Oxidative Stress and Hepatic Inflammation

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 November 2021) | Viewed by 13207

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Special Issue Information

Dear Colleagues, 

Hepatic inflammation is an important public health problem due to its being a chronic symptom, and liver disease has emerged as one of the leading causes of death and illness worldwide. The global burden of liver disease is poised to swell yet further due to health-modulating factors such as extension of life expectancy, increasingly sedentary lifestyles, and over-nutrition. 

Chronic pathologic processes include viral infection, alcoholic liver disease, non-alcoholic steatohepatitis (NASH), and autoimmune diseases. Depending on the type of underlying liver injury, several mechanisms exist to trigger immune reactions. Chronic immune reactions lead to liver fibrosis. Understanding the mechanisms of inflammation and fibrosis is critically important to developing treatments for chronic liver diseases. 

Over the past few decades, clinical and experimental studies have provided a substantial amount of evidence that oxidative stress, which is defined as an imbalance between oxygen radical production and scavenging, increases in the hepatocyte and at a systemic level during hepatic inflammation. At physiological levels, reactive oxygen species play important roles in intracellular pathways and redox signaling, but at higher levels they may induce cellular dysfunction and damage. Despite extensive investigation, however, the molecular pathways and drug development involved in hepatic-inflammation-associated oxidative stress remain incompletely understood. 

This Special Issue aims to provide a compact overview of the basic mechanisms of, and novel developments in research on, the role of oxidative stress in hepatic inflammation pathophysiology, contributing to a better understanding of the disease. We invite investigators to contribute original research and review articles that will help us to elucidate the effects of oxidative stress on hepatic inflammation. We encourage the submission of studies describing in vitro and in vivo experiments, as well as clinical studies describing the mechanisms, signaling pathways, novel targets, and therapies for hepatic inflammation. 

Dr. Seon-Heui Cha
Guest Editor

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Keywords

  • hepatic inflammation
  • hepatitis
  • non-alcoholic fatty liver disease (NAFLD)
  • non-alcoholic steatohepatitis (NASH)
  • oxidative stress

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Published Papers (3 papers)

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Research

21 pages, 3737 KiB  
Article
Hepatoprotective Effect of Bee Bread in Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) Rats: Impact on Oxidative Stress and Inflammation
by Zaida Zakaria, Zaidatul Akmal Othman, Joseph Bagi Suleiman, Nur Asyilla Che Jalil, Wan Syaheedah Wan Ghazali, Victor Udo Nna and Mahaneem Mohamed
Antioxidants 2021, 10(12), 2031; https://doi.org/10.3390/antiox10122031 - 20 Dec 2021
Cited by 16 | Viewed by 4549
Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a pathological accumulation of hepatic lipid closely linked with many metabolic disorders, oxidative stress and inflammation. We aimed to evaluate the hepatoprotective effect of bee bread on oxidative stress and inflammatory parameters in MAFLD rats. Twenty-eight [...] Read more.
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a pathological accumulation of hepatic lipid closely linked with many metabolic disorders, oxidative stress and inflammation. We aimed to evaluate the hepatoprotective effect of bee bread on oxidative stress and inflammatory parameters in MAFLD rats. Twenty-eight male Sprague-Dawley rats were assigned into four groups (n = 7/group): normal control (NC), high-fat diet (HFD), bee bread (HFD + Bb, HFD + 0.5 g/kg/day bee bread) and orlistat (HFD + Or, HFD + 10 mg/kg/day orlistat) groups. After 12 weeks, the HFD group demonstrated significantly higher body weight gain, serum levels of lipids (TG, TC, LDL), liver enzymes (AST, ALT, ALP) and adiponectin, liver lipids (TG, TC) and insulin resistance (HOMA-IR). Furthermore, the HFD group showed significantly decreased antioxidant enzyme activities (GPx, GST, GR, SOD, CAT) and GSH level, and increased liver oxidative stress (TBARS, NO), translocation of Nrf2 to the nucleus, Keap1 expression and inflammation (TNF-α, NF-κβ, MCP-1) together with histopathological alterations (steatosis, hepatocyte hypertrophy, inflammatory cell infiltration, collagen deposition), which indicated the presence of non-alcoholic steatohepatitis (NASH) and fibrosis. Bee bread significantly attenuated all these changes exerted by HFD feeding. In conclusion, our results suggest that bee bread might have antioxidant, anti-inflammatory, anti-steatotic and anti-fibrotic effects that are beneficial in protecting liver progression towards NASH and fibrosis. Full article
(This article belongs to the Special Issue Oxidative Stress and Hepatic Inflammation)
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16 pages, 4685 KiB  
Article
Diosmin Alleviates Doxorubicin-Induced Liver Injury via Modulation of Oxidative Stress-Mediated Hepatic Inflammation and Apoptosis via NfkB and MAPK Pathway: A Preclinical Study
by Abdullah F. AlAsmari, Metab Alharbi, Faleh Alqahtani, Fawaz Alasmari, Mohammed AlSwayyed, Sami I. Alzarea, Ibrahim A. Al-Alallah, Adel Alghamdi, Hassan M. Hakami, Meshal K. Alyousef, Youssef Sari and Nemat Ali
Antioxidants 2021, 10(12), 1998; https://doi.org/10.3390/antiox10121998 - 15 Dec 2021
Cited by 38 | Viewed by 4479
Abstract
Hepatotoxicity caused by chemotherapeutic drugs (e.g., doxorubicin) is of critical concern in cancer therapy. This study focused on investigating the modulatory effects of diosmin against doxorubicin-induced hepatotoxicity in Male Wistar rats. Male Wistar rats were randomly divided into four groups: Group I was [...] Read more.
Hepatotoxicity caused by chemotherapeutic drugs (e.g., doxorubicin) is of critical concern in cancer therapy. This study focused on investigating the modulatory effects of diosmin against doxorubicin-induced hepatotoxicity in Male Wistar rats. Male Wistar rats were randomly divided into four groups: Group I was served as control, Group II was treated with doxorubicin (20 mg/kg, intraperitoneal, i.p.), Group III was treated with a combination of doxorubicin and low-dose diosmin (100 mg/kg orally), and Group IV was treated with a combination of doxorubicin and high-dose diosmin (200 mg/kg orally) supplementation. A single dose of doxorubicin (i.p.) caused hepatic impairment, as shown by increases in the concentrations of serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. Doxorubicin produced histological abnormalities in the liver. In addition, a single injection of doxorubicin increased lipid peroxidation and reduced glutathione, catalase, and superoxide dismutase (SOD) levels. Importantly, pre-treatment with diosmin restored hepatic antioxidant factors and serum enzymatic activities and reduced the inflammatory and apoptotic-mediated proteins and genes. These findings demonstrate that diosmin has a protective effect against doxorubicin-induced hepatotoxicity. Full article
(This article belongs to the Special Issue Oxidative Stress and Hepatic Inflammation)
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11 pages, 3214 KiB  
Article
Rutaecarpine Protects against Acetaminophen-Induced Acute Liver Injury in Mice by Activating Antioxidant Enzymes
by Jae Ho Choi, Sun Woo Jin, Gi Ho Lee, Eun Hee Han, Yong Pil Hwang and Hye Gwang Jeong
Antioxidants 2021, 10(1), 86; https://doi.org/10.3390/antiox10010086 - 10 Jan 2021
Cited by 20 | Viewed by 3406
Abstract
Rutaecarpine, an indolopyridoquinazolinone alkaloid isolated from the unripe fruit of Evodia rutaecarpa, is used to treat hypertension, postpartum hemorrhage, dysentery, and amenorrhea as a traditional medicine in Asia. We investigated the effect of rutaecarpine on acetaminophen-induced hepatotoxicity in mice. Rutaecarpine was administered [...] Read more.
Rutaecarpine, an indolopyridoquinazolinone alkaloid isolated from the unripe fruit of Evodia rutaecarpa, is used to treat hypertension, postpartum hemorrhage, dysentery, and amenorrhea as a traditional medicine in Asia. We investigated the effect of rutaecarpine on acetaminophen-induced hepatotoxicity in mice. Rutaecarpine was administered orally daily for seven consecutive days, followed by intraperitoneal injection of acetaminophen in mice on day seven to induce hepatotoxicity. Rutaecarpine pretreatment significantly decreased acetaminophen-induced serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) activities and hepatic malondialdehyde content and prevented acetaminophen-induced hepatic glutathione depletion. Furthermore, CYP2E1 expression was decreased by rutaecarpine pretreatment in a dose-dependent manner. Rutaecarpine pretreatment inhibited acetaminophen-induced expression of inflammatory cytokines by inhibiting NF-κB activation by JNK1/2. Also, rutaecarpine pretreatment promoted Nrf2-mediated activation of the antioxidant enzymes GCLC, HO-1, and NQO1. This indicates that the protective effect of rutaecarpine during acetaminophen-induced acute liver injury is mediated by the activation of antioxidant enzymes. Therefore, rutaecarpine has a protective effect of APAP-induced liver damage. Full article
(This article belongs to the Special Issue Oxidative Stress and Hepatic Inflammation)
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