Extracts from Erythronium japonicum and Corylopsis coreana Uyeki reduce 1,3-dichloro-2-propanol-mediated oxidative stress in human hepatic cells

Abstract Reducing oxidative stress is an effective method to prevent hepatic ischaemia/reperfusion injury (HIRI). This study focuses on the role of propofol on the oxidative stress of hepatic cells and the involved lncRNA-TUG1/Brahma-related gene 1 (Brg1) pathway in HIRI mice. The mouse HIRI model was established and was intraperitoneally injected with propofol postconditioning. Hepatic injury indexes were used to evaluate HIRI. The oxidative stress was indicated by increasing 8-isoprostane concentration. Mouse hepatic cell line AML12 was treated with hypoxia and subsequent reoxygenation (H/R). The targeted regulation of lncRNA-TUG1 on Brg1 was proved by RNA pull-down, RIP (RNA-binding protein immunoprecipitation) and the expression level of Brg1 responds to silencing or overexpression of lncRNA-TUG1. Propofol alleviates HIRI and induces the upregulation of lncRNA-TUG1 in the mouse HIRI model. Propofol increases cell viability and lncRNA-TUG1 expression level in H/R-treated hepatic cells. In H/R plus propofol-treated hepatic cells, lncRNA-TUG1 silencing reduces cell viability and increased oxidative stress. LncRNA-TUG1 interacts with Brg1 protein and keeps its level via inhibiting its degradation. Brg1 overexpression reverses lncRNA-TUG1 induced the reduction of cell viability and the increase in oxidative stress. LncRNA-TUG1 silencing abrogates the protective role of propofol against HIRI in the mouse HIRI model. LncRNA-TUG1 has a targeted regulation of Brg1, and thereby affects the oxidative stress induced by HIRI. This pathway mediates the protective effect of propofol against HIRI of hepatic cell.

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An aqueous extract of Zingiber officinale Roscoe protects mouse primary hepatic cells against hydrogen peroxide-induced oxidative stress

Biotechnology and Bioprocess Engineering ◽

10.1007/s12257-011-0433-8 ◽

2012 ◽

Vol 17 (1) ◽

pp. 168-175 ◽

Cited By ~ 4

Author(s):

Su Young Oh ◽

Ji-hye Lee ◽

Ji Seon Lee ◽

Sanghee Seo ◽

Jinyeul Ma

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Aqueous Extract ◽

Zingiber Officinale ◽

Hepatic Cells ◽

Zingiber Officinale Roscoe

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Tartary buckwheat flavonoids protect hepatic cells against high glucose-induced oxidative stress and insulin resistance via MAPK signaling pathways

Food & Function ◽

10.1039/c5fo01467k ◽

2016 ◽

Vol 7 (3) ◽

pp. 1523-1536 ◽

Cited By ~ 14

Author(s):

Yuanyuan Hu ◽

Zuoxu Hou ◽

Dongyang Liu ◽

Xingbin Yang

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Signaling Pathways ◽

High Glucose ◽

Crucial Role ◽

Mapk Signaling ◽

Tartary Buckwheat ◽

Hepatic Cells ◽

Chronic Complication ◽

Mapk Signaling Pathways

Oxidative stress plays a crucial role in chronic complication of diabetes.

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Silybin counteracts lipid excess and oxidative stress in cultured steatotic hepatic cells

World Journal of Gastroenterology ◽

10.3748/wjg.v22.i26.6016 ◽

2016 ◽

Vol 22 (26) ◽

pp. 6016 ◽

Cited By ~ 19

Author(s):

Giulia Vecchione ◽

Elena Grasselli ◽

Adriana Voci ◽

Francesca Baldini ◽

Ignazio Grattagliano ◽

...

Keyword(s):

Oxidative Stress ◽

Hepatic Cells ◽

And Oxidative Stress

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Autophagy in Triptolide-Mediated Cytotoxicity in Hepatic Cells

International Journal of Toxicology ◽

10.1177/1091581819864518 ◽

2019 ◽

Vol 38 (5) ◽

pp. 436-444 ◽

Cited By ~ 1

Author(s):

Yan Ming Wei ◽

Zhi Hua Luan ◽

Bi Wang Liu ◽

Yong Hui Wang ◽

Yin Xia Chang ◽

...

Keyword(s):

Oxidative Stress ◽

Chinese Herb ◽

Normal Liver ◽

Caspase 9 ◽

Tripterygium Wilfordii Hook F ◽

Hepatic Cells ◽

Traditional Chinese Herb ◽

Intracellular Process ◽

Tripterygium Wilfordii Hook ◽

Related Proteins

Triptolide is a major active ingredient isolated from the traditional Chinese herb Tripterygium wilfordii Hook F. However, its use in clinical practice is limited due to its severe hepatotoxicity. Autophagy, a highly conserved intracellular process, is essential for maintaining cytoplasmic homeostasis. Considering that abnormalities in autophagy are closely associated with drug-mediated hepatotoxicity, we applied human normal liver HL7702 cells to elucidate the roles of autophagy in triptolide-induced hepatotoxicity. Our study revealed that triptolide was cytotoxic to HL7702 cells. It markedly increased autophagosome formation and expression of autophagy-related proteins, namely Beclin1 and microtubule-associated protein 1 light chain 3II, and induced oxidative stress. These proautophagic effects were counteracted by pretreatment with N-acetylcysteine, a reactive oxygen species scavenger. Moreover, the pharmacological suppression of autophagy further exacerbated triptolide-elicited decrease in cell viability, increase in lactate dehydrogenase leakage, and activation of apoptosis proteases (caspase 3 and caspase 9). Our findings suggest that triptolide-induced oxidative stress consequently enhances autophagic activity, and autophagy is a cytoprotective mechanism against triptolide-induced cytotoxicity in HL7702 cells.

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Antioxidant and Anti-Apoptotic Properties of Oat Bran Protein Hydrolysates in Stressed Hepatic Cells

Foods ◽

10.3390/foods8050160 ◽

2019 ◽

Vol 8 (5) ◽

pp. 160 ◽

Cited By ~ 4

Author(s):

Ramak Esfandi ◽

William G. Willmore ◽

Apollinaire Tsopmo

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzyme ◽

Caspase 3 ◽

Stress Proteins ◽

Protein Hydrolysates ◽

Cellular Damage ◽

Enzyme Assays ◽

Antioxidant Enzyme Activities ◽

Hepatic Cells ◽

Oat Bran

The objective of this work was to find out how the method to extract proteins and subsequent enzymatic hydrolysis affect the ability of hepatic cells to resist oxidative stress. Proteins were isolated from oat brans in the presence of Cellulase (CPI) or Viscozyme (VPI). Four protein hydrolysates were produced from CPI and four others from VPI when they treated with Alcalase, Flavourzyme, Papain, or Protamex. Apart from CPI-Papain that reduced the viability of cell by 20%, no other hydrolysate was cytotoxic in the hepatic HepG2 cells. In the cytoprotection test, VPI-Papain and VPI-Flavourzyme fully prevented the damage due to peroxyl radical while CPI-Papain and CPI-Alcalase enhanced the cellular damage. Cells treated with VPI-hydrolysates reduced intracellular reactive oxygen species (ROS) by 20–40% and, also increased the intracellular concentration of glutathione, compared to CPI-hydrolysates. In antioxidant enzyme assays, although all hydrolysates enhanced the activity of both superoxide dismutase and catalase by up to 2- and 3.4-fold, respectively relative the control cells, the largest increase was due to VPI-Papain and VPI-Flavourzyme hydrolysates. In caspase-3 assays, hydrolysates with reduced ROS or enhanced antioxidant enzyme activities were able to reduce the activity of the pro-apoptotic enzyme, caspase-3 indicating that they prevented oxidative stress-induced cell death.

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Alteration of hepatic cells glucose metabolism as a non-cholinergic detoxication mechanism in counteracting diazinon-induced oxidative stress

Human & Experimental Toxicology ◽

10.1177/0960327106075064 ◽

2006 ◽

Vol 25 (12) ◽

pp. 697-703 ◽

Cited By ~ 59

Author(s):

Fatemeh Teimouri ◽

Nasim Amirkabirian ◽

Hadi Esmaily ◽

Azadeh Mohammadirad ◽

Atousa Aliahmadi ◽

...

Keyword(s):

Oxidative Stress ◽

Plasma Glucose ◽

Phosphoenolpyruvate Carboxykinase ◽

Liver Lipid ◽

Liver Homogenate ◽

Thiobarbituric Acid ◽

Predisposing Factor ◽

Cholinergic Mechanism ◽

Hepatic Cells ◽

Total Antioxidant

The aim of this study was to evaluate effects of acute exposure to various doses of diazinon, a widely used synthetic organophosphorus (OP) insecticide on plasma glucose, hepatic cells key enzymes of glycogenolysis and gluconeogenesis, and oxidative stress in rats. Diazinon was administered by gavage at doses of 15, 30 and 60 mg/kg. The liver was perfused and removed under anaesthesia. The activities of glycogen phosphorylase (GP), phosphoenolpyruvate carboxykinase (PEPCK), thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity (TAC) were analysed in liver homogenate. Administration of diazinon (15, 30 and 60 mg/kg) increased plasma glucose concentrations by 101.43% (P=0.001), 103.68% (P=0.000) and 160.65% (P=0.000) of control, respectively. Diazinon (15, 30 and 60 mg/kg) increased hepatic GP activity by 43.5% (P=0.05), 70.3% (P=0.00) and 117.2% (P=0.02) of control, respectively. In addition, diazinon (30 and 60 mg/kg) increased hepatic PEPCK by 77.3% (P=0.000) and 93.5% (P=0.000) of control, respectively. Diazinon (30 and 60 mg/kg) decreased liver TAC by 38% (P=0.046) and 48% (P=0.000) of control, respectively. Also diazinon (30 and 60 mg/kg) increased hepatic cell liver lipid peroxidation by 77% (P=0.05) and 280% (P=0.000) of control. The correlations between plasma glucose and hepatic cells TBARS (r2=0.537, P=0.02), between plasma glucose and ChE activity (r2=0.81, P=0.049) and between plasma glucose and hepatic cells GP activity (r2=0.833, P=0.04) were significant. It is concluded that the liver cells are a site of toxic action of diazinon. Diazinon increases glucose release from liver into blood through activation of glycogenolysis and gluconeogenesis as a detoxication non-cholinergic mechanism to overwhelm diazinon-induced toxic stress. The results are in accordance with the hypothesis that OPs are a predisposing factor of diabetes.

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