Down-regulation of miR-192-5p protects from oxidative stress-induced acute liver injury

2016 ◽  
Vol 130 (14) ◽  
pp. 1197-1207 ◽  
Author(s):  
Sanchari Roy ◽  
Fabian Benz ◽  
Jan Alder ◽  
Heike Bantel ◽  
Joern Janssen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Liver Injury ◽  
Therapeutic Approach ◽  
Acute Liver Injury ◽  
Down Regulation

In the present study, we demonstrate that miR-192-5p is critically involved in the regulation of cell death during acute liver injury, highlighting a potential miR-based therapeutic approach in this setting.

Down regulation of DJ-1 enhances cell death by oxidative stress, ER stress, and proteasome inhibition

2003 ◽  
Vol 312 (4) ◽  
pp. 1342-1348 ◽  
Author(s):  
Takanori Yokota ◽  
Kanako Sugawara ◽  
Kaoru Ito ◽  
Ryosuke Takahashi ◽  
Hiroyoshi Ariga ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Er Stress ◽  
Proteasome Inhibition ◽  
Down Regulation

Sinomenine attenuates alcohol-induced acute liver injury via inhibiting oxidative stress, inflammation and apoptosis in mice

2021 ◽  
pp. 112759
Author(s):  
Hui Fan ◽  
Tingting Tu ◽  
Xiao Zhang ◽  
Qiankun Yang ◽  
Jinxin Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Acute Liver Injury

scholarly journals The Late-Stage Protective Effect of Mito-TEMPO against Acetaminophen-Induced Hepatotoxicity in Mouse and Three-Dimensional Cell Culture Models

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 965
Author(s):  
Mohammad Abdullah-Al-Shoeb ◽  
Kenta Sasaki ◽  
Saori Kikutani ◽  
Nanami Namba ◽  
Keiichi Ueno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Culture ◽  
Liver Injury ◽  
Protective Effect ◽  
Acute Liver Injury ◽  
Three Dimensional ◽  
3D Cell Culture ◽  
Cell Culture Model ◽  
Culture Model ◽  
Apap Hepatotoxicity

An overdose of acetaminophen (APAP), the most common cause of acute liver injury, induces oxidative stress that subsequently causes mitochondrial impairment and hepatic necroptosis. N-acetyl-L-cysteine (NAC), the only recognized drug against APAP hepatotoxicity, is less effective the later it is administered. This study evaluated the protective effect of mitochondria-specific Mito-TEMPO (Mito-T) on APAP-induced acute liver injury in C57BL/6J male mice, and a three dimensional (3D)-cell culture model containing the human hepatoblastoma cell line HepG2. The administration of Mito-T (20 mg/kg, i.p.) 1 h after APAP (400 mg/kg, i.p.) injection markedly attenuated the APAP-induced elevated serum transaminase activity and hepatic necrosis. However, Mito-T treatment did not affect key factors in the development of APAP liver injury including the activation of c-jun N-terminal kinases (JNK), and expression of the transcription factor C/EBP homologous protein (CHOP) in the liver. However, Mito-T significantly reduced the APAP-induced increase in the hepatic oxidative stress marker, nitrotyrosine, and DNA fragmentation. Mito-T markedly attenuated cytotoxicity induced by APAP in the HepG2 3D-cell culture model. Moreover, liver regeneration after APAP hepatotoxicity was not affected by Mito-T, demonstrated by no changes in proliferating cell nuclear antigen formation. Therefore, Mito-T was hepatoprotective at the late-stage of APAP overdose in mice.

scholarly journals Liver Autophagy in Anorexia Nervosa and Acute Liver Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Marouane Kheloufi ◽  
Chantal M. Boulanger ◽  
François Durand ◽  
Pierre-Emmanuel Rautou
Keyword(s):  
Cell Death ◽  
Anorexia Nervosa ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Mechanism ◽  
Liver Insufficiency ◽  
Electron Microscopy Analysis ◽  
Microscopy Analysis ◽  
Rescue Mechanism ◽  
Liver Cell Death

Autophagy, a lysosomal catabolic pathway for long-lived proteins and damaged organelles, is crucial for cell homeostasis, and survival under stressful conditions. During starvation, autophagy is induced in numerous organisms ranging from yeast to mammals, and promotes survival by supplying nutrients and energy. In the early neonatal period, when transplacental nutrients supply is interrupted, starvation-induced autophagy is crucial for neonates’ survival. In adult animals, autophagy provides amino acids and participates in glucose metabolism following starvation. In patients with anorexia nervosa, autophagy appears initially protective, allowing cells to copes with nutrient deprivation. However, when starvation is critically prolonged and when body mass index reaches 13 kg/m2or lower, acute liver insufficiency occurs with features of autophagic cell death, which can be observed by electron microscopy analysis of liver biopsy samples. In acetaminophen overdose, a classic cause of severe liver injury, autophagy is induced as a protective mechanism. Pharmacological enhancement of autophagy protects against acetaminophen-induced necrosis. Autophagy is also activated as a rescue mechanism in response to Efavirenz-induced mitochondrial dysfunction. However, Efavirenz overdose blocks autophagy leading to liver cell death. In conclusion, in acute liver injury, autophagy appears as a protective mechanism that can be however blocked or overwhelmed.

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