scholarly journals Vitamin C deficiency attenuates liver fibrosis by way of up-regulated peroxisome proliferator-activated receptor-gamma expression in senescence marker protein 30 knockout mice

Hepatology ◽  
2009 ◽  
Vol 51 (5) ◽  
pp. 1766-1777 ◽  
Author(s):  
Jin-Kyu Park ◽  
Mi-Ran Ki ◽  
Hye-Rim Lee ◽  
Il-Hwa Hong ◽  
Ae-Ri Ji ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Vitamin C ◽  
Knockout Mice ◽  
Peroxisome Proliferator ◽  
Marker Protein ◽  
Peroxisome Proliferator Activated Receptor ◽  
Vitamin C Deficiency

Chronic vitamin C insufficiency aggravated thioacetamide-induced liver fibrosis in gulo-knockout mice

2014 ◽  
Vol 67 ◽  
pp. 81-90 ◽  
Author(s):  
Jin-Hee Kim ◽  
Young-Joo Jeong ◽  
Jun-Man Hong ◽  
Hang-Rae Kim ◽  
Jae Seung Kang ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Vitamin C ◽  
Knockout Mice

Adult Cartilage-Specific Peroxisome Proliferator–Activated Receptor Gamma Knockout Mice Exhibit the Spontaneous Osteoarthritis Phenotype

2013 ◽  
Vol 182 (4) ◽  
pp. 1099-1106 ◽  
Author(s):  
Faezeh Vasheghani ◽  
Roxana Monemdjou ◽  
Hassan Fahmi ◽  
Yue Zhang ◽  
Gemma Perez ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Role of peroxisome proliferator-activated receptor-α in ileum tight junction alteration in mouse model of restraint stress

2009 ◽  
Vol 297 (3) ◽  
pp. G488-G505 ◽  
Author(s):  
Emanuela Mazzon ◽  
Concetta Crisafulli ◽  
Maria Galuppo ◽  
Salvatore Cuzzocrea
Keyword(s):  
Tight Junction ◽  
Knockout Mice ◽  
Restraint Stress ◽  
Immobilization Stress ◽  
Peroxisome Proliferator ◽  
Barrier Dysfunction ◽  
Peroxisome Proliferator Activated Receptor ◽  
Significant Augmentation ◽  
Tight Junction Permeability

Restraint stress induces permeability changes in the small intestine, but little is known about the role of endogenous peroxisome proliferator-activated receptor-α (PPAR-α) ligand in the defects of the tight junction function. In the present study, we used PPAR-α knockout mice to understand the roles of endogenous PPAR-α on ileum altered permeability function in models of immobilization stress. The absence of a functional PPAR-α gene in PPAR-α knockout mice resulted in a significant augmentation of the degree of 1) TNF-α production in ileum tissues; 2) the alteration of zonula occludens-1, occludin, and β-catenin (immunohistochemistry); and 3) apoptosis (terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining, Bax, Bcl-2 expression). Taken together, our results demonstrate that endogenous PPAR-α ligands reduce the degree of tight junction permeability in the ileum tissues associated with immobilization stress, suggesting a possible role of endogenous PPAR-α ligands on ileum barrier dysfunction.

scholarly journals PPARg Dysfunction in the Medial Prefrontal Cortex Mediates High-Fat Diet-Induced Depression

2021 ◽  
Author(s):  
Cong-Cong Fu ◽  
Xin-Yi Zhang ◽  
Liu Xu ◽  
Hui-Xian Huang ◽  
Shuang Xu ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Peroxisome Proliferator ◽  
Obese Mice ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Increased Risk ◽  
Bidirectional Association

Abstract ObjectiveEpidemiological studies suggest a bidirectional association between depression and obesity; however, the biological mechanisms that link the development of depression to a metabolic disorder remain unclear. Even though nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ) agonists show anti-depressive effect, and high-fat diet-(HFD)-induced PPARγ dysfunction is involved in the pathogenesis of metabolic disorders, the neuronal PPARg has never been studied in HFD-induced depression. Thus, we aimed to investigate the effect of neuronal PPARγ on depressive-like behaviors in HFD-induced obese mice. MethodsWe fed male C57BL/6J mice with HFD to generate obese mice and conducted a series of behavioral tests to assess the effects of HFD feeding on depression. We generated neuron-specific PPARγ knockout mice (NKO) to determine whether neuronal PPARg deficiency was correlated with depressive-like behaviors. To further prove whether PPARγ in the medial prefrontal cortex (mPFC) neurons is involved in depressive-like behaviors, we applied AAV- CaMKIIa-Cre approach to specifically knockout PPARγ in the mPFC neurons of LoxP mice and used AAV-syn-PPARγ vectors to overexpress PPARγ in the mPFC neurons of NKO mice. ResultsWe observed a low mPFC PPARγ level and an increase in depressive-like behaviors in the HFD-fed mice. Moreover, neuronal-specific PPARγ deficiency in mice induced depressive-like behaviors, which could be abolished by imipramine. Furthermore, overexpressing PPARg in the mPFC reversed the depressive-like behaviors in HFD-fed mice as well as in neuronal-specific PPARγ knockout mice. ConclusionsThese results implicate that dysregulation of neuronal PPARγ in the mPFC may contribute to an increased risk for depression in obese populations.

scholarly journals Effect of Resistance Exercise and Liposomal Vitamin C on Some Factors of Mitochondrial Dynamics and Biogenesis

2021 ◽  
Vol 11 (1) ◽  
pp. 82-97
Author(s):  
Mostafa Khodabandeh ◽  
◽  
Maghsoud Peeri ◽  
Mohammad Ali Azarbayjani ◽  
Hasan Matinhomaee ◽  
...  
Keyword(s):  
Vitamin C ◽  
Resistance Exercise ◽  
Liver Tissue ◽  
Mitochondrial Dynamics ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Collagen Deposition ◽  
Peroxisome Proliferator Activated Receptor ◽  
Significance Level ◽  
Male Wistar Rats

Objective: Aging is associated with some changes in the liver function including increased collagen deposition and decreased mitochondrial function. This study aims to evaluate the effect of resistance exercise and vitamin C intake on the expression of Peroxisome Proliferator-Activated Receptor-Γ Coactivator-1α (PGC-1α) and Mitofusin 1 (MFn1) genes and collagen deposition in older rats. Methods: This is an experimental study conducted on 25 male Wistar rats aged 24 weeks and weighted 280-320 g. They were randomly divided into five groups of young control, older exercise, older vitamin C, older exercise + vitamin C, and older control. In the supplementation groups, rats were given liposomal vitamin C (100 mg/kg per body weight) by gavage daily. One-way ANOVA was used to examine the difference between the groups and Tukey’s post hoc test was used to determine the location of group differences. For all analyses, the significance level was set at 0.05. Results: Aging significantly reduced the expression of PGC-1α and MFn1 and increased collagen deposition in the liver tissue of rats (P=0.001). In the older exercise + vitamin C group, a significant increase in PGC-1α expression was observed compared to the older control group (P=0.001), but there was no significant changes in MFn1 expression. A significant decrease in collagen deposition was reported in the older exercise, older vitamin C, and older exercise + vitamin C groups compared to the older control group (P=0.001). Conclusion: Resistance exercise combined with vitamin C intake reduces collagen deposition in liver tissue and increases PGC-1α expression in older rats.

scholarly journals Short hairpin RNA attenuates liver fibrosis by regulating the peroxisome proliferator-activated receptor-γ and nuclear factor-κB pathways in hepatitis B virus-induced liver fibrosis in mice

2019 ◽  
Author(s):  
Lei Ye ◽  
Jiaqi Cao ◽  
Liying Sun ◽  
Ting Chen ◽  
Wuping Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Nuclear Factor Κb ◽  
Differentially Expressed ◽  
Peroxisome Proliferator ◽  
Differentially Expressed Proteins ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Ppar Signaling

Abstract Background: Progressive liver fibrosis, caused by chronic viral infection and metabolic disorders, results in the development of cirrhosis and hepatocellular carcinoma. However, no antifibrotic therapies have been approved to date. In our previous study, adeno-associated virus (AAV) short hairpin RNAs (shRNAs) targeting hepatitis B virus (HBV) and transforming growth factor (TGF)-β administration could persistently inhibit HBV replication and concomitantly prevent liver fibrosis. However, the differentially expressed proteins and critical regulatory networks of AAVshRNA treatment remain unclear. Accordingly, in this study, our major goal was we aimed to analyze differentially expressed proteins in the liver of AAV-shRNAs-treated mice with HBV infection and liver fibrosis using isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomics and to elucidate the underlying antifibrotic mechanisms. Results: In total 2743 proteins were recognized by iTRAQ-based quantitative proteomics analysis. Gene ontology analysis suggested that the differentially expressed proteins were mostly participated in peptide metabolism in the biological process category, cytosolic ribosomes in the cell component category, and structural constituents of ribosomes in the molecular function category. Kyoto Encyclopedia of Genes and Genomespathway analysis indicated that oxidative stress and the peroxisome proliferator-activated receptor (PPAR) signaling pathway were actived after treatment. Verification studies showed that AAVshRNAs inhibited hepatic stellate cell activation and inflammation by suppressing nuclear factor-κB p65 phosphorylation and α-smooth muscle actin expression via upregulation of PPAR-γ. Hepatocytes steatosis was also decreased by activating PPAR signaling pathway and improving lipid metabolism. TGF-β level was decreased owning to increase PPAR-γ expression and directly inhibition using AAVshRNAs targeting TGF-β. TGF-β-induced oxidative stress was suppressed by increasing glutathione S-transferase Pi 1 and reducing peroxiredoxin 1. Conclusions: Our results indicated that AAV-shRNAs were effective for modulating liver fibrosis by reducing oxidative stress, inflammation and activating PPAR signaling pathway.

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