Oxidative Stress in Nonalcoholic Steatohepatitis

2016 ◽  
pp. 349-361
Author(s):  
Akinobu Takaki ◽  
Daisuke Uchida ◽  
Kazuhide Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Nonalcoholic Steatohepatitis

II. Cytochrome P-450 enzymes and oxidative stress

2001 ◽  
Vol 281 (5) ◽  
pp. G1135-G1139 ◽  
Author(s):  
Graham Robertson ◽  
Isabelle Leclercq ◽  
Geoffrey C. Farrell
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Molecular Oxygen ◽  
Hepatic Steatosis ◽  
Nonalcoholic Steatohepatitis ◽  
Acid Oxidation ◽  
Cellular Injury ◽  
Second Hit ◽  
Cytochrome P 450 ◽  
And Oxidative Stress

Oxidative stress is present in the liver of humans with steatosis and nonalcoholic steatohepatitis (NASH) and is a plausible mediator of cellular injury, inflammatory recruitment, and fibrogenesis. CYPs 2E1 and 4A are the microsomal oxidases involved with fatty acid oxidation. Both enzymes can reduce molecular oxygen to produce prooxidant species, which, if not countered efficiently by antioxidants, create oxidative stress. In this theme article, we present the evidence that, in the context of hepatic steatosis, CYPs 2E1 and 4A could generate the “second hit” of cellular injury, particularly when antioxidant reserves are depleted, and propose ways in which this could contribute to the pathogenesis of NASH.

scholarly journals Current and Potential Therapies Targeting Inflammation in NASH

2021 ◽  
Vol 12 ◽  
Author(s):  
Somaya Albhaisi ◽  
Mazen Noureddin
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Adipose Tissue ◽  
Liver Disease ◽  
Immune Responses ◽  
Nonalcoholic Steatohepatitis ◽  
Targeted Therapies ◽  
Fatty Liver Disease ◽  
Hepatocellular Injury ◽  
Nonalcoholic Fatty Liver

Nonalcoholic steatohepatitis (NASH) is the advanced form of nonalcoholic fatty liver disease (NAFLD). It is characterized by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis. Inflammation plays a key role in the progression of NASH and can be provoked by intrahepatic (e.g., lipotoxicity, immune responses, oxidative stress and cell death) and extrahepatic sources (adipose tissue or gut). The identification of triggers of inflammation is central to understanding the mechanisms in NASH development and progression and in designing targeted therapies that can halt or reverse the disease. In this review, we summarize the current and potential therapies targeting inflammation in NASH.

Upregulation of osteopontin expression is involved in the development of nonalcoholic steatohepatitis in a dietary murine model

2004 ◽  
Vol 287 (1) ◽  
pp. G264-G273 ◽  
Author(s):  
Atul Sahai ◽  
Padmini Malladi ◽  
Hector Melin-Aldana ◽  
Richard M. Green ◽  
Peter F. Whitington
Keyword(s):  
Oxidative Stress ◽  
Mrna Expression ◽  
Nonalcoholic Steatohepatitis ◽  
Transforming Growth Factor ◽  
Control Diet ◽  
Transforming Growth Factor Β ◽  
Collagen I ◽  
Tnf Α ◽  
Th1 Cytokine

The pathogenesis of nonalcoholic steatohepatitis (NASH) is poorly defined. Feeding mice a diet deficient in methionine and choline (MCD diet) induces experimental NASH. Osteopontin (OPN) is a Th1 cytokine that plays an important role in several fibroinflammatory diseases. We examined the role of OPN in the development of experimental NASH. A/J mice were fed MCD or control diet for up to 12 wk, and serum alanine aminotransferase (ALT), liver histology, oxidative stress, and the expressions of OPN, TNF-α, and collagen I were assessed at various time points. MCD diet-fed mice developed hepatic steatosis starting after 1 wk and inflammation by 2 wk; serum ALT increased from day 3. Hepatic collagen I mRNA expression increased during 1–4 wk, and fibrosis appeared at 8 wk. OPN protein expression was markedly increased on day 1 of MCD diet and persisted up to 8 wk, whereas OPN mRNA expression was increased at week 4. TNF-α expression was increased from day 3 to 2 wk, and evidence of oxidative stress did not appear until 8 wk. Increased expression of OPN was predominantly localized in hepatocytes. Hepatocytes in culture also produced OPN, which was stimulated by transforming growth factor-β and TNF-α. Moreover, MCD diet-induced increases in serum ALT levels, hepatic inflammation, and fibrosis were markedly reduced in OPN−/− mice when compared with OPN+/+ mice. In conclusion, our results demonstrate an upregulation of OPN expression early in the development of steatohepatitis and suggest an important role for OPN in signaling the onset of liver injury and fibrosis in experimental NASH.

Integrative transcriptomics and metabolomics explore the mechanism of kaempferol on improving nonalcoholic steatohepatitis

2020 ◽  
Vol 11 (11) ◽  
pp. 10058-10069
Author(s):  
Yifei Lu ◽  
Mingmei Shao ◽  
Hongjiao Xiang ◽  
Peiyong Zheng ◽  
Tao Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Energy Metabolism ◽  
Nonalcoholic Steatohepatitis ◽  
Alcoholic Steatohepatitis ◽  
Integration Analysis

By integration analysis of transcriptomics and metabolomics, Kaempferol was found to improve non-alcoholic steatohepatitis in mice probably through regulating energy metabolism, lipid metabolism, oxidative stress and inflammation-related pathways.

Fucoxanthin inhibits hepatic oxidative stress, inflammation, and fibrosis in diet-induced nonalcoholic steatohepatitis model mice

2020 ◽  
Vol 528 (2) ◽  
pp. 305-310 ◽  
Author(s):  
Naoki Takatani ◽  
Yuka Kono ◽  
Fumiaki Beppu ◽  
Yuko Okamatsu-Ogura ◽  
Yumiko Yamano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nonalcoholic Steatohepatitis ◽  
Hepatic Oxidative Stress

Serotonin Mediates Oxidative Stress and Mitochondrial Toxicity in a Murine Model of Nonalcoholic Steatohepatitis

2007 ◽  
Vol 133 (2) ◽  
pp. 608-618 ◽  
Author(s):  
Antonio Nocito ◽  
Felix Dahm ◽  
Wolfram Jochum ◽  
Jae Hwi Jang ◽  
Panco Georgiev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Murine Model ◽  
Nonalcoholic Steatohepatitis ◽  
Mitochondrial Toxicity
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