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      Hepatoprotective effect of essential oils of Nepeta cataria L. on acetaminophen-induced liver dysfunction

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          Abstract

          Nepeta cataria L. has long been used in folk food and medicine for several functions. Essential oils (EOs) were extracted from Nepeta cataria L. by supercritical fluid extraction. The results of animal experiments showed that EOs from Nepeta cataria L. significantly attenuated acetaminophen-induced liver damage. Further study confirmed that EOs were able to increase mRNA expression of uridine diphosphate glucuronosyltransferases (UGTs) and sulfotransferases (SULTs), as well as inhibit CYP2E1 activities, and thereby suppressed toxic intermediate formation. Nrf-2 activation might be involved in EOs-induced up-regulation of Phase II enzymes. Collectively, our data provide evidence that EOs protect the liver against acetaminophen-induced liver injury mainly by accelerating acetaminophen harmless metabolism, implying that EOs can be considered as a potential natural resource to develop hepatoprotective agent.

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          Acetaminophen-Induced Hepatotoxicity: a Comprehensive Update

          Eric Yoon, Arooj Babar, Moaz Choudhary … (2016)
          Abstract Hepatic injury and subsequent hepatic failure due to both intentional and non-intentional overdose of acetaminophen (APAP) has affected patients for decades, and involves the cornerstone metabolic pathways which take place in the microsomes within hepatocytes. APAP hepatotoxicity remains a global issue; in the United States, in particular, it accounts for more than 50% of overdose-related acute liver failure and approximately 20% of the liver transplant cases. The pathophysiology, disease course and management of acute liver failure secondary to APAP toxicity remain to be precisely elucidated, and adverse patient outcomes with increased morbidity and mortality continue to occur. Although APAP hepatotoxicity follows a predictable timeline of hepatic failure, its clinical presentation might vary. N-acetylcysteine (NAC) therapy is considered as the mainstay therapy, but liver transplantation might represent a life-saving procedure for selected patients. Future research focus in this field may benefit from shifting towards obtaining antidotal knowledge at the molecular level, with focus on the underlying molecular signaling pathways.
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            Oxidative stress during acetaminophen hepatotoxicity: Sources, pathophysiological role and therapeutic potential

            Kuo Du, Anup Ramachandran, Hartmut Jaeschke (2016)
            Acetaminophen (APAP) hepatotoxicity is characterized by an extensive oxidative stress. However, its source, pathophysiological role and possible therapeutic potential if targeted, have been controversially described. Earlier studies argued for cytochrome P450-generated reactive oxygen species (ROS) during APAP metabolism, which resulted in massive lipid peroxidation and subsequent liver injury. However, subsequent studies convincingly challenged this assumption and the current paradigm suggests that mitochondria are the main source of ROS, which impair mitochondrial function and are responsible for cell signaling resulting in cell death. Although immune cells can be a source of ROS in other models, no reliable evidence exists to support a role for immune cell-derived ROS in APAP hepatotoxicity. Recent studies suggest that mitochondrial targeted antioxidants can be viable therapeutic agents against hepatotoxicity induced by APAP overdose, and re-purposing existing drugs to target oxidative stress and other concurrent signaling events can be a promising strategy to increase its potential application in patients with APAP overdose.
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              4-Hydroxyphenylacetic Acid Prevents Acute APAP-Induced Liver Injury by Increasing Phase II and Antioxidant Enzymes in Mice

              Hongqiong Zhao, Zhihui Jiang, Xuemei Chang … (2018)
              Acetaminophen (APAP) overdose is the principal cause of drug-induced acute liver failure. 4-hydroxyphenylacetic acid (4-HPA), a major microbiota-derived metabolite of polyphenols, is involved in the antioxidative action. This study seeks to investigate the ability of 4-HPA to protect against APAP-induced hepatotoxicity, as well as the putative mechanisms involved. Mice were treated with 4-HPA (6, 12, or 25 mg/kg) for 3 days, 1 h after the last administration of 4-HPA, a single dose of APAP was intraperitoneally infused for mice. APAP caused a remarkable increase of oxidative stress markers, peroxynitrite formation, and fewer activated phase II enzymes. 4-HPA increased Nrf2 translocation to the nucleus and enhanced the activity of phase II and antioxidant enzymes, and could thereby ameliorate APAP-induced liver injury. Studies reveal that 4-HPA, as an active area of bioactive dietary constituents, could protect the liver against APAP-induced injury, implying that 4-HPA could be a new promising strategy and natural hepatoprotective drug.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biosci Rep
                Journal ID (iso-abbrev): Biosci. Rep
                Journal ID (hwp): ppbioscirep
                Journal ID (publisher-id): BSR
                Title: Bioscience Reports
                Publisher: Portland Press Ltd.
                ISSN (Print): 0144-8463
                ISSN (Electronic): 1573-4935
                Publication date (Electronic preprint): 23 July 2019
                Publication date Collection: 30 August 2019
                Publication date (Electronic): 07 August 2019
                Volume: 39
                Issue: 8
                Electronic Location Identifier: BSR20190697
                Affiliations
                [1 ]Department of Tranditional Chinese Medicine, The Affiliated Hospital of Yan’an University, Shaanxi 71600, Yan’an, China
                [2 ]Department of Traditional Chinese Medicine, Shaanxi People’s Hospital, Shaanxi 710068, Xi’an, China
                [3 ]Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China
                Author notes
                Correspondence: Feng Qiao ( yuqiaofeng19701222@ 123456163.com )
                Author information
                http://orcid.org/0000-0002-5617-2755
                Article
                DOI: 10.1042/BSR20190697
                PMC ID: 6684950
                PubMed ID: 31337687
                SO-VID: 5515a903-cf31-480e-ba31-3f71f91ba6c9
                Copyright © © 2019 The Author(s).
                License:

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                Date received : 25 March 2019
                Date revision received : 24 June 2019
                Date accepted : 16 July 2019
                Page count
                Pages: 9
                Categories
                Subject: Research Articles
                Subject: Research Article
                Subject: 8
                Subject: 39
                Subject: 36
                Subject: 45

                ScienceOpen disciplines: Life sciences
                Keywords: essential oil,hepatoprotective,nepeta cataria l.
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: essential oil, hepatoprotective, nepeta cataria l.

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