scholarly journals Hepatoprotective Potential of Pomegranate in Curbing the Incidence of Acute Liver Injury by Alleviating Oxidative Stress and Inflammatory Response

2021 ◽  
Vol 12 ◽  
Author(s):  
Hamid Ali ◽  
Azra Jahan ◽  
Samrana Samrana ◽  
Abid Ali ◽  
Safdar Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Crude Extract ◽  
Defense Mechanism ◽  
Elevated Serum ◽  
Punica Granatum ◽  
Protective Mechanism ◽  
Central Vein ◽  
Scavenging Activity ◽  
Aqueous Fraction

Hepatitis is an inflammatory disease of the liver and is considered one of the leading causes of death worldwide. Due to its scavenging activity, Punica granatum may be used for the treatment and prevention of liver diseases. The current study investigated the protective mechanism underlying the effects of pomegranate against a rat model of carbon tetrachloride–induced liver injury. Intraperitoneal injection of CCl4 resulted in liver inflammation, oxidative stress, and accumulation of lipid in hepatocytes. CCl4 induced a downregulation of superoxide dismutase (SOD), glutathione (GSH), and melonaldehyde (MDA). Pomegranate protection was assessed in terms of biochemical parameters, histopathology, and immunohistochemistry. Promegranate administration decreased inflammation, elevated serum enzymes and ROS production, and countered the debilitating effects caused by CCl4. In addition, CCl4-induced histological changes were absent in the crude pomegranate extract group, which also enhanced the scavenging activity of reactive oxygen species by enhancing the antioxidant defense mechanism as confirmed by detecting MDA, SOD, and GSH expressions. The migration of CD68+ macrophages was halted at the injured area of the central vein and the number of macrophages was reduced to the normal control by the crude extract compared to the positive control silymarin group. Likewise, protective effects of ethylacetate and the aqueous fraction of the crude extract were also observed. However, the butanol and n-hexane fractions displayed increased levels of ALT, AST, and ALP as compared to silymarin. About 25% damage to hepatocytes was observed in the butanol and n-hexane group by histopathological examination, which is a little better compared to the CCl4-treated group. The crude extract and its ethyl acetate and aqueous fractions may be accountable for the hepatoprotective potential of Punica granatum, which was further confirmed by in vivo experiments. Together, these findings confirm that pomegranate exerts hepatoprotective activity against CCl4-induced oxidative stress and liver damage.

scholarly journals Arctium lappa Root Extract Prevents Lead-Induced Liver Injury by Attenuating Oxidative Stress and Inflammation, and Activating Akt/GSK-3β Signaling

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 582
Author(s):  
Ahlam Alhusaini ◽  
Laila Fadda ◽  
Iman H. Hasan ◽  
Hanaa M. Ali ◽  
Naglaa F. El Orabi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Dna Fragmentation ◽  
Caspase 3 ◽  
Glycogen Synthase ◽  
Elevated Serum ◽  
Antioxidant Defenses ◽  
Root Extract ◽  
Arctium Lappa ◽  
Gsk 3Β

Arctium lappa L. (A. lappa) is a popular medicinal plant with promising hepatoprotective activity. This study investigated the protective effect of A. lappa root extract (ALRE) on lead (Pb) hepatotoxicity, pointing to its ability to modulate oxidative stress, inflammation, and protein kinase B/Akt/glycogen synthase kinase (GSK)-3β signaling. Rats received 50 mg/kg lead acetate (Pb(Ac)2) and 200 mg/kg ALRE or vitamin C (Vit. C) for 7 days, and blood and liver samples were collected. Pb(Ac)2 provoked hepatotoxicity manifested by elevated serum transaminases and lactate dehydrogenase, and decreased total protein. Histopathological alterations, including distorted lobular hepatic architecture, microsteatotic changes, congestion, and massive necrosis were observed in Pb(II)-induced rats. ALRE ameliorated liver function and prevented all histological alterations. Pb(II) increased hepatic lipid peroxidation (LPO), nitric oxide (NO), caspase-3, and DNA fragmentation, and serum C-reactive protein, tumor necrosis factor-α, and interleukin-1β. Cellular antioxidants, and Akt and GSK-3β phosphorylation levels were decreased in the liver of Pb(II)-induced rats. ALRE ameliorated LPO, NO, caspase-3, DNA fragmentation and inflammatory mediators, and boosted antioxidant defenses in Pb(II)-induced rats. In addition, ALRE activated Akt and inhibited GSK-3β in the liver of Pb(II)-induced rats. In conclusion, ALRE inhibits liver injury in Pb(II)-intoxicated rats by attenuating oxidative injury and inflammation, and activation of Akt/GSK-3β signaling pathway.

Caffeine affects HFD-induced hepatic steatosis by multifactorial intervention

2017 ◽  
Vol 37 (9) ◽  
pp. 983-990 ◽  
Author(s):  
MG Helal ◽  
SE Ayoub ◽  
WF Elkashefand ◽  
TM Ibrahim
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Fatty Acid Synthase ◽  
De Novo ◽  
Histopathological Examination ◽  
Elevated Serum ◽  
De Novo Lipogenesis ◽  
Control Group ◽  
Standard Diet ◽  
And Oxidative Stress

The incidence of nonalcoholic fatty liver disease (NAFLD) is considered a risk factor for hepatic fibrosis. Therefore, there is critical need to develop novel cheap and effective therapeutic approaches to prevent and reverse NAFLD. Caffeine is commonly consumed beverage and has antioxidant and anti-inflammatory activities. This study examined whether caffeine can ameliorate liver injury induced by high-fat diet (HFD) feeding. Four groups of rats were used and treated for 16 weeks as follows: control group, rats were fed a standard diet; HFD group, rats were fed HFD; and caffeine 20 and caffeine 30 groups, rats were fed HFD for 16 weeks in addition to different doses of caffeine (20 or 30 mg/kg, respectively) for last 8 weeks. The HFD-induced liver injury is determined biochemically by evaluating serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin, bilirubin, triglycerides, cholesterol, and high-density lipoprotein-cholesterol and by histopathological examination. Tissue malondialdehyde, total nitrate/nitrite, and glutathione concentration were also measured. Real-time reverse transcription polymerase chain reaction technique was used to determine the expression of lipogenic enzyme genes. Caffeine treatment significantly decreased the elevated serum ALT, AST, and bilirubin and increased the reduced albumin level. Interestingly, the hepatic mRNA expression of Fatty acid synthase and acetyl CoA carboxylase was decreased by caffeine, while the protein expression of hepatic carnitine palmitoyltransferase 1 and proliferation-activated receptor α was increased. Furthermore, caffeine reduced tissue lipid peroxidation and oxidative stress. These effects suggest that caffeine could improve HFD-induced hepatic injury by suppressing inflammatory response and oxidative stress and regulating hepatic de novo lipogenesis and β-oxidation.

scholarly journals Ameliorative Effect of Beta vulgaris Root Extract on Chlorpyrifos-Induced Oxidative Stress, Inflammation and Liver Injury in Rats

Biomolecules ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 261 ◽  
Author(s):  
Gadah Albasher ◽  
Rafa Almeer ◽  
Fatimah O. Al-Otibi ◽  
Noorah Al-Kubaisi ◽  
Ayman M. Mahmoud
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Liver Injury ◽  
Inflammatory Cytokines ◽  
Elevated Serum ◽  
Serum Levels ◽  
Antioxidant Defenses ◽  
Root Extract ◽  
Histological Alterations ◽  
Pro Inflammatory Cytokines

Exposure to organophosphorus insecticides causes several health problems to animals and humans. Red beetroot (RBR) is rich in antioxidant ingredients and possesses a promising hepatoprotective activity. This study evaluated the potential of RBR extract to prevent chlorpyrifos (CPF)-induced liver injury, with an emphasis on oxidative stress, inflammation and apoptosis. Rats received 10 mg/kg CPF and were treated with 300 mg/kg RBR extract for 28 days. CPF caused liver injury evidenced by elevated serum levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and bilirubin, along with several histological alterations. Hepatic lipid peroxidation (LPO) and nitric oxide (NO) levels, as well as inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines were increased in CPF-intoxicated rats. RBR prevented CPF-induced histological alterations, and ameliorated liver function, LPO, NO, iNOS and pro-inflammatory cytokines. RBR boosted glutathione and antioxidant enzymes, and increased Nrf2 expression. In addition, RBR diminished Bax and caspase-3, and increased Bcl-2 expression. In conclusion, RBR prevented CPF-induced liver injury via attenuation of oxidative stress, inflammation and apoptosis. RBR enhanced antioxidant defenses, suggesting that it could be used as a potential therapeutic intervention to minimize CPF hepatotoxicity.

Heat-Processed Scutellariae Radix Protects Hepatic Inflammation through the Amelioration of Oxidative Stress in Lipopolysaccharide-Induced Mice

2017 ◽  
Vol 45 (06) ◽  
pp. 1233-1252 ◽  
Author(s):  
Chan Hum Park ◽  
Mi-Rae Shin ◽  
Byung Kwan An ◽  
Hyun Woo Joh ◽  
Jang Cheon Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Elevated Serum ◽  
Intercellular Adhesion Molecule ◽  
Activator Protein 1 ◽  
Intercellular Adhesion Molecule 1 ◽  
Scutellariae Radix ◽  
Hepatocellular Damage ◽  
Chemotactic Protein ◽  
Nitrite Nitrate

The present study evaluated the effects of heat-processed Scutellariae Radix (Scutellaria baicalensis) on lipopolysaccharide (LPS)-induced liver injury in mice. Scutellariae Radix heat-processed at 160[Formula: see text]C or 180[Formula: see text]C was orally administered at a dose of 100 mg/kg body weight for three days before the intraperitoneal injection of LPS, and the effects were compared with those of vehicle-treated LPS administered to control mice. The administration of Scutellariae Radix decreased the elevated serum monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6), reactive oxygen species (ROS), nitrite/nitrate, peroxynitrite, and hepatic functional parameters, and reduced the increased ROS in the liver. The augmented expressions of hepatic oxidative stress and inflammation-related proteins, phospho-p38, phosphorylated extracellular signal-regulated kinase, phosphorylated c-Jun N-terminal kinase, nuclear factor-[Formula: see text] B p65, activator protein-1, cyclooxygenase-2, inducible nitric oxide synthase, MCP-1, intercellular adhesion molecule-1, tumor necrosis factor-[Formula: see text], and IL-6, were downregulated by the heat-processed Scutellariae Radix. Hematoxylin-eosin staining showed that the increased hepatocellular damage in the liver of LPS-treated mice improved with the administration of heat-processed Scutellariae Radix. Overall, the ameliorative effects of Scutellariae Radix were superior to those when heat-processed at 180[Formula: see text]C. Our results indicate that heat-processed Scutellariae Radix acts as an anti-inflammatory agent by ameliorating oxidative stress in the liver of mice with LPS-induced liver injury.

scholarly journals Baicalin Ameliorates Liver Injury Induced by Chronic plus Binge Ethanol Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and NRF2 in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Ping He ◽  
Yafeng Wu ◽  
Jianchao Shun ◽  
Yaodong Liang ◽  
Mingliang Cheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Transcription Factor ◽  
Liver Injury ◽  
Cell Activation ◽  
Antioxidant Defense ◽  
Defense Mechanism ◽  
Nuclear Translocation ◽  
Transcriptional Level ◽  
Binge Ethanol

Alcoholic liver injury leads to serious complication including death. The potential role of baicalin at the transcription level in mice model of alcohol injury is not known yet. In this study, we examined the effect of baicalin against chronic plus binge ethanol model in mice and understanding the mechanism of protection. Liver function, histology, steatosis, inflammation, NF-κB activity, oxidative stress sources, nuclear translocation of NRF2 transcription factor, and cell death were assessed. Treatment with baicalin ameliorated ethanol-induced oxidative stress, inflammation, and cell death. Baicalin attenuated ethanol-induced proinflammatory molecules such as TNF-α, IL-1β, MIP-2, and MCP-1 and reversed redox-sensitive transcription factor NF-κB activation. Baicalin also modulated Kupffer cell activation in vitro. Baicalin inhibited ethanol-induced expression of reactive oxygen species (ROS) generating enzymes NOX2, p67phox, xanthine oxidase, and iNOS in addition to CYP2E1 activities. Baicalin also enhanced ethanol-induced NRF2 nuclear translocation and increased downstream target gene HO-1 as antioxidant defense. Finally, baicalin reduced significant apoptotic and necrotic cell death. Our study suggests that baicalin ameliorates chronic plus binge ethanol-induced liver injury involving molecular crosstalk of multiple pathways at the transcriptional level and through upregulation of antioxidant defense mechanism.

Metabolomics and Pharmacological Screening of Aspergillus versicolor Isolated from Hyrtios erectus Red Sea Sponge; Egypt

2020 ◽  
Vol 16 (7) ◽  
pp. 1083-1102
Author(s):  
Mohamed A. Shreadah ◽  
Nehad M.A. El Moneam ◽  
Samy A. El-Assar ◽  
Asmaa Nabil-Adam
Keyword(s):  
Oxidative Stress ◽  
Red Sea ◽  
Crude Extract ◽  
Quantitative Methods ◽  
Total Phenolic ◽  
Aspergillus Versicolor ◽  
Crude Extracts ◽  
Study Results ◽  
Anti Inflammatory ◽  
Pharmacological Screening

Background: Aspergillus Versicolor is a marine-derived fungus isolated from Hyrtios Erectus Red Sea sponge. Methods: The aim of this study was to carry out a pharmacological screening and investigation for the in vitro biological activity (antioxidant, cholinergic, antidiabetic and anticancer) of Aspergillus Versicolor crude extract’s active compounds by using different qualitative and quantitative methods. Results: The present study results showed that Aspergillus Versicolor crude extracts contain 0.6 mg total phenolic/mg crude extract. Aspergillus Versicolor also showed a potent antioxidative capacity by decreasing the oxidation of ABTS. The anticancer and inhibitory effects of Aspergillus Versicolor crude extracts on PTK and SHKI were found to be 75.29 % and 80.76%; respectively. The AChE inhibitory assay revealed that Aspergillus Versicolor extracts had an inhibitory percentage of 86.67%. Furthermore, the anti-inflammatory activity using COX1, COX2, TNF, and IL6 was 77.32, 85.21 %, 59.83%, and 56.15%; respectively. Additionally, the anti-viral effect using reverse transcriptase enzyme showed high antiviral activity with 92.10 %. Conclusion: The current study confirmed that the Aspergillus versicolor crude extract and its active constituents showed strong effects on diminishing the oxidative stress, neurodegenerative damage, antiinflammatory, anti-cancer and anti-viral, suggesting their beneficial role as a promising fermented product in the treatment of cancer, oxidative stress, Alzheimer's, anti-inflammatory and anti-viral diseases.

Glabridin attenuates paracetamol-induced liver injury in mice via CYP2E1-mediated inhibition of oxidative stress

2021 ◽  
pp. 1-9
Author(s):  
Shipra Bhatt ◽  
Ankita Sharma ◽  
Ashish Dogra ◽  
Priyanka Sharma ◽  
Amit Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury

A polysaccharide of PFP-1 from Pleurotus geesteranus attenuates alcoholic liver diseases via Nrf2 and NF-κB signaling pathways

2021 ◽  
Author(s):  
Xinling Song ◽  
Wenxue Sun ◽  
Wenxin Cai ◽  
Le Jia ◽  
Jianjun Zhang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Liver Injury ◽  
Signaling Pathways ◽  
Alcoholic Liver Disease ◽  
Fruiting Body ◽  
Liver Diseases ◽  
Alcoholic Liver Diseases

A polysaccharide named as PFP-1 was isolated from Pleurotus geesteranus fruiting body, and the potential investigations on ameliorating oxidative stress and liver injury against alcoholic liver disease (ALD) were processed...

scholarly journals Protective Effect of Osmundacetone against Neurological Cell Death Caused by Oxidative Glutamate Toxicity

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 328
Author(s):  
Tuy An Trinh ◽  
Young Hye Seo ◽  
Sungyoul Choi ◽  
Jun Lee ◽  
Ki Sung Kang
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Defense Mechanism ◽  
Neuroprotective Effect ◽  
Glutamate Release ◽  
Chromatin Condensation ◽  
Critical Role ◽  
Glutamate Toxicity ◽  
Heme Oxygenase 1 ◽  
Brain Functions

Oxidative stress is one of the main causes of brain cell death in neurological disorders. The use of natural antioxidants to maintain redox homeostasis contributes to alleviating neurodegeneration. Glutamate is an excitatory neurotransmitter that plays a critical role in many brain functions. However, excessive glutamate release induces excitotoxicity and oxidative stress, leading to programmed cell death. Our study aimed to evaluate the effect of osmundacetone (OAC), isolated from Elsholtzia ciliata (Thunb.) Hylander, against glutamate-induced oxidative toxicity in HT22 hippocampal cells. The effect of OAC treatment on excess reactive oxygen species (ROS), intracellular calcium levels, chromatin condensation, apoptosis, and the expression level of oxidative stress-related proteins was evaluated. OAC showed a neuroprotective effect against glutamate toxicity at a concentration of 2 μM. By diminishing the accumulation of ROS, as well as stimulating the expression of heat shock protein 70 (HSP70) and heme oxygenase-1 (HO-1), OAC triggered the self-defense mechanism in neuronal cells. The anti-apoptotic effect of OAC was demonstrated through its inhibition of chromatin condensation, calcium accumulation, and reduction of apoptotic cells. OAC significantly suppressed the phosphorylation of mitogen-activated protein kinases (MAPKs), including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 kinases. Thus, OAC could be a potential agent for supportive treatment of neurodegenerative diseases.

scholarly journals Maresin 1 protects the liver against ischemia/reperfusion injury via the ALXR/Akt signaling pathway

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Da Tang ◽  
Guang Fu ◽  
Wenbo Li ◽  
Ping Sun ◽  
Patricia A. Loughran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Serum Aminotransferase ◽  
Primary Mouse ◽  
Maresin 1

Abstract Background Hepatic ischemia/reperfusion (I/R) injury can be a major complication following liver surgery contributing to post-operative liver dysfunction. Maresin 1 (MaR1), a pro-resolving lipid mediator, has been shown to suppress I/R injury. However, the mechanisms that account for the protective effects of MaR1 in I/R injury remain unknown. Methods WT (C57BL/6J) mice were subjected to partial hepatic warm ischemia for 60mins followed by reperfusion. Mice were treated with MaR1 (5-20 ng/mouse), Boc2 (Lipoxin A4 receptor antagonist), LY294002 (Akt inhibitor) or corresponding controls just prior to liver I/R or at the beginning of reperfusion. Blood and liver samples were collected at 6 h post-reperfusion. Serum aminotransferase, histopathologic changes, inflammatory cytokines, and oxidative stress were analyzed to evaluate liver injury. Signaling pathways were also investigated in vitro using primary mouse hepatocyte (HC) cultures to identify underlying mechanisms for MaR1 in liver I/R injury. Results MaR1 treatment significantly reduced ALT and AST levels, diminished necrotic areas, suppressed inflammatory responses, attenuated oxidative stress and decreased hepatocyte apoptosis in liver after I/R. Akt signaling was significantly increased in the MaR1-treated liver I/R group compared with controls. The protective effect of MaR1 was abrogated by pretreatment with Boc2, which together with MaR1-induced Akt activation. MaR1-mediated liver protection was reversed by inhibition of Akt. Conclusions MaR1 protects the liver against hepatic I/R injury via an ALXR/Akt signaling pathway. MaR1 may represent a novel therapeutic agent to mitigate the detrimental effects of I/R-induced liver injury.

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