Literature DB >> 27596680

Antcin H Protects Against Acute Liver Injury Through Disruption of the Interaction of c-Jun-N-Terminal Kinase with Mitochondria.

Yazhen Huo1,2, Sanda Win2, Tin Aung Than2, Shutao Yin1, Min Ye3, Hongbo Hu1, Neil Kaplowitz2.   

Abstract

AIM: Antrodia Camphorate (AC) is a mushroom that is widely used in Asian countries to prevent and treat various diseases, including liver diseases. However, the active ingredients that contribute to the biological functions remain elusive. The purpose of the present study is to test the hepatoprotective effect of Antcin H, a major triterpenoid chemical isolated from AC, in murine models of acute liver injury.
RESULTS: We found that Antcin H pretreatment protected against liver injury in both acetaminophen (APAP) and galactosamine/tumor necrosis factor (TNF)α models. More importantly, Antcin H also offered a significant protection against acetaminophen-induced liver injury when it was given 1 h after acetaminophen. The protection was verified in primary mouse hepatocytes. Antcin H prevented sustained c-Jun-N-terminal kinase (JNK) activation in both models. We excluded an effect of Antcin H on acetaminophen metabolism and TNF receptor signaling and excluded a direct effect as a free radical scavenger or JNK inhibitor. Since the sustained JNK activation through its interaction with mitochondrial Sab, leading to increased mitochondrial reactive oxygen species (ROS), is pivotal in both models, we examined the effect of Antcin H on p-JNK binding to mitochondria and impairment of mitochondrial respiration. Antcin H inhibited the direct effect of p-JNK on isolated mitochondrial function and binding to isolated mitochondria. Innovation and
Conclusion: Our study has identified Antcin H as a novel active ingredient that contributes to the hepatoprotective effect of AC, and Antcin H protects against liver injury through disruption of the binding of p-JNK to Sab, which interferes with the ROS-dependent self-sustaining activation of MAPK cascade. Antioxid. Redox Signal. 26, 207-220.

Entities:  

Keywords:  Antcin H; Antrodia Camphorate; ROS; c-Jun-N-terminal kinase; liver injury; mitochondria

Mesh:

Substances:

Year:  2016        PMID: 27596680      PMCID: PMC5312552          DOI: 10.1089/ars.2016.6833

Source DB:  PubMed          Journal:  Antioxid Redox Signal        ISSN: 1523-0864            Impact factor:   8.401


  47 in total

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4.  Deletion of apoptosis signal-regulating kinase 1 attenuates acetaminophen-induced liver injury by inhibiting c-Jun N-terminal kinase activation.

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6.  Inhibitory effects of antrodins A-E from Antrodia cinnamomea and their metabolites on hepatitis C virus protease.

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Review 8.  Protective effects of Antrodia cinnamomea against liver injury.

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10.  Review of Pharmacological Effects of Antrodia camphorata and Its Bioactive Compounds.

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1.  Mitochondrial depolarization and repolarization in the early stages of acetaminophen hepatotoxicity in mice.

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Review 2.  Acetaminophen Toxicity: Novel Insights Into Mechanisms and Future Perspectives.

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Review 3.  A mitochondrial journey through acetaminophen hepatotoxicity.

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Review 4.  New insights into the role and mechanism of c-Jun-N-terminal kinase signaling in the pathobiology of liver diseases.

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Review 6.  Drug-Induced Liver Injury: Cascade of Events Leading to Cell Death, Apoptosis or Necrosis.

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Review 7.  The Regulation of JNK Signaling Pathways in Cell Death through the Interplay with Mitochondrial SAB and Upstream Post-Translational Effects.

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Review 9.  Mechanisms of acetaminophen-induced liver injury and its implications for therapeutic interventions.

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Review 10.  Functional Role of p53 in the Regulation of Chemical-Induced Oxidative Stress.

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