scholarly journals Corrigendum to: Magnesium isoglycyrrhizinate prevents cadmium-induced activation of JNK and apoptotic hepatocyte death by reversing ROS-inactivated PP2A

2021 ◽  
Author(s):  
Xiaoling Chen ◽  
Xiaoxue Wang ◽  
Liu Yang ◽  
Hongjiang Xu ◽  
Yiqun Wu ◽  
...  
Keyword(s):  
Hepatocyte Death ◽  
Magnesium Isoglycyrrhizinate

scholarly journals Magnesium Isoglycyrrhizinate Ameliorates Concanavalin A-Induced Liver Injury by Inhibiting Autophagy

2022 ◽  
Vol 12 ◽  
Author(s):  
Zihao Fan ◽  
Yuxian Li ◽  
Sisi Chen ◽  
Ling Xu ◽  
Yuan Tian ◽  
...  
Keyword(s):  
Liver Injury ◽  
Protective Effect ◽  
Concanavalin A ◽  
Severe Liver ◽  
Cytokine Levels ◽  
Therapeutic Mechanism ◽  
Severe Liver Dysfunction ◽  
Hepatocyte Death ◽  
Magnesium Isoglycyrrhizinate

Background and Aims: Acute liver failure (ALF) is a type of liver injury that is caused by multiple factors and leads to severe liver dysfunction; however, current treatments for ALF are insufficient. Magnesium isoglycyrrhizinate (MgIG), a novel glycyrrhizin extracted from the traditional Chinese medicine licorice, has a significant protective effect against concanavalin A (ConA)-induced liver injury, but its underlying therapeutic mechanism is unclear. Hence, this study aims to explore the potential therapeutic mechanism of MgIG against ConA-induced immune liver injury.Methods: ConA (20 mg/kg, i. v.) was administered for 12 h to construct an immune liver injury model, and the treatment group was given MgIG (30 mg/kg, i. p.) injection 1 h in advance. Lethality, liver injury, cytokine levels, and hepatocyte death were evaluated. The level of autophagy was evaluated by electron microscopy, RT-PCR and western blotting, and hepatocyte death was assessed in vitro by flow cytometry.Results: MgIG significantly increased the survival rate of mice and ameliorated severe liver injury mediated by ConA. The decrease in the number of autophagosomes, downregulation of LC3b expression and upregulation of p62 expression indicated that MgIG significantly inhibited ConA-induced autophagy in the liver. Reactivation of autophagy by rapamycin (RAPA) reversed the protective effect of MgIG against ConA-induced liver injury. Compared with MgIG treatment, activation of autophagy by RAPA also promoted the expression of liver inflammation markers (IL-1β, IL-6, TNF-α, CXCL-1, CXCL-2, CXCL-10, etc.) and hepatocyte death. In vitro experiments also showed that MgIG reduced ConA-induced hepatocyte death but did not decrease hepatocyte apoptosis by inhibiting autophagy.Conclusion: MgIG significantly ameliorated ConA-induced immune liver injury in mice by inhibiting autophagy. This study provides theoretical support for the ability of MgIG to protect against liver injury in clinical practice.

Danshensu Rescues Ischemia/Reperfusion Caused Human Hepatocyte Death

2018 ◽  
Vol 17 (2) ◽  
pp. 117-121
Author(s):  
Sun Maw-Sheng ◽  
Liang Chun-Ya ◽  
Hsieh Po-Chun ◽  
Kuo Chan-Yen
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Oxygen Species ◽  
Good Strategy ◽  
Ros Accumulation ◽  
Dichlorofluorescin Diacetate ◽  
Hepatocyte Damage ◽  
Hepatocyte Death

Apoptosis of hepatocyte, under ischemia/reperfusion (IR) conditions, has been identified as an essential process in the progression of liver transplantation. Under these conditions, mitochondria can become a threat to the cell because of their capacity to generate reactive oxygen species (ROS). Additionally, ROS overproduction may induce inflammation. As ROS accumulation appears to cause hepatocyte damage or death, there has been considerable interest in identifying the candidate natural products involved and in developing strategies to reduce oxidative stress. In this study, we use Danshensu as a candidate product to speculate whether has the protective effect on apoptotic hepatocyte upon IR. To speculate the apoptotic phenomena was reversed by Danshensu, we detected the p53, cleaved-caspase 3 expression by western blotting, as well as caspase-3 activity. Additionally, we analyzed the ROS levels by 2′,7′-dichlorofluorescin diacetate (DCF-DA) staining. We also detected the cell viability by WST-1. Results showed that Danshensu alleviated hypoxia-caused cell apoptosis via ROS overproduction. We suggested that Danshensu is a good strategy for treating hepatocyte damage upon IR.

scholarly journals Hepatocyte Turnover in Chronic HCV-Induced Liver Injury and Cirrhosis

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Nikolaos P. Karidis ◽  
Ioanna Delladetsima ◽  
Stamatios Theocharis
Keyword(s):  
Current Evidence ◽  
Hepatocellular Injury ◽  
Ongoing Research ◽  
Molecular Events ◽  
Parenchymal Liver ◽  
B Virus ◽  
Multistep Process ◽  
Differential Gene ◽  
Chronic Hcv ◽  
Hepatocyte Death

Chronic hepatitis C virus (HCV) infection may eventually lead to progressive liver fibrosis and cirrhosis through a complex, multistep process involving hepatocyte death and regeneration. Despite common pathogenetic pathways present in all forms of liver cirrhosis irrespective of etiology, hepatocyte turnover and related molecular events in HCV-induced cirrhosis are increasingly being distinguished from even “similar” causes, such as hepatitis B virus- (HBV-) related cirrhosis. New insights in HCV-induced hepatocellular injury, differential gene expression, and regenerative pathways have recently revealed a different pattern of progression to irreversible parenchymal liver damage. A shift to the significant role of the host immune response rather than the direct effect of HCV on hepatocytes and the imbalance between antiapoptotic and proapoptotic signals have been investigated in several studies but need to be further elucidated. The present review aims to comprehensively summarize the current evidence on HCV-induced hepatocellular turnover with a view to outline the significant trends of ongoing research.

scholarly journals Magnesium Isoglycyrrhizinate Reduces Hepatic Lipotoxicity through Regulating Metabolic Abnormalities

2021 ◽  
Vol 22 (11) ◽  
pp. 5884
Author(s):  
Li Lu ◽  
Kun Hao ◽  
Yu Hong ◽  
Jie Liu ◽  
Jinwei Zhu ◽  
...  
Keyword(s):  
Metabolic Diseases ◽  
Lipid Synthesis ◽  
Total Lipid Content ◽  
Metabolic Activation ◽  
Metabolite Profile ◽  
Metabolic Enzymes ◽  
Antagonistic Effect ◽  
Heparg Cells ◽  
Hepatic Lipotoxicity ◽  
Magnesium Isoglycyrrhizinate

The excessive accumulation of lipids in hepatocytes induces a type of cytotoxicity called hepatic lipotoxicity, which is a fundamental contributor to liver metabolic diseases (such as NAFLD). Magnesium isoglycyrrhizinate (MGIG), a magnesium salt of the stereoisomer of natural glycyrrhizic acid, is widely used as a safe and effective liver protectant. However, the mechanism by which MGIG protects against NAFLD remains unknown. Based on the significant correlation between NAFLD and the reprogramming of liver metabolism, we aimed to explore the beneficial effects of MGIG from a metabolic viewpoint in this paper. We treated HepaRG cells with palmitic acid (PA, a saturated fatty acid of C16:0) to induce lipotoxicity and then evaluated the antagonistic effect of MGIG on lipotoxicity by investigating the cell survival rate, DNA proliferation rate, organelle damage, and endoplasmic reticulum stress (ERS). Metabolomics, lipidomics, and isotope tracing were used to investigate changes in the metabolite profile, lipid profile, and lipid flux in HepaRG cells under different intervention conditions. The results showed that MGIG can indeed protect hepatocytes against PA-induced cytotoxicity and ERS. In response to the metabolic abnormality of lipotoxicity, MGIG curtailed the metabolic activation of lipids induced by PA. The content of total lipids and saturated lipids containing C16:0 chains increased significantly after PA stimulation and then decreased significantly or even returned to normal levels after MGIG intervention. Lipidomic data show that glycerides and glycerophospholipids were the two most affected lipids. For excessive lipid accumulation in hepatocytes, MGIG can downregulate the expression of the metabolic enzymes (GPATs and DAGTs) involved in triglyceride biosynthesis. In conclusion, MGIG has a positive regulatory effect on the metabolic disorders that occur in hepatocytes under lipotoxicity, and the main mechanisms of this effect are in lipid metabolism, including reducing the total lipid content, reducing lipid saturation, inhibiting glyceride and glycerophospholipid metabolism, and downregulating the expression of metabolic enzymes in lipid synthesis.

scholarly journals Prevention and Therapeutic Effects and Mechanisms of Tanshinone IIA Sodium Sulfonate on Acute Liver Injury Mice Model

2016 ◽  
Vol 2016 ◽  
pp. 1-8
Author(s):  
Lunjie Lu ◽  
Jun Zhou ◽  
Jingying Zhang ◽  
Jun Che ◽  
Yang Jiao ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Salvia Miltiorrhiza ◽  
Water Soluble ◽  
Tanshinone Iia ◽  
Therapeutic Effects ◽  
Mice Model ◽  
Sodium Sulfonate ◽  
Pharmacologically Active ◽  
Magnesium Isoglycyrrhizinate

Tanshinone IIA sodium sulfonate (TSS) is a water-soluble derivative of tanshinone IIA, which is the main pharmacologically active component of Salvia miltiorrhiza. This study aimed to verify the preventive and therapeutic effects of TSS and its combined therapeutic effects with magnesium isoglycyrrhizinate (MI) in D-galactosamine- (D-Gal-) induced acute liver injury (ALI) in mice. The potential regulatory mechanisms of TSS on ALI were also examined. Our results may provide a basis for the development of novel therapeutics for ALI.

Apocynum venetum Attenuates Acetaminophen-Induced Liver Injury in Mice

2015 ◽  
Vol 43 (03) ◽  
pp. 457-476 ◽  
Author(s):  
Wenyan Xie ◽  
Chen Chen ◽  
Zhihui Jiang ◽  
Jian Wang ◽  
Matthias F. Melzig ◽  
...  
Keyword(s):  
Liver Injury ◽  
Histopathological Examination ◽  
Folk Medicine ◽  
Analgesic Drug ◽  
Once Daily ◽  
Apocynum Venetum ◽  
Anti Oxidant ◽  
Underlying Mechanisms ◽  
Serum Aminotransferases ◽  
Hepatocyte Death

Apocynum venetum L. (A. venetum) has long been used in oriental folk medicine for the treatment of some liver diseases; however, the underlying mechanisms remain to be fully elucidated. Acetaminphen (APAP) is a widely used analgesic drug that can cause acute liver injury in overdose situations. In this study, we investigated the potential protective effect of A. venetum leaf extract (ALE) against APAP-induced hepatotoxicity. Mice were intragastrically administered with ALE once daily for 3 consecutive days prior to receiving a single intraperitoneal injection of APAP. The APAP group showed severe liver injury characterized by the noticeable fluctuations in the following parameters: serum aminotransferases; hepatic malondialdehyde (MDA), 3-nitrotyrosine (3-NT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH). These liver damages induced by APAP were significantly attenuated by ALE pretreatments. A collective analysis of histopathological examination, DNA laddering and western blot for caspase-3 and cytochrome c indicated that the ALE is also capable of preventing APAP-induced hepatocyte death. Hyperoside, isoquercitrin and their derivatives have been identified as the major components of ALE using HPLC-MS/MS. Taken together, the A. venetum possesses hepatoprotective effects partially due to its anti-oxidant action.

scholarly journals SLAMF1 Mediates Hepatocyte Death in a Model of Non‐Alcoholic Steatohepatitis

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Oscar Gomez Torres ◽  
Shripa Amatya ◽  
Hrishikesh Samant ◽  
Jonathan Alexander ◽  
Emma Burgos‐Ramos ◽  
...  
Keyword(s):  
Alcoholic Steatohepatitis ◽  
Hepatocyte Death
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