Oxidative Stress in Nonalcoholic Fatty Liver Disease

Marı́, Montserrat; Morales, Albert; Colell, Anna; Garcı́a-Ruiz, Carmen; Fernández‐Checa, José C.

doi:10.1007/978-3-319-15539-5_12

Cited by 7 publications

(9 citation statements)

References 168 publications

(99 reference statements)

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“…According to previous studies, oxidative stress and inflammation are highly involved during the pathogenesis of NAFLD [11,13]. In our study, AGT treatment enhanced the SOD activity, GPx activity and reduced the MDA levels, indicating that AGT potentiated the oxidant defense mechanisms, along with the improved Nrf-2/HO-1 pathway both in liver and intestine.…”

Section: Discussionsupporting

confidence: 75%

“…As the hepatic manifestation of the metabolic syndrome, NAFLD comprises a spectrum of liver diseases, including benign steatosis, steatohepatitis, cirrhosis and even hepatocellular carcinoma ultimately [11,12]. The pathophysiology of NAFLD involves gut-derived microbial components, lipotoxicity, oxidative stress and inflammation, which might be observed in the liver, but might be also originated from other tissues such as the gastrointestinal tract [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Apigetrin attenuates high fat diet-induced intestinal inflammation and nonalcoholic fatty liver disease (NAFLD) process

Liu¹,

Li²,

Liu³

et al. 2017

Oncotarget

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Obesity and non-alcoholic fatty liver disease (NAFLD) are characterized by abnormal gut inflammation, and microbiota. Apigetrin (AGT), a flavonoid isolated from various herbal medicines such as Matricaria chamomilla and Scutellaria baicalensis Georgi, has a number of beneficial health effects, including anti-inflammatory and anti-oxidative bioactivities. In the present study, we attempted to explore the metabolic impact of AGT on high fat diet (HFD)-induced NAFLD and to investigate the consequent anti-diabetic effects associated with gut microbiota. C57BL/6J mice were fed with normal diet (ND) or HFD. And the mice with HFD were gavaged daily with or without AGT for 56 days. The gut microbiota composition was measured using 16s rRNA gene sequences. The results indicated that AGT reduced the weight gain, visceral and subcutaneous fat of HFD-feeding mice. AGT administration increased insulin sensitivity as evidenced by the improved insulin tolerance. AGT treatment also reduced liver weight and triglyceride (TG) accumulation, associated with the blunted hepatic oxidative stress and inflammation. Further, AGT administration could lower serum lipopolysaccharide (LPS) levels, intestinal glucose uptake, TG content, as well as prevent intestinal inflammation and oxidative stress. AGT decreased the secretion of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β, by inactivating nuclear factor-κB (NF-κB) pathway; and increased the levels of anti-oxidants, such as superoxide dismutase (SOD), heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf-2). Of note, AGT reduced the intestinal bacterial overgrowth. Further more, the anti-oxidant and anti-inflammatory effects of AGT were confirmed in LPS-and fructose-stimulated cells in vitro. The results above indicated that AGT showed beneficial metabolic effects to attenuate HFD-induced NAFLD and intestinal injury.

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Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Apigetrin attenuates high fat diet-induced intestinal inflammation and nonalcoholic fatty liver disease (NAFLD) process

Liu¹,

Li²,

Liu³

et al. 2017

Oncotarget

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“…There are two types of SOD including the specific mitochondrial matrix containing the manganese active site ( 40 ) (MnSOD or SOD2), which eliminates O2 •− formed in the matrix or on the inner side of the inner membrane, and SOD containing copper and zinc ( 41 ) instead of manganese SOD (copper-zinc SOD or SOD1) located in the cytoplasm of eukaryotic cells. The second mechanism is associated with cytochrome c in the intermembrane space that can reduce O2 •− ( 42 ) to regenerate oxygen in the process ( 43 ), glutathione peroxidase which mostly decomposes O2 •− and OH • ( 44 ), and catalase, the major detoxifying enzyme identified in peroxisomes ( 45 ). Ubiquinol (QH2) is another carrier appearing to have a detoxifying role against ROS, acting as a reducing agent in the elimination of various peroxides in the presence of succinate ( 46 ).…”

Section: Oxidative Stressmentioning

confidence: 99%

Role of oxidative stress in Alzheimer's disease

2016

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Alzheimer's disease (AD) is the most common cause of disability in individuals aged >65 years worldwide. AD is characterized by the abnormal deposition of amyloid β (Aβ) peptide, and intracellular accumulation of neurofibrillary tangles of hyperphosphorylated τ protein and dementia. The neurotoxic oligomer Aβ peptide, which is the neuropathological diagnostic criterion of the disease, together with τ protein, are mediators of the neurodegeneration that is among the main causative factors. However, these phenomena are mainly initiated and enhanced by oxidative stress, a process referring to an imbalance between antioxidants and oxidants in favour of oxidants. This imbalance can occur as a result of increased free radicals or a decrease in antioxidant defense, free radicals being a species that contains one or more unpaired electrons in its outer shell. The major source of potent free radicals is the reduction of molecular oxygen in water, that initially yields the superoxide radical, which produces hydrogen peroxide by the addition of an electron. The reduction of hydrogen peroxide produces highly reactive hydroxyl radicals, termed reactive oxygen species (ROS) that can react with lipids, proteins, nucleic acids, and other molecules and may also alter their structures and functions. Thus, tissues and organs, particularly the brain, a vulnerable organ, are affected by ROS due to its composition. The brain is largely composed of easily oxidizable lipids while featuring a high oxygen consumption rate. The current review examined the role of oxidative stress in AD.

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“…Consequently, mitochondria in NASH patients are big and have crystalline inclusions, which indicate mitochondrial dysfunction and liver injury [ 22 , 28 ]. Mitochondrial dysfunction is also characterized by mitochondrial outer membrane permeabilization, promoting protein release to the cytosol, cell death and loss of mitochondrial integrity [ 29 ].…”

Section: Oxidative Stress In Nafld Progressionmentioning

confidence: 99%

“…Both ω- and β- oxidation are increased in NASH, leading to augmented generation of ROS and promoting OS. Moreover, peroxisomal β-oxidation products are further metabolized in the mitochondrial tricarboxylic acid cycle, thus the functionality of this organelle is exceeded [ 29 , 32 ].…”

Section: Oxidative Stress In Nafld Progressionmentioning

confidence: 99%

The Interplay between Oxidative Stress and miRNAs in Obesity-Associated Hepatic and Vascular Complications

et al. 2020

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Nowadays, the obesity pandemic is one of the most relevant health issues worldwide. This condition is tightly related to comorbidities such as non-alcoholic fatty liver disease (NAFLD) and cardiovascular diseases (CVDs), namely atherosclerosis. Dysregulated lipid metabolism and inflammation link these three diseases, leading to a subsequent increase of oxidative stress (OS) causing severe cellular damage. On the other hand, microRNAs (miRNAs) are short, single-stranded, non-coding RNAs that act as post-transcriptional negative regulators of gene expression, thus being involved in the molecular mechanisms that promote the development of many pathologies including obesity and its comorbidities. The involvement of miRNAs in promoting or opposing OS in disease progression is becoming more evident. Some miRNAs, such as miR-200a and miR.421, seem to play important roles in OS control in NAFLD. On the other hand, miR-92a and miR-133, among others, are important in the development of atherosclerosis. Moreover, since both diseases are linked to obesity, they share common altered miRNAs, being miR-34a and miR-21 related to OS. This review summarizes the latest advances in the knowledge about the mechanisms of oxidative stress (OS) generation in obesity-associated NAFLD and atherosclerosis, as well as the role played by miRNAs in the regulation of such mechanisms.

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Oxidative Stress in Nonalcoholic Fatty Liver Disease

Cited by 7 publications

References 168 publications

Apigetrin attenuates high fat diet-induced intestinal inflammation and nonalcoholic fatty liver disease (NAFLD) process

Apigetrin attenuates high fat diet-induced intestinal inflammation and nonalcoholic fatty liver disease (NAFLD) process

Role of oxidative stress in Alzheimer's disease

The Interplay between Oxidative Stress and miRNAs in Obesity-Associated Hepatic and Vascular Complications

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