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Oxidative Stress in Hepatic Injury

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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 (20 March 2023) | Viewed by 50154

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Dr. Hyeong-Geug Kim

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Guest Editor

Department of Biochemistry and Molecular Biology, School of Medicine, Indiana University, Indianapolis, IN MS1021B, USA
Interests: liver immunology; alcoholic liver diseases; non-alcoholic steatohepatitis; epigenetic regulator; metabolic syndrome; hepatocellular carcinoma

Dr. Gi-Sang Bae

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Guest Editor

1. Department of Pharmacology, School of Korean Medicine, Wonkwang University, Iksan 54538, Republic of Korea 2. Research Center of Traditional Korean Medicine, Wonkwang University, Iksan 54538, Republic of Korea
Interests: inflammation; pancreatitis; immunology; liver injury
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Oxidative stress plays critical roles in various liver diseases including alcoholic liver diseases (ALD), non-alcoholic steatohepatitis (NASH), viral infection of hepatitis (HBV or HCV), and drug-induced liver disease. During oxidative stress in liver injury, free radicals such as reactive oxygen species (ROS) and reactive nitrogen species (RNS) are mostly generated at the initial stage, then they can rapidly react with hepatocyte’s protein, lipids, and DNA. These conditions directly disrupt the cellular and molecular level of the structure–function relationship of the hepatocyte in different sites; however, the pathophysiological mechanisms remain unclear, and there no effective therapeutics are accessible.

We invite you to submit your recent research findings or a review article to this Special Issue, which will bring together current research concerning oxidative stress in the liver and potent antioxidant effects of therapeutics, including drug candidates or target molecules. This Special Issue invites in vitro experiments, in vivo experiments using preclinical animal models, and clinical trials. Studies relating to any of the following topics are welcome: Oxidative stress-related target molecules; regulation of redox status of liver injury; possible drug candidates of antioxidant effects of drugs during liver injury; molecular levels of oxidative stress features on various hepatic tissue oxidations; metabolism and oxidative stress during chronic liver injury; epigenetic regular and oxidative stress in liver injury; crosstalk of oxidative hepatic oxidation and hepatic inflammation in acute/chronic liver injury; comparison analysis of drug-induced liver tissue oxidation; and endoplasmic stress and oxidative stress in liver tissue.

We sincerely anticipate your valuable contribution.

Dr. Hyeong-Geug Kim
Dr. Gi-Sang Bae
Guest Editors

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Keywords

Hepatic tissue oxidation
Redox homeostasis
Free radicals
Alcoholic liver injury
Non-alcoholic fatty liver diseases
Epigenetic regulator

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Published Papers (11 papers)

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Research

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14 pages, 1568 KiB

Open AccessArticle

Hangover-Relieving Effect of Ginseng Berry Kombucha Fermented by Saccharomyces cerevisiae and Gluconobacter oxydans in Ethanol-Treated Cells and Mice Model

by Eun Jung Choi, Hyeongyeong Kim, Ki-Bae Hong, Hyung Joo Suh and Yejin Ahn

Antioxidants 2023, 12(3), 774; https://doi.org/10.3390/antiox12030774 - 22 Mar 2023

Cited by 16 | Viewed by 3713

Abstract

This study aimed to evaluate the hangover relieving effect of ginseng berry kombucha (GBK) fermented with Saccharomyces cerevisiae and Gluconobacter oxydans in in vitro and in vivo models. The antioxidant activity and oxidative stress inhibitory effect of GBK were evaluated in ethanol-treated human liver HepG2 cells. In addition, biochemical and behavioral analyses of ethanol treated male ICR mice were performed to confirm the anti-hangover effect of GBK. The radical scavenging activity of GBK was increased by fermentation, and the total ginsenoside content of GBK was 70.24 μg/mL. In HepG2 cells, in which oxidative stress was induced using ethanol, GBK significantly increased the expression of antioxidant enzymes by upregulating the Nrf2/Keap1 pathway. Moreover, GBK (15 and 30 mg/kg) significantly reduced blood ethanol and acetaldehyde concentrations in ethanol-treated mice. GBK significantly increased the levels of alcohol-metabolizing enzymes, including alcohol dehydrogenase and acetaldehyde dehydrogenase. The balance beam test and elevated plus maze test revealed that high-dose GBK significantly ameliorated ethanol-induced behavioral changes. Collectively, GBK exerted a protective effect against ethanol-induced liver damage by regulating the Nrf2/Keap1 pathway. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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14 pages, 3616 KiB

Open AccessArticle

Co-Treatments of Gardeniae Fructus and Silymarin Ameliorates Excessive Oxidative Stress-Driven Liver Fibrosis by Regulation of Hepatic Sirtuin1 Activities Using Thioacetamide-Induced Mice Model

by Jin A Lee, Mi-Rae Shin, JeongWon Choi, MinJu Kim, Hae-Jin Park and Seong-Soo Roh

Antioxidants 2023, 12(1), 97; https://doi.org/10.3390/antiox12010097 - 30 Dec 2022

Cited by 6 | Viewed by 2601

Abstract

Gardeniae Fructus (GF, the dried ripe fruits of Gardenia jasminoides Ellis) has traditionally been used to treat various diseases in East Asian countries, such as liver disease. Silymarin is a well-known medicine used to treat numerous liver diseases globally. The present study was purposed to evaluate the synergistic effects of GF and silymarin on the thioacetamide (TAA)-induced liver fibrosis of a mouse model. Mice were orally administered with distilled water, GF (100 mg/kg, GF 100), silymarin (100 mg/kg, Sily 100), and GF and silymarin mixtures (50 and 100 mg/kg, GS 50 and 100). The GS group showed remarkable amelioration of liver injury in the serum levels and histopathology by observing the inflamed cell infiltrations and decreases in necrotic bodies through the liver tissue. TAA caused liver tissue oxidation, which was evidenced by the abnormal statuses of lipid peroxidation and deteriorations in the total glutathione in the hepatic protein levels; moreover, the immunohistochemistry supported the increases in the positive signals against 4-hydroxyneal and 8-OHdG through the liver tissue. These alterations corresponded well to hepatic inflammation by an increase in F4/80 positive cells and increases in pro-inflammatory cytokines in the hepatic protein levels; however, administration with GS, especially the high dose group, not only remarkably reduced oxidative stress and DNA damage in the liver cells but also considerably diminished pro-inflammatory cytokines, which were driven by Kupffer cell activations, as compared with each of the single treatment groups. The pharmacological properties of GS prolonged liver fibrosis by the amelioration of hepatic stellate cells’ (HSCs’) activation that is dominantly expressed by huge extracellular matrix (ECM) molecules including α-smooth muscle actin, and collagen type1 and 3, respectively. We further figured out that GS ameliorated HSCs activated by the regulation of Sirtuin 1 (Sirt1) activities in the hepatic protein levels, and this finding excellently reenacted the transforming growth factor-β-treated LX-2-cells-induced cell death signals depending on the Sirt1 activities. Future studies need to reveal the pharmacological roles of GS on the specific cell types during the liver fibrosis condition. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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10 pages, 497 KiB

Open AccessArticle

Role of Oxidative Stress and Lipid Peroxidation in the Pathophysiology of NAFLD

by Marta Martín-Fernández, Víctor Arroyo, Carmen Carnicero, Rebeca Sigüenza, Reyes Busta, Natalia Mora, Beatriz Antolín, Eduardo Tamayo, Patricia Aspichueta, Irene Carnicero-Frutos, Hugo Gonzalo-Benito and Rocío Aller

Antioxidants 2022, 11(11), 2217; https://doi.org/10.3390/antiox11112217 - 10 Nov 2022

Cited by 44 | Viewed by 4862

Abstract

Non-alcoholic fatty liver disease (NAFLD) is characterised by an excess of hepatic fat that can progress to steatohepatitis, fibrosis, cirrhosis and hepatocarcinoma. The imbalance between lipid uptake/lipogenesis and lipid oxidation/secretion in the liver is a major feature of NAFLD. Given the lack of a non-invasive and reliable methods for the diagnosis of non-alcoholic steatohepatitis (NASH), it is important to find serum markers that are capable of discriminating or defining patients with this stage of NASH. Blood samples were obtained from 152 Caucasian subjects with biopsy-proven NAFLD due to persistently elevated liver enzyme levels. Metabolites representative of oxidative stress were assessed. The findings derived from this work revealed that NAFLD patients with a NASH score of ≥ 4 showed significantly higher levels of lipid peroxidation (LPO). Indeed, LPO levels above the optimal operating point (OOP) of 315.39 μM are an independent risk factor for presenting a NASH score of ≥ 4 (OR: 4.71; 95% CI: 1.68–13.19; p = 0.003). The area under the curve (AUC = 0.81, 95% CI = 0.73–0.89, p < 0.001) shows a good discrimination ability of the model. Therefore, understanding the molecular mechanisms underlying the basal inflammation present in these patients is postulated as a possible source of biomarkers and therapeutic targets in NASH. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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20 pages, 4057 KiB

Open AccessArticle

Effects of the Gut Microbiota and Barrier Function on Melatonin Efficacy in Alleviating Liver Injury

by Hao Zhang, Xiaoyun Liu, Mabrouk Elsabagh, Ying Zhang, Yi Ma, Yaqian Jin, Mengzhi Wang, Hongrong Wang and Honghua Jiang

Antioxidants 2022, 11(9), 1727; https://doi.org/10.3390/antiox11091727 - 31 Aug 2022

Cited by 9 | Viewed by 2542

Abstract

Environmental cadmium (Cd) exposure has been associated with severe liver injury. In contrast, melatonin (Mel) is a candidate drug therapy for Cd-induced liver injury due to its diverse hepatoprotective activities. However, the precise molecular mechanism by which Mel alleviates the Cd-induced liver injury, as well as the Mel–gut microbiota interaction in liver health, remains unknown. In this study, mice were given oral gavage CdCl₂ and Mel for 10 weeks before the collection of liver tissues and colonic contents. The role of the gut microbiota in Mel’s efficacy in alleviating the Cd-induced liver injury was evaluated by the gut microbiota depletion technique in the presence of antibiotic treatment and gut microbiota transplantation (GMT). Our results revealed that the oral administration of Mel supplementation mitigated liver inflammation, endoplasmic reticulum (ER) stress and mitophagy, improved the oxidation of fatty acids, and counteracted intestinal microbial dysbiosis in mice suffering from liver injury. It was interesting to find that neither Mel nor Cd administration induced any changes in the liver of antibiotic-treated mice. By adopting the GMT approach where gut microbiota collected from mice in the control (CON), Cd, or Mel + Cd treatment groups was colonized in mice, it was found that gut microbiota was involved in Cd-induced liver injury. Therefore, the gut microbiota is involved in the Mel-mediated mitigation of ER stress, liver inflammation and mitophagy, and the improved oxidation of fatty acids in mice suffering from Cd-induced liver injury. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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19 pages, 2780 KiB

Open AccessArticle

The Azadirachta indica (Neem) Seed Oil Reduced Chronic Redox-Homeostasis Imbalance in a Mice Experimental Model on Ochratoxine A-Induced Hepatotoxicity

by Galina Nikolova, Julian Ananiev, Veselin Ivanov, Kamelia Petkova-Parlapanska, Ekaterina Georgieva and Yanka Karamalakova

Antioxidants 2022, 11(9), 1678; https://doi.org/10.3390/antiox11091678 - 28 Aug 2022

Cited by 5 | Viewed by 2817

Abstract

Liver damage severity depends on both the dose and the exposure duration. Oxidative stress may increase the Ochratoxine-A (OTA) hepatotoxicity and many antioxidants may counteract toxic liver function. The present study aims to investigate the hepatoprotective potential of Azadirachta indicaA (A. indica; neem oil) seed oil to reduce acute oxidative disorders and residual OTA toxicity in a 28-day experimental model. The activity of antioxidant and hepatic enzymes, cytokines and the levels of oxidative stress biomarkers –MDA, GSPx, Hydroxiproline, GST, PCC, AGEs, PGC-1, and STIR-1 were analyzed by ELISA. The free radicals ROS and RNS levels were measured by EPR. The protective effects were studied in BALB/C mice treated with A. indica seed oil (170 mg/kg), alone and in combination with OTA (1.25 mg/kg), by gavage daily for 28 days. At the end of the experiment, mice treated with OTA showed changes in liver and antioxidant enzymes, and oxidative stress parameters in the liver and blood. A. indica oil significantly reduced oxidative stress and lipid peroxidation compared to the OTA group. In addition, the hepatic histological evaluation showed significant adipose tissue accumulation in OTA-treated tissues, while treatment with 170 mg/kg A. indica oil showed moderate adipose tissue accumulation. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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14 pages, 3291 KiB

Open AccessArticle

Alanyl-Glutamine Protects against Lipopolysaccharide-Induced Liver Injury in Mice via Alleviating Oxidative Stress, Inhibiting Inflammation, and Regulating Autophagy

by Jiaji Hu, Hanglu Ying, Yigang Zheng, Huabin Ma, Long Li and Yufen Zhao

Antioxidants 2022, 11(6), 1070; https://doi.org/10.3390/antiox11061070 - 27 May 2022

Cited by 13 | Viewed by 3986

Abstract

Acute liver injury is a worldwide problem with a high rate of morbidity and mortality, and effective pharmacological therapies are still urgently needed. Alanyl-glutamine (Ala-Gln), a dipeptide formed from L-alanine and L-glutamine, is known as a protective compound that is involved in various tissue injuries, but there are limited reports regarding the effects of Ala-Gln in acute liver injury. This present study aimed to investigate the protective effects of Ala-Gln in lipopolysaccharide (LPS)-induced acute liver injury in mice, with a focus on inflammatory responses and oxidative stress. The acute liver injury induced using LPS (50 μg/kg) and D-galactosamine (D-Gal) (400 mg/kg) stimulation in mice was significantly attenuated after Ala-Gln treatment (500 and 1500 mg/kg), as evidenced by reduced plasma alanine transaminase (ALT) (p < 0.01, p < 0.001), aspartate transaminase (AST) (p < 0.05, p < 0.001), and lactate dehydrogenase (LDH) (p < 0.01, p < 0.001) levels, and accompanied by improved histopathological changes. In addition, LPS/D-Gal-induced hepatic apoptosis was also alleviated by Ala-Gln administration, as shown by a greatly decreased ratio of TUNEL-positive hepatocytes, from approximately 10% to 2%, and markedly reduced protein levels of cleaved caspase-3 (p < 0.05, p < 0.001) in liver. Moreover, we found that LPS/D-Gal-triggered oxidative stress was suppressed after Ala-Gln treatment, the effect of which might be dependent on the elevation of SOD and GPX activities, and on GSH levels in liver. Interestingly, we observed that Ala-Gln clearly inhibited LPS/D-Gal exposure-induced macrophage accumulation and the production of proinflammatory factors in the liver. Furthermore, Ala-Gln greatly regulated autophagy in the liver in LPS/D-Gal-treated mice. Using RAW264.7 cells, we confirmed the anti-inflammatory role of Ala-Gln-targeting macrophages. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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18 pages, 3234 KiB

Open AccessArticle

N-Acetylcysteine Reverses Monocrotophos Exposure-Induced Hepatic Oxidative Damage via Mitigating Apoptosis, Inflammation and Structural Changes in Rats

by Jagjeet Singh, Annu Phogat, Chandra Prakash, Sunil Kumar Chhikara, Sandeep Singh, Vinay Malik and Vijay Kumar

Antioxidants 2022, 11(1), 90; https://doi.org/10.3390/antiox11010090 - 30 Dec 2021

Cited by 17 | Viewed by 3112

Abstract

Oxidative stress-mediated tissue damage is primarily involved in hepatic injuries and dysfunctioning. Natural antioxidants have been shown to exert hepatoprotective, anti-inflammatory and antiapoptotic properties. The present study evaluated the effect of N-acetylcysteine (NAC) against monocrotophos (MCP) exposure-induced toxicity in the rat liver. Albino Wistar rats were divided into four groups: (1) control, (2) NAC-treated, (3) MCP-exposure, (4) NAC and MCP-coexposure group. The dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) were administered orally for 28 days. Exposure to MCP caused a significant increase in lipid peroxidation, protein oxidation and decreased glutathione content along with the depletion of antioxidant enzyme activities. Further MCP exposure increased pro-inflammatory cytokines levels and upregulated Bax and Caspase-3 expressions. MCP exposure also caused an array of structural alternations in liver tissue, as depicted by the histological and electron microscopic analysis. Thepretreatment of NAC improved glutathione content, restored antioxidant enzyme activities, prevented oxidation of lipids and proteins, decreased pro-inflammatory cytokines levels and normalized apoptotic protein expression. Treatment of NAC also prevented histological and ultrastructural alternations. Thus, the study represents the therapeutic efficacy and antioxidant potential of NAC against MCP exposure in the rat liver. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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17 pages, 4677 KiB

Open AccessArticle

Gardeniae Fructus Attenuates Thioacetamide-Induced Liver Fibrosis in Mice via Both AMPK/SIRT1/NF-κB Pathway and Nrf2 Signaling

by Mi-Rae Shin, Jin A Lee, Minju Kim, Sehui Lee, Minhyuck Oh, Jimin Moon, Joo-Won Nam, Hyukjae Choi, Yeun-Ja Mun and Seong-Soo Roh

Antioxidants 2021, 10(11), 1837; https://doi.org/10.3390/antiox10111837 - 19 Nov 2021

Cited by 33 | Viewed by 3989

Abstract

Liver fibrosis, which means a sort of the excessive accumulation of extracellular matrices (ECMs) components through the liver tissue, is considered as tissue repair or wound-healing status. This pathological stage potentially leads to cirrhosis, if not controlled, it progressively results in hepatocellular carcinoma. Herein, we investigated the pharmacological properties and underlying mechanisms of Gardeniae Fructus (GF) against thioacetamide (TAA)-induced liver fibrosis of mice model. GF not only attenuated hepatic tissue oxidation but also improved hepatic inflammation. We further confirmed that GF led to ameliorating liver fibrosis by ECMs degradations. Regarding the possible underlying mechanism of GF, we observed GF regulated epigenetic regulator, Sirtuin 1 (SIRT1), in TAA-injected liver tissue. These alterations were well supported by SIRT1 related signaling pathways through regulations of its downstream proteins including, AMP-activated protein kinase (AMPK), p47^phox, NADPH oxidase 2, nuclear factor erythroid 2–related factor 2 (Nrf2), and heme oxygenase-1, respectively. To validate the possible mechanism of GF, we used HepG2 cells with hydrogen peroxide treated oxidative stress and chronic exposure conditions via deteriorations of cellular SIRT1. Moreover, GF remarkably attenuated ECMs accumulations in transforming growth factor–β1-induced LX-2 cells relying on the SIRT1 existence. Taken together, GF attenuated liver fibrosis through AMPK/SIRT1 pathway as well as Nrf2 signaling cascades. Therefore, GF could be a clinical remedy for liver fibrosis patients in the future. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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14 pages, 5601 KiB

Open AccessArticle

Zerumbone Exhibit Protective Effect against Zearalenone Induced Toxicity via Ameliorating Inflammation and Oxidative Stress Induced Apoptosis

by Hamad Mohammed AbuZahra, Peramaiyan Rajendran and Mohammad Bani Ismail

Antioxidants 2021, 10(10), 1593; https://doi.org/10.3390/antiox10101593 - 12 Oct 2021

Cited by 31 | Viewed by 3522

Abstract

Zearalenone are widely occurring food contaminants that cause hepatotoxicity. This research work aimed to investigate how zerumbone, a plant-derived dietary compound, can fight ZEA-induced hepatotoxicity. ZER is found to increase the cells’ toxin resistance. This study was performed on mice challenged with ZEA. The administration of ZER decreased the level of alkaline phosphatase and alanine aminotransferase (ALT). Simultaneously, ZER attenuated the inflammatory response via significantly reducing the levels of pro-inflammatory factors, including interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) in serum. Pretreatment with ZER reduced the hepatic malondialdehyde (MDA) concentration, as well as the depletion of hepatic superoxide dismutase (SOD), hepatic glutathione (GSH), and hepatic catalase (CAT). Moreover, it significantly ameliorated ZEA-induced liver damage and histological hepatocyte changes. ZER also relieved ZEA-induced apoptosis by regulating the PI3K/AKT pathway and Nrf2 and HO-1 expression. Furthermore, ZER increasingly activated Bcl2 and suppressed apoptosis marker proteins. Our findings suggest that ZER exhibits the ability to prevent ZEA-induced liver injury and present the underlying molecular basis for potential applications of ZER to cure liver injuries. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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16 pages, 3094 KiB

Open AccessArticle

Ethyl Acetate Fraction of Amomum villosum var. xanthioides Attenuates Hepatic Endoplasmic Reticulum Stress-Induced Non-Alcoholic Steatohepatitis via Improvement of Antioxidant Capacities

by Jung-Hyo Cho, Jong-Suk Lee, Hyeong-Geug Kim, Hye Won Lee, Zhigang Fang, Hyeok-Hee Kwon, Dong Woon Kim, Chang-Min Lee and Jin-Woo Jeong

Antioxidants 2021, 10(7), 998; https://doi.org/10.3390/antiox10070998 - 23 Jun 2021

Cited by 17 | Viewed by 3307

Abstract

Non-alcoholic fatty liver disease (NAFLD), including non-alcoholic steatohepatitis (NASH), affects 25% of the global population. Despite the prevalence of NAFLD worldwide, effective therapeutics are currently lacking. Amomum villosum var. xanthioides (Wall. ex Baker) T.L.Wu & S.J.Chen (AX) is a medicinal herb traditionally used for treating digestive tract disorders in countries across Asia. We aimed to examine the pharmacological effects of the ethyl acetate fraction of AX (AXEF) against tunicamycin (TM)-induced ER stress in a NASH mouse model using C57/BL6J male mice. Following TM injections (2 mg/kg), the mice were orally administrated AXEF (12.5, 25, or 50 mg/kg), silymarin (50 mg/kg), or distilled water daily for 5 days, and the outcomes for fatty liver, inflammation, and oxidative stress were measured in serum or liver tissue levels. AXEF drastically attenuated hepatic ER stress-induced NASH as indicated by decreases in lipid droplet accumulations, serum liver enzymes, hepatic inflammations, and cell death signals in the hepatic tissue and/or serum levels. Interestingly, AXEF showed potent antioxidant effects by quenching reactive oxidative stress and its final product lipid peroxide in the hepatic tissue, specifically an increase in metallothionein (MT). To confirm the underlying actions of AXEF, we observed that AXEF increases MT1 gene promoter activities in the physiological levels. Collectively, AXEF showed antioxidant properties on TM-induced ER stress in a NASH mice model through the improvement of MTs. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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25 pages, 1994 KiB

Open AccessReview

Oxidative Stress Is a Key Modulator in the Development of Nonalcoholic Fatty Liver Disease

by Yuanqiang Ma, Gyurim Lee, Su-Young Heo and Yoon-Seok Roh

Antioxidants 2022, 11(1), 91; https://doi.org/10.3390/antiox11010091 - 30 Dec 2021

Cited by 110 | Viewed by 13624

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, and scientific studies consistently report that NAFLD development can be accelerated by oxidative stress. Oxidative stress can induce the progression of NAFLD to NASH by stimulating Kupffer cells, hepatic stellate cells, and hepatocytes. Therefore, studies are underway to identify the role of antioxidants in the treatment of NAFLD. In this review, we have summarized the origins of reactive oxygen species (ROS) in cells, the relationship between ROS and NAFLD, and have discussed the use of antioxidants as therapeutic agents for NAFLD. Full article

(This article belongs to the Special Issue Oxidative Stress in Hepatic Injury)

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