P < 0.01), and the contents of T-AOC, GSH-PX, IL-4 and IL-10 in the liver were significantly increased (P < 0.0 5 or P < 0.01). There were 380 mRNA and 178 protein differentially expressed between GP2 group and GP3 group. Part of DEGs was randomly selected for QPCR verification, and the expression results of randomly selected FABP1, SLC16A1, GPT2, AACS and other genes were verified by QPCR to be consistent with the sequencing results, which demonstrated the accuracy of transcriptation-associated proteomics sequencing. The results showed that SMPs could alleviate the oxidative stress and inflammatory damage caused by FFC in the liver of chicken and restore the normal function of the liver. SMPs may alleviate the liver damage caused by FFC by regulating the drug metabolism - cytopigment P450, PPAR signaling pathway, MAPK signaling pathway, glutathione metabolism and other pathways.

scholarly journals Adalimumab Ameliorates Abdominal Aorta Cross Clamping Which Induced Liver Injury in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Erkan Cure ◽  
Medine Cumhur Cure ◽  
Levent Tumkaya ◽  
Yildiray Kalkan ◽  
Ibrahim Aydin ◽  
...  
Keyword(s):  
Liver Injury ◽  
Abdominal Aorta ◽  
Liver Tissue ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels

The aim of this study was to investigate the possible protective effects of adalimumab (ADA) on cell damage in rat liver tissue during ischemia/reperfusion (I/R) injury of infrarenal abdominal aorta. Thirty male Wistar-albino rats were divided into three groups: control, I/R, and I/R+ADA, each group containing 10 animals. Laparotomy without I/R injury was performed in the control group animals. Laparotomy in the I/R group was followed by two hours of infrarenal abdominal aortic cross ligation and then two hours of reperfusion. ADA (50 mg/kg) was administered intraperitoneally as a single dose, to the I/R+ADA group, five days before I/R. The tumor necrosis factor-alpha (TNF-α) (pg/mg protein) and nitric oxide (NO) (µmol/g protein) levels in the I/R group (430.8 ± 70.1, 8.0 ± 1.1, resp.) were significantly higher than those in the I/R+ADA group (338.0 ± 71.6,P=0.006; 6.3 ± 1.2,P=0.008) and the control group (345.5 ± 53.3,P=0.008; 6.5 ± 1.5,P=0.010, resp.). I/R causes severe histopathological injury to the liver tissue, but ADA leads to much less histopathological changes. ADA treatment significantly decreased the severity of liver I/R injury. ADA pretreatment may have protective effects on experimental liver injury.

scholarly journals Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-κB Signaling Pathway in Type 2 Diabetic Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Li-ping Han ◽  
Chun-jun Li ◽  
Bei Sun ◽  
Yun Xie ◽  
Yue Guan ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Diabetic Rats ◽  
Inflammatory Factors ◽  
Hepatic Tissue ◽  
Control Group ◽  
Dependent Manner ◽  
Protective Effects ◽  
Type 2 Diabetic

Immune and inflammatory pathways play a central role in the pathogenesis of diabetic liver injury. Celastrol is a potent immunosuppressive and anti-inflammatory agent. So far, there is no evidence regarding the mechanism of innate immune alterations of celastrol on diabetic liver injury in type 2 diabetic animal models. The present study was aimed at investigating protective effects of celastrol on the liver injury in diabetic rats and at elucidating the possible involved mechanisms. We analyzed the liver histopathological and biochemical changes and the expressions of TLR4 mediated signaling pathway. Compared to the normal control group, diabetic rats were found to have obvious steatohepatitis and proinflammatory cytokine activities were significantly upregulated. Celastrol-treated diabetic rats show reduced hepatic inflammation and macrophages infiltration. The expressions of TLR4, MyD88, NF-κB, and downstream inflammatory factors IL-1βand TNFαin the hepatic tissue of treated rats were downregulated in a dose-dependent manner. We firstly found that celastrol treatment could delay the progression of diabetic liver disease in type 2 diabetic rats via inhibition of TLR4/MyD88/NF-κB signaling cascade pathways and its downstream inflammatory effectors.

scholarly journals Anti-Oxidative and Immuno-Protective Effect of Camel Milk on Radiation-Induced Intestinal Injury in C57BL/6 J Mice

Dose-Response ◽  
2021 ◽  
Vol 19 (1) ◽  
pp. 155932582110037
Author(s):  
Yu-Zhong Chen ◽  
Chao Li ◽  
Jia Gu ◽  
Si-chen Lv ◽  
Jia-ying Song ◽  
...  
Keyword(s):  
Survival Rate ◽  
Protective Effect ◽  
Survival Time ◽  
Intestinal Injury ◽  
Camel Milk ◽  
Whole Body ◽  
Inflammatory Factors ◽  
Control Group ◽  
Irradiation Group ◽  
Radiation Induced

Purpose: The main objective is to investigate the protective effect of camel milk (CM) on radiation-induced intestinal injury. Methods: The C57BL/6 J mice in 2 experiments were assigned into control group (Con), irradiation group (IR), and CM+irradiation group (CM+IR). After receiving the CM via gavage for 14 days, the mice in the first experiment were exposed to 6 Gy X-ray whole body irradiation, and survival rate was compared among the groups. Mice in the second experiment were exposed to 4 Gy irradiation and sacrificed at day 7. The small intestines were collected to examine the histopathological changes and to determine the anti-oxidative index and HMGB1/TLR4 inflammatory pathway. Fasting blood was used to measure serum pro-inflammatory factors. Results: Compared with the IR group, the survival time was prolonged, and survival rate was increased in the CM+IR group. CM increased levels of SOD and GSH and decreased MDA in the jejunum. Furthermore, intestinal protein expression of HMGB1/TLR4 pathway (TLR4, NF-κB, and HMGB1) was up-regulated by CM intervention. CM decreased the serum levels of TNF-α and IL-1β and increased IL-10 level. Conclusions: CM extended the survival time and had a protective effect against radiation-induced jejunum injury by regulation of antioxidant capacity and HMGB1/TLR4/NF-κB/MyD88 inflammatory signaling pathway.

scholarly journals Thymoquinone Attenuates Immune Mediated Liver Injury Induced by Concanavalin A in Mice

2021 ◽  
Vol 30 (2) ◽  
pp. 50-57
Author(s):  
Halla A. Ahmad ◽  
Sarmed H. Kathem
Keyword(s):  
Liver Injury ◽  
Inflammatory Cytokines ◽  
Liver Damage ◽  
Concanavalin A ◽  
Liver Tissue ◽  
Tissue Homogenate ◽  
Control Group ◽  
Dependent Manner ◽  
Immune Mediated ◽  
Dose Dependent

Autoimmune hepatitis is an inflammatory disease and its incidence has been increasing. The features of hepatitis are the release of inflammatory cytokines, the elevation of AST and ALT, and hepatocyte apoptosis and necrosis. Concanavalin A considered as essential model represents the acute immune-mediated liver damage in rodents. Thymoquinone is well known herbal compound that exert hepatoprotective, anti-inflammatory, and antioxidant activity. In this study, we focus on the immunoregulatory and liver protective effect of thymoquinone in a mouse model of concanavalin A-induced liver injury. Twenty-four male mice were randomly divided into four groups each containing six animals: Negative control group, concanavalin A model group, thymoquinone 15mg/kg group, and thymoquinone 30mg/kg group. Blood was collected to detect the activities of alanine transaminase (ALT) and aspartate transaminase (AST) as well as liver tissue for the detection of tumor necrosis factor  levels, after 8 hours of concanavalin A injection. Injecting mice with concanavalin resulted in a dramatic increase in serum level of both ALT and AST which indicate severe liver tissue damage with a significant increase in inflammatory cytokines TNF alpha - and INF  levels, with a notable increase in NF-kB gene expression in mice liver tissue homogenate. Thymoquinone pretreatment revealed a dose-dependent increase in liver tissue protection. Conclusion: Thymoquinone has hepatoprotective and immune modulatory effects in concanavalin A induced immune mediated liver damage. Thymoquinone exerted its effect through attenuating NF and its downstream effectors TNF  and INF  in a dose dependent manner.

Pregabalin, a GABA Analogue Protects against Carbon Tetrachloride-Induced Oxidative Stress and Liver Injury in Rats

2021 ◽  
Vol 11 ◽  
Author(s):  
Omar M.E. Abdel-Salam ◽  
Eman R. Youness ◽  
Fatma A. Morsy ◽  
Amany Ameen Sleem
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Dna Fragmentation ◽  
Liver Tissue ◽  
Paraoxonase 1 ◽  
Control Group ◽  
Acute Administration ◽  
Synthetic Analogue ◽  
Serum Aminotransferases

Pregabalin is a synthetic analogue of the neurotransmitter g-aminobutyric acid (GABA) and is used in the treatment of epilepsy and neuropathic pain. The aim of this study was to investigate the effect of pregabalin on toxic liver injury caused by the acute administration of carbon tetrachloride (CCl4). Rats were orally treated with CCl4 for two successive days either alone or along with intraperitoneal pregabalin at doses of 7 and 14 mg/kg. The control group received the vehicle (olive oil). Liver oxidative stress and damage were assessed by determining serum and/or liver tissue levels of malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), DNA fragmentation, serum aminotransferases, paraoxonase-1 (PON-1), and hepatic histopathology. Results showed that CCl4 significantly (i) increased MDA and NO and decreased PON-1 in both serum and liver tissue, and (ii) decreased liver GSH content and induced marked hepatic DNA fragmentation. CCl4 treatment caused liver tissue injury as evidenced by significantly increased serum aminotransferases. In line with the above biochemical changes, the liver of CCl4-treated rats exhibited massive steatosis, vacuolar degeneration, cloudy swelling, and necrosis. In CCl4-treated rats, pregabalin given at the dose of 14 mg/kg significantly reduced the increments in MDA, NO, serum aminotransferases, and hepatic DNA fragmentation. Liver GSH was unaltered but hepatic and serum PON-1 activity increased after administering pregabalin which also improved, though not normalized, liver tissue histopathology. Collectively, these results suggest that the administration of pregabalin is associated with a reduction in experimental liver injury caused by CCl4. (First online: Apr 12, 2021)

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.

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