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Biomedicines
Special Issues
Cell Death and Inflammation in Liver Diseases
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Cell Death and Inflammation in Liver Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 6087

Special Issue Editors

Dr. Muhammad Farooq

E-Mail Website
Guest Editor
Department of Clinical Sciences, University of Veterinary and Animal Sciences, Lahore, Pakistan
Interests: RIPK1 in hepatitis; cell death and inflammation; murine hepatitis; murine NAFLD; murine NASH; murine HCC; RIPK1
Dr. Muhammad Imran Arshad

E-Mail Website
Guest Editor
Institute of Microbiology, University of Agriculture of Faisalabad, Faisalabad, Pakistan
Interests: necroptosis and liver diseases; cytokines and hepatitis; immunotherapy; PPAR-γ and liver pathophysiology; microRNAs and hepatitis

Special Issue Information

Dear Colleagues,

Cell death and inflammation are key critical events in the progression of hepatitis, which may be caused by a variety of infectious or non-infectious agents. Significant progress has been made in understanding the role of inflammation and cell death in hepatitis. Furthermore, mechanistic studies, identification of the regulators of cell death, nuclear receptors, the use of inflammatory cytokines as diagnostic or prognostic markers, and therapeutic trials targeting cell death and inflammation in various liver diseases, are being studied both in animal models as well as humans.

This Special Issue will focus on the role of cell death pathways and inflammation in liver pathologies, including, but not limited to: drug-induced liver injury (DILI), viral hepatitis, bacterial hepatitis, alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), hepatocellular carcinoma (HCC), immune-mediated hepatitis, as well as approaches to the modulation of cell death and inflammation for the treatment of liver diseases. We cordially invite researchers from this vast discipline to submit original or review articles pertaining to this issue (animal model, cell/tissue culture and clinical studies on liver diseases).

Dr. Muhammad Farooq
Dr. Muhammad Imran Arshad
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cell death
  • apoptosis
  • necroptosis
  • regulated cell death
  • hepatitis
  • NAFLD
  • ALD
  • viral hepatitis
  • inflammation
  • biomarkers
  • immunity
  • NASH, therapeutic
  • liver
  • hepatitis

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Published Papers (3 papers)

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Research

21 pages, 8900 KiB  
Article
Genistein and Sex Hormone Supplementation Modulated Hepatic PPARα, δ, and γ Subtypes and STAT1 Expressions in a NASH Rat Model with Bilateral Orchidectomy
by Fatist Okrit, Maneerat Chayanupatkul, Prasong Siriviriyakul, Natcha Wanpiyarat and Duangporn Werawatganon
Biomedicines 2024, 12(3), 483; https://doi.org/10.3390/biomedicines12030483 - 21 Feb 2024
Cited by 1 | Viewed by 1922
Abstract
Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that is characterized by hepatic inflammation and steatosis. Currently, limited data exist regarding the risk of NASH in transgender women and the treatment options for this particular population. The use [...] Read more.
Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that is characterized by hepatic inflammation and steatosis. Currently, limited data exist regarding the risk of NASH in transgender women and the treatment options for this particular population. The use of testosterone supplementation is unfavorable for transgender women, and estrogen supplementation is linked to an increased risk of breast cancer; thus, an isoflavone derivative compound known as “genistein” could serve as a viable substitute for a hormone supplement in this context. The purpose of this study was to investigate the treatment effects and mechanisms of actions of genistein and sex hormones in orchidectomized (ORX) rats with nonalcoholic steatohepatitis induced via a high-fat high-fructose diet (HFHF) model. Male Sprague-Dawley rats (n = 42) were randomly assigned into seven groups; control, ORX + standard diet, HFHF, ORX + HFHF, ORX + HFHF diet + testosterone (50 mg/kg body weight (BW) once weekly), ORX + HFHF diet + estradiol (1.6 mg/kg BW daily), and ORX + HFHF diet + genistein (16 mg/kg BW daily). The duration of the study was 6 weeks. Some parts of liver tissue were used for histological examination by H&E staining. The determination of fat accumulation was performed using Oil Red O staining. SREBP1c and FAS gene expression were quantified using real-time PCR technique. The levels of all types of peroxisome proliferator-activated receptors (PPARs; α, δ, γ), proteins, and signal transducer and activator of transcription 1 (STAT1) signaling pathway were determined by both immunoblotting and immunohistochemistry. Rats in the ORX + HFHF group had the highest degree of hepatic steatosis, lobular inflammation, and hepatocyte ballooning, and showed higher levels of genes related to de novo lipogenesis, including SREBP1c and FAS. The expression of PPARγ and STAT1 were upregulated, while the expression of PPARα and PPARδ were downregulated in the ORX + HFHF group. Testosterone, estradiol and genistein treatments improved NASH histopathology together with the reversal of all types of PPAR protein expressions. Interestingly, genistein decreased the levels of STAT1 protein expression more than those of testosterone and estradiol treatment. Genistein and sex hormone treatment could ameliorate NASH through the upregulation of PPARα, and PPARδ, and the suppression of PPARγ and STAT1 expression. Full article
(This article belongs to the Special Issue Cell Death and Inflammation in Liver Diseases)
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16 pages, 3782 KiB  
Article
Apocynin, an NADPH Oxidase Enzyme Inhibitor, Prevents Amebic Liver Abscess in Hamster
by Germán Higuera-Martínez, Ivonne Maciel Arciniega-Martínez, Rosa Adriana Jarillo-Luna, Luz María Cárdenas-Jaramillo, David Levaro-Loquio, Maritza Velásquez-Torres, Edgar Abarca-Rojano, Aldo Arturo Reséndiz-Albor and Judith Pacheco-Yépez
Biomedicines 2023, 11(8), 2322; https://doi.org/10.3390/biomedicines11082322 - 21 Aug 2023
Cited by 2 | Viewed by 1404
Abstract
Amebiasis is an intestinal infection caused by Entamoeba histolytica. Amebic liver abscess (ALA) is the most common extraintestinal complication of amebiasis. In animal models of ALA, neutrophils have been shown to be the first cells to come into contact with Entamoeba histolytica [...] Read more.
Amebiasis is an intestinal infection caused by Entamoeba histolytica. Amebic liver abscess (ALA) is the most common extraintestinal complication of amebiasis. In animal models of ALA, neutrophils have been shown to be the first cells to come into contact with Entamoeba histolytica during the initial phase of ALA. One of the multiple mechanisms by which neutrophils exhibit amebicidal activity is through reactive oxygen species (ROS) and the enzyme NADPH oxidase (NOX2), which generates and transports electrons to subsequently reduce molecular oxygen into superoxide anion. Previous reports have shown that ROS release in the susceptible animal species (hamster) is mainly stimulated by the pathogen, in turn provoking such an exacerbated inflammatory reaction that it is unable to be controlled and results in the death of the animal model. Apocynin is a natural inhibitor of NADPH oxidase. No information is available on the role of NOX in the evolution of ALA in the hamster, a susceptible model. Our study showed that administration of a selective NADPH oxidase 2 (NOX2) enzyme inhibitor significantly decreases the percentage of ALA, the size of inflammatory foci, the number of neutrophils, and NOX activity indicated by the reduction in superoxide anion (O2−) production. Moreover, in vitro, the apocynin damages amoebae. Our results showed that apocynin administration induces a decrease in the activity of NOX that could favor a decrease in ALA progression. Full article
(This article belongs to the Special Issue Cell Death and Inflammation in Liver Diseases)
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11 pages, 1868 KiB  
Article
Calcitriol Protects against Acetaminophen-Induced Hepatotoxicity in Mice
by Supachaya Sriphoosanaphan, Pakkapon Rattanachaisit, Kanjana Somanawat, Natcha Wanpiyarat, Piyawat Komolmit and Duangporn Werawatganon
Biomedicines 2023, 11(6), 1534; https://doi.org/10.3390/biomedicines11061534 - 25 May 2023
Cited by 3 | Viewed by 2164
Abstract
Acetaminophen (APAP) overdose is one of the major causes of acute liver failure. Severe liver inflammation and the production of oxidative stress occur due to toxic APAP metabolites and glutathione depletion. Growing evidence has proved that vitamin D (VD) exerts anti-inflammatory and antioxidative [...] Read more.
Acetaminophen (APAP) overdose is one of the major causes of acute liver failure. Severe liver inflammation and the production of oxidative stress occur due to toxic APAP metabolites and glutathione depletion. Growing evidence has proved that vitamin D (VD) exerts anti-inflammatory and antioxidative functions. Our objective was to explore the protective role of calcitriol (VD3) in acute APAP-induced liver injury. Methods: Adult male mice were randomized into three groups; control (n = 8), APAP (n = 8), and VD3 group (n = 8). All mice, except controls, received oral administration of APAP (400 mg/kg) and were sacrificed 24 h later. In the VD3 group, calcitriol (10 µg/kg) was injected intraperitoneally 24 h before and after exposure to APAP. Blood samples were collected to assess serum aminotransferase and inflammatory cytokines [tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6)]. Liver tissues were analyzed for hepatic glutathione (GSH), malondialdehyde (MDA), and histopathology. Results: APAP administration significantly increased serum aminotransferase, inflammatory cytokines, and induced cellular inflammation and necrosis. APAP also depleted hepatic GSH and elevated oxidative stress, as indicated by high MDA levels. In the APAP group, 25% of the mice (two out of eight) died, while no deaths occurred in the VD3 group. Treatment with calcitriol significantly reduced serum aminotransferase, TNF-α, and IL-6 levels in the VD3 group compared to the APAP group. Additionally, VD3 effectively restored GSH reserves, reduced lipid peroxidation, and attenuated hepatotoxicity. Conclusions: These findings demonstrate that VD3 prevents APAP-induced acute liver injury and reduces mortality in mice through its anti-inflammatory and antioxidative activity. Thus, VD3 might be a novel treatment strategy for APAP-induced hepatotoxicity. Full article
(This article belongs to the Special Issue Cell Death and Inflammation in Liver Diseases)
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