Ablation of catalase promotes non-alcoholic fatty liver via oxidative stress and mitochondrial dysfunction in diet-induced obese mice

Shin, Su; Cho, Hyun Woo; Song, Suk-Won; Bae, Jae Hoon; Im, Seung Soon; Hwang, Inha; Ha, Hunjoo; Song, Dong Hyun

doi:10.1007/s00424-018-02250-3

Cited by 27 publications

(25 citation statements)

References 65 publications

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“…This consequence was also associated with effective modulation of protein kinase B (AKT), extracellular signal-regulated kinases (ERK), NF-κB and the reappearance of β-catenin. These beneficial effects by NAC administration were consistent with the suppression of fatty liver development, NLRP3 and caspase-1 activity, while improving the hepatic mitochondrial function in MCD/catalase knockout mice [63,73]. Table 3.…”

Section: Impact Of Nac On Lipid Accumulation Oxidative Stress and Insupporting

confidence: 62%

N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

et al. 2020

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Impaired adipose tissue function and insulin resistance remain instrumental in promoting hepatic lipid accumulation in conditions of metabolic syndrome. In fact, enhanced lipid accumulation together with oxidative stress and an abnormal inflammatory response underpin the development and severity of non-alcoholic fatty liver disease (NAFLD). There are currently no specific protective drugs against NAFLD, and effective interventions involving regular exercise and healthy diets have proved difficult to achieve and maintain. Alternatively, due to its antioxidant and anti-inflammatory properties, there has been growing interest in understanding the therapeutic effects of N-acetyl cysteine (NAC) against metabolic complications, including NAFLD. Here, reviewed evidence suggests that NAC blocks hepatic lipid accumulation in preclinical models of NAFLD. This is in part through the effective regulation of a fatty acid scavenger molecule (CD36) and transcriptional factors such as sterol regulatory element-binding protein (SREBP)-1c/-2 and peroxisome proliferator-activated receptor gamma (PPARγ). Importantly, NAC appears effective in improving liver function by reducing pro-inflammatory markers such as interleukin (IL)-6 IL-1β, tumour necrosis factor alpha (TNF-α) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). This was primarily through the attenuation of lipid peroxidation and enhancements in intracellular response antioxidants, particularly glutathione. Very few clinical studies support the beneficial effects of NAC against NAFLD-related complications, thus well-organized randomized clinical trials are still necessary to confirm its therapeutic potential.

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Section: Impact Of Nac On Lipid Accumulation Oxidative Stress and Insupporting

confidence: 62%

N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

et al. 2020

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“…Defective autophagy is closely associated with mitochondrial oxidative stress (Scherz-Shouval and Elazar, 2011), which reflects an imbalance between availability of ROS and the cellular antioxidant system (Shin et al, 2019). Next, we investigated whether Cori played a key role in reducing ROS levels in PA/ OA treated cells models of NAFLD.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported the decrease of antioxidant activity in obese or overweight patients of NAFLD (Krzystek-Korpacka et al, 2013). Supplement with antioxidant may attenuate ROSinduced mitochondrial dysfunction of ob/ob mice (Shin et al, 2019). Of note, Cori has been reported to exhibit strong antioxidant activity for acute liver failure (Lv et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Excessive ROS production overwhelmed the capacity of antioxidant defense system, which further promoted oxidative stress (Shin et al, 2019). To determine whether Cori enhanced the activities of enzymes involved in antioxidant defense system, we next investigated major antioxidant enzymes levels in AML12 cells.…”

Section: Cori Suppressed Intracellular Pa/oa Induced Ros Levelsmentioning

confidence: 99%

“…Protein was extracted from AML12 cells or liver tissues with RIPA buffer (50 mM Tris HCl, pH 8.0, 150 mM NaCl, 5 mM EDTA, 1% Nonidet P-40, 0.5% sodium deoxycholate, 1 mM PMSF, 1 mM NaVO4, 1 mM NaF, 0.1% SDS), and protease inhibitor cocktail (Roche, Germany). Immunobloting was then performed as described previously (Shin et al, 2019). In brief, lysates were centrifuged (13,000 × g for 15 min) and the supernatant was collected for the following protein quantification using BCA Protein Assay Kit (Pierce).…”

Section: Western Blot Analysismentioning

confidence: 99%

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Corilagin Alleviates Nonalcoholic Fatty Liver Disease in High-Fat Diet-Induced C57BL/6 Mice by Ameliorating Oxidative Stress and Restoring Autophagic Flux

et al. 2020

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Corilagin (Cori) possesses multiple biological activities. To determine whether Cori can exert protective effects against nonalcoholic fatty liver disease (NAFLD) and its potential mechanisms. C57BL/6 mice were fed with high-fat diet (HFD) alone or in combination with Cori (20 mg/kg, i.p.) and AML12 cells were exposed to 200 mM PA/OA with or without Cori (10 mM or 20 mM). Phenotypes and key indicators relevant to NAFLD were examined both in vivo and in vitro. In this study, Cori significantly ameliorated hepatic steatosis, confirmed by improved serum lipid profiles, and hepatic TC, TG contents, and the gene expression related to lipid metabolism in livers of HFD mice. Moreover, Cori attenuated HFD-mediated autophagy (including mitophagy) blockage by restoring autophagic flux, evidenced by increased number of autophagic double vesicles containing mitochondria, elevated LC3II protein levels, decreased p62 protein levels, as well as enhanced colocalization of autophagy-related protein (LC3, Parkin) and mitochondria. In accordance with this, Cori also reduced the accumulation of ROS and MDA levels, and enhanced the activities of antioxidative enzymes including SOD, GSH-Px, and CAT. In addition, Cori treatment improved mitochondrial dysfunction, evidenced by increased mitochondrial membrane potential (DYm). In parallel with this, Cori decreased mitochondrial DNA oxidative damage, while increased mitochondrial biogenesis related transcription factors expression, mitochondrial DNA content and oxygen consumption rate (OCR). In conclusion, these results demonstrate that Cori is a potential candidate for

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Effects of a collagen hyaluronic acid silk‐fibroin patch with the electroconductive element polyaniline on left ventricular remodeling in an infarct heart model

et al. 2022

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Biodegradable cardiac patches have been able to induce improvement in left ventricular (LV) remodeling. A novel scaffold patch made with collagen and silk-fibroin (COL-SF) was further associated to polyaniline (PANi) to increase conductivity. Thus, this study investigated the safety of the association of PANi to a patch, and the improvement in LV remodeling in a myocardial infarct (MI) rat model. Wistar rats underwent MI induction. MI was confirmed with echocardiographic and after 2 weeks, animals (n = 10/group) were randomized into: (a) COL-SF hyaluronic acid patch, (b) PANi hyaluronic acid patch, (c) MI Control (just repeat thoracotomy). Healthy animals were also followed. Echocardiography was performed at pre-treatment, and at 2-, 4-, and 8-weeks post-treatment. Hearts underwent hemodynamic evaluation on Langendorff apparatus and histology for LV thickness and percent of infarct size. Liver, kidneys, and blood samples were evaluated for biochemical, hematological, oxidative stress, and histology. There was a tendency of lower %infarct size in patched animals. LV thickness was higher in the patched animals than controls.Functional echocardiographic indices %Fractional shortening and %LV ejection fraction decreased in the MI control group, but not in the patched animals. PANi presented higher %LVEF versus MI control. PANi presented higher liver transaminases; no morphological changes were observed in histology. Elevation of antioxidant markers was observed. COL-SF and PANi patches were able to induce better remodeling features compared to MI controls on %infarct size and LV thickness and have not presented echocardiographic worsening. Polyaniline may present a slight improvement on LV remodeling, despite associated to signs of hepatotoxicity and pro-oxidant effect.

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Ablation of catalase promotes non-alcoholic fatty liver via oxidative stress and mitochondrial dysfunction in diet-induced obese mice

Cited by 27 publications

References 65 publications

N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

Corilagin Alleviates Nonalcoholic Fatty Liver Disease in High-Fat Diet-Induced C57BL/6 Mice by Ameliorating Oxidative Stress and Restoring Autophagic Flux

Effects of a collagen hyaluronic acid silk‐fibroin patch with the electroconductive element polyaniline on left ventricular remodeling in an infarct heart model

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