scholarly journals Liver Histopathological Analysis of 24 Postmortem Findings of Patients With COVID-19 in China

2021 ◽  
Vol 8 ◽  
Author(s):  
Huikuan Chu ◽  
Li Peng ◽  
Lilin Hu ◽  
Yixin Zhu ◽  
Jinfang Zhao ◽  
...  
Keyword(s):  
Liver Injury ◽  
Ultrastructural Changes ◽  
Histopathological Analysis ◽  
Hepatocellular Necrosis ◽  
Obstructive Cholestasis ◽  
Male Patients ◽  
Underlying Diseases ◽  
Viral Inclusions ◽  
Lobular Inflammation ◽  
Liver Tissues

Although the pathologic investigation of liver injury was observed in a couple of cases in China, the detailed description of liver histopathologic and ultrastructural changes in a relatively larger series of liver tissues from COVID-19 patients is lacking. Samples from the liver were obtained from 24 COVID-19 cases from February 1 to April 1, 2020. Light microscopy showed that all liver sections had different degrees of liver injury manifested as swelling of the hepatocytes, hepatocellular necrosis, steatosis, lobular inflammation, portal inflammation, dilatation of sinusoids, and so on. SARS-CoV-2 induced liver injury might be independent of pre-existing Schistosoma infection or obstructive cholestasis. Patients combined with respiratory failure had more severe hepatocellular necrosis and male patients were more susceptible to liver injury. Although coronavirus particles or viral inclusions were not detected in the liver tissues for all cases, vacuolar degenerations in hepatocytes, edematous of mitochondria with the disruption of cristae, and expansions of the endoplasmic reticulum were observed. In conclusion, pathologic changes of liver tissues provide us a further understanding of liver injury in COVID-19 patients. Changes in the liver seem to be related to the underlying diseases/conditions.

scholarly journals Lemon Balm and Dandelion Leaf Extracts Synergistically Protect against Carbon Tetrachloride-Induced Acute Liver Injury in Mice

2021 ◽  
Vol 11 (1) ◽  
pp. 390
Author(s):  
Beom-Rak Choi ◽  
Il-Je Cho ◽  
Su-Jin Jung ◽  
Jae-Kwang Kim ◽  
Dae-Geon Lee ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Antioxidant Activities ◽  
Body Weight Gain ◽  
Histopathological Analysis ◽  
Related Factor ◽  
Mrna Levels ◽  
Protective Effects ◽  
Lemon Balm

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.

scholarly journals Simultaneous Inhibition of Three Major Cytokines and Its Therapeutic Effects: A Peptide-Based Novel Therapy against Endotoxemia in Mice

2021 ◽  
Vol 11 (5) ◽  
pp. 436
Author(s):  
Hung-Jen Shih ◽  
Chao-Yuan Chang ◽  
Milton Chiang ◽  
Van Long Le ◽  
Hao-Jen Hsu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Therapeutic Effects ◽  
The Novel ◽  
Tissue Water ◽  
Novel Therapy ◽  
Binding Domains ◽  
Tnf Α ◽  
Simultaneous Inhibition ◽  
Factor Α ◽  
Liver Tissues

Three major cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6, mediate endotoxemia-induced liver injury. With the similar structures to the binding domains of the three cytokines to their cognate receptors, the novel peptide KCF18 can simultaneously inhibit TNF-α, IL-1β, and IL-6. We elucidated whether KCF18 can alleviate injury of liver in endotoxemic mice. Adult male mice (BALB/cJ) were intraperitoneally (i.p.) administered lipopolysaccharide (LPS, 15 mg/kg; LPS group) or LPS with KCF18 (LKCF group). Mice in the LKCF group received KCF18 (i.p.) at 2 h (0.6 mg/kg), 4 h (0.3 mg/kg), 6 h (0.3 mg/kg), and 8 h (0.3mg/kg) after LPS administration. Mice were sacrificed after receiving LPS for 24 h. Our results indicated that the binding levels of the three cytokines to their cognate receptors in liver tissues in the LKCF group were significantly lower than those in the LPS group (all p < 0.05). The liver injury level, as measured by performing functional and histological analyses and by determining the tissue water content and vascular permeability (all p < 0.05), was significantly lower in the LKCF group than in the LPS group. Similarly, the levels of inflammation (macrophage activation, cytokine upregulation, and leukocyte infiltration), oxidation, necroptosis, pyroptosis, and apoptosis (all p < 0.05) in liver tissues in the LKCF group were significantly lower than those in the LPS group. In conclusion, the KCF18 peptide–based simultaneous inhibition of TNF-α, IL-1β, and IL-6 can alleviate liver injury in mice with endotoxemia.

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

scholarly journals Evaluation of hepatoprotective potential of methanolic extract of the plant dolichos biflorus linn

2016 ◽  
Vol 2 (5) ◽  
pp. 116
Author(s):  
Deepthi B ◽  
Ashoka Shenoy M ◽  
Karunakar Hegde
Keyword(s):  
Body Weight ◽  
Liver Injury ◽  
Methanolic Extract ◽  
Histopathological Study ◽  
Histopathological Analysis ◽  
Standard Drug ◽  
Dolichos Biflorus ◽  
Liver Functions ◽  
Dose Dependent ◽  
Endogenous Enzymes

Present study is to evaluate the hepatoprotective potential of methanolic extract of the plant Dolichos biflorus Linn. against paracetamol and alcohol induced hepatotoxicity in rats. Oral administration of plant extract in two doses 200mg/kg and 400mg/kg body weight were subjected for the evaluation of hepatoprotective potential against alcohol (2ml/100g) and PCM (2g/kg) induced liver injury. Silymarin (25mg/kg) was used as a standard drug. The parameters like SGPT, SGO, ALP, TB and endogenous enzymes were estimated to assess the liver functions. In addition histopathological study was also carried out. Both the lower (200mg/kg) and higher dose (400mg/kg) of D.biflorus extract showed dose dependent significant decrease in SGPT, SGOT, ALP and TB levels when compared with toxic control. Both extracts showed decrease in LPO and increase in GSH, SOD and CAT levels. Hepatoprotective effect was also confirmed by histopathological analysis of liver which showed less damage in extract treated rats. The results obtained were comparable with that of the standard. The present study concluded that Dolichos biflorus Linn. plant were found to be effective against hepatotoxicity induced by Alcohol and Paracetamol.

scholarly journals Acute Bacterial Meningitis in Qatar: A Hospital-Based Study from 2009 to 2013

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Fahmi Yousef Khan ◽  
Mohammed Abu-Khattab ◽  
Eman Abdulrahman Almaslamani ◽  
Abubaker Ahmed Hassan ◽  
Shehab Fareed Mohamed ◽  
...  
Keyword(s):  
Bacterial Meningitis ◽  
Causative Agent ◽  
Medical Condition ◽  
Acute Bacterial Meningitis ◽  
Coagulase Negative Staphylococci ◽  
Inappropriate Treatment ◽  
Common Medical Condition ◽  
Male Patients ◽  
The Common ◽  
Underlying Diseases

Background and Objectives. Bacterial meningitis is a common medical condition in Qatar. The aim of this study was to describe the clinical characteristics of bacterial meningitis, the frequency of each pathogen, and its sensitivity to antibiotics and risk factors for death.Patients and Methods. This retrospective study was conducted at Hamad General Hospital between January 1, 2009, and December 31, 2013.Results. We identified 117 episodes of acute bacterial meningitis in 110 patients. Their mean age was26.4±22.3years (range: 2–74) and 81 (69.2%) of them were male patients. Fifty-nine episodes (50.4%) were community-acquired infection and fever was the most frequent symptom (94%), whereas neurosurgery is the most common underlying condition. Coagulase-negative staphylococci were the most common causative agent, of which 95% were oxacillin-resistant, while 63.3% ofAcinetobacterspp. showed resistance to meropenem. The in-hospital mortality was 14 (12%). Only the presence of underlying diseases, hypotension, and inappropriate treatment were found to be independent predictors of mortality.Conclusion. Acute bacterial meningitis predominantly affected adults and coagulase-negative staphylococci species were the common causative agent in Qatar with majority of infections occurring nosocomially. More than 90% of all implicated coagulase-negative staphylococci strains were oxacillin-resistant.

scholarly journals Tumor Necrosis Factor α-dependent Up-regulation of Lrh-1 and Mrp3(Abcc3) Reduces Liver Injury in Obstructive Cholestasis

2003 ◽  
Vol 278 (38) ◽  
pp. 36688-36698 ◽  
Author(s):  
Alan Bohan ◽  
Wen-Sheng Chen ◽  
Lee A. Denson ◽  
Matthew A. Held ◽  
James L. Boyer
Keyword(s):  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Obstructive Cholestasis ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Malarial Infection of Female BWF1 Lupus Mice Alters the Redox State in Kidney and Liver Tissues and Confers Protection against Lupus Nephritis

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Saleh Al-Quraishy ◽  
Mostafa A. Abdel-Maksoud ◽  
Azza El-Amir ◽  
Fathy A. Abdel-Ghaffar ◽  
Gamal Badr
Keyword(s):  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Redox State ◽  
Ultrastructural Changes ◽  
Liver And Kidney ◽  
Gamma Irradiated ◽  
Kidney Functions ◽  
Tropical Infections ◽  
Liver Tissues

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by an imbalanced redox state and increased apoptosis. Tropical infections, particularly malaria, may confer protection against SLE. Oxidative stress is a hallmark of SLE. We have measured changes in the levels of nitric oxide (NO), hydrogen peroxide (H2O2), malondialdehyde (MDA), and reduced glutathione (GSH) in both kidney and liver tissues of female BWF1 lupus mice, an experimental model of SLE, after infection with either live or gamma-irradiated malaria. We observed a decrease in NO, H2O2, and MDA levels in kidney tissues after infection of lupus mice with live malaria. Similarly, the levels of NO and H2O2were significantly decreased in the liver tissues of lupus mice after infection with live malaria. Conversely, GSH levels were obviously increased in both kidney and liver tissues after infection of lupus mice with either live or gamma-irradiated malaria. Liver and kidney functions were significantly altered after infection of lupus mice with live malaria. We further investigated the ultrastructural changes and detected the number of apoptotic cells in kidney and liver tissues in situ by electron microscopy and TUNEL assays. Our data reveal that infection of lupus mice with malaria confers protection against lupus nephritis.

scholarly journals Loss of orphan receptor small heterodimer partner sensitizes mice to liver injury from obstructive cholestasis

Hepatology ◽  
2008 ◽  
Vol 47 (5) ◽  
pp. 1578-1586 ◽  
Author(s):  
Young Joo Park ◽  
Mohammed Qatanani ◽  
Steven S. Chua ◽  
Jennifer L. LaRey ◽  
Stacy A. Johnson ◽  
...  
Keyword(s):  
Liver Injury ◽  
Orphan Receptor ◽  
Small Heterodimer Partner ◽  
Obstructive Cholestasis

scholarly journals Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis

10.3791/52438 ◽  
2015 ◽  
Author(s):  
Carmen G. Tag ◽  
Sibille Sauer-Lehnen ◽  
Sabine Weiskirchen ◽  
Erawan Borkham-Kamphorst ◽  
René H. Tolba ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Bile Duct Ligation ◽  
Duct Ligation ◽  
Obstructive Cholestasis

Rosiglitazone protects rat liver against acute liver injury associated with the NF-κB signaling pathway

2016 ◽  
Vol 94 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Wei Chen ◽  
Yuan-Jie Lin ◽  
Xu-Ya Zhou ◽  
Hao Chen ◽  
Yong Jin
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Rat Liver ◽  
Receptor Subtype ◽  
Histopathological Analysis ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Serum Aminotransferase

Rosiglitazone, which is mainly used in the treatment of diabetes mellitus, is also involved in the regulation of inflammation. The peroxisome proliferator-activated receptor (PPAR)-γ receptor subtype appears to play a pivotal role in the regulation of inflammation. However, the exact mechanism for the protective effects of rosiglitazone against inflammation such as liver injury remains unclear. The aim of this study was to investigate the effects of rosiglitazone on inflammation in the liver of rats treated with D-GaIN/LPS. Male Sprague–Dawley rats were injected with D-GaIN/LPS with or without pre-administration of rosiglitazone (3, 10, or 30 mg/kg, intraperitoneal injection). Our data showed that rosiglitazone significantly inhibited D-GaIN/LPS-induced hepatotoxicity in a dose-dependent manner, as indicated by both diagnostic indicators of liver damage (serum aminotransferase activities) and histopathological analysis. Western blot analysis showed that rosiglitazone significantly decreased protein expression levels of COX-2 and production of pro-inflammatory markers, including TNF-α and IL-6, in D-GaIN/LPS-treated rat liver. The results indicated that the inhibition of D-GaIN/LPS-induced inflammation by rosiglitazone can be attributed, at least partially, to its capacity to regulate the the immunoregulatory transcription factor nuclear factor kappa B (NF-κB) signaling pathway.

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