scholarly journals MagnoliaExtract (BL153) Ameliorates Kidney Damage in a High Fat Diet-Induced Obesity Mouse Model

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Wenpeng Cui ◽  
Yangwei Wang ◽  
Qiang Chen ◽  
Weixia Sun ◽  
Lu Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
Kidney Damage ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Plasminogen Activator Inhibitor 1 ◽  
Hexokinase Ii ◽  
Functional Changes

Accumulating evidence demonstrated that obesity is a risk factor for renal structural and functional changes, leading to the end-stage renal disease which imposes a heavy economic burden on the community. However, no effective therapeutic method for obesity-associated kidney disease is available. In the present study, we explored the therapeutic potential of amagnoliaextract (BL153) for treating obesity-associated kidney damage in a high fat diet- (HFD-) induced mouse model. The results showed that inflammation markers (tumor necrosis factor-αand plasminogen activator inhibitor-1) and oxidative stress markers (3-nitrotyrosine and 4-hydroxy-2-nonenal) were all significantly increased in the kidney of HFD-fed mice compared to mice fed with a low fat diet (LFD). Additionally, proteinuria and renal structure changes in HFD-fed mice were much more severe than that in LFD-fed mice. However, all these alterations were attenuated by BL153 treatment, accompanied by upregulation of peroxisome proliferator-activated receptor-γcoactivator-1α(PGC-1α) and hexokinase II (HK II) expression in the kidney. The present study indicates that BL153 administration may be a novel approach for renoprotection in obese individuals by antiinflammation and anti-oxidative stress most likely via upregulation of PGC-1αand HK II signal in the kidney.

An experimental MODEL study to investigate the pathogenesis of oxaliplatin-induced liver injury.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 184-184
Author(s):  
Stuart M. Robinson ◽  
Jelena Mann ◽  
Derek M. Manas ◽  
Derek A. Mann ◽  
Steve A. White
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
Negative Impact ◽  
Acid Synthesis ◽  
Sinusoidal Obstruction Syndrome ◽  
High Fat ◽  
Expression Of Genes ◽  
Folfox Chemotherapy

184 Background: Oxaliplatin based chemotherapy is widely utilized pre-operatively in patients with colorectal liver metastases. Its use is associated with injury to the liver in the form of sinusoidal obstruction syndrome (SOS) the presence of which can have a negative impact on surgical outcomes. The pathogenesis of this condition is poorly understood. Methods: C57Bl/6 mice (n=10 per group) were treated with 5-FU/oxaliplatin/folinic acid chemotherapy (FOLFOX) weekly for 5 weeks or their respective vehicle controls. Animals were culled one week following the final treatment and liver tissue harvested for histological and biochemical analysis. mRNA was extracted from snap frozen liver and subject to genome wide expression analysis the results of which were confirmed using qRT-PCR. To determine the effect of background steatosis on the development of liver injury the experiment was repeated using mice maintained on a high fat diet. To assess the ability of antioxidants to prevent SOS development diet was supplemented with 3% butylated hydroxyanisole (BHA). Results: H&E stained tissue sections confirmed the presence of SOS in all FOLFOX treated animals. Microarray identified changes in expression of over 604 genes in the liver of animals with FOLFOX induced SOS. In particular there was increased expression of genes implicated in oxidative stress (e.g. Metallothionein 1; 22 fold; p<0.001), cell cycle arrest (e.g. p21; 21 fold; p<0.001) and angiogenesis (VEGF-A; 2 fold; p<0.001). Administration of the antioxidant BHA alongside chemotherapy prevented the development of SOS confirming the role of oxidative stress in the pathogenesis of this condition. There was down regulation of a number of genes implicated in fatty acid synthesis (e.g. FASN; 8 fold; p<0.001). In support of this mice maintained on a high fat diet treated with FOLFOX do not develop steatosis unlike those treated with vehicle alone. Conclusions: FOLFOX chemotherapy is specifically associated with SOS and not hepatic steatosis. We have identified some of the molecular pathways involved in the pathogenesis of this condition. Manipulation of these pathways may be of therapeutic potential in preventing the development of chemotherapy-associated liver injury.

scholarly journals Leaf powder supplementation of Senna alexandrina ameliorates oxidative stress, inflammation, and hepatic steatosis in high-fat diet-fed obese rats

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250261
Author(s):  
Shariful Islam Nayan ◽  
Faizul Islam Chowdhury ◽  
Noushin Akter ◽  
Md Mizanur Rahman ◽  
Saima Selim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
High Fat ◽  
Gene Expressions ◽  
Alcoholic Fatty Liver ◽  
Leaf Powder ◽  
Natural Leaf ◽  
Senna Alexandrina

Obesity is an enduring medical issue that has raised concerns around the world. Natural plant extracts have shown therapeutic potential in preventing oxidative stress and inflammation related to obesity complications. In this study, Senna alexandrina Mill. leaves were utilized to treat high-fat diet-related metabolic disorders and non-alcoholic fatty liver diseases. Plasma biochemical assays were conducted to determine the lipid profiles and oxidative stress parameters, and the gene expression of antioxidant enzymes and inflammatory mediators was measured. Histological stained livers of high-fat diet-fed rats were observed. S. alexandrina leaf powder supplementation prevented the increase in cholesterol and triglyceride levels in high-fat diet-fed rats. Moreover, S. alexandrina leaves also reduced lipid peroxidation and nitric oxide production in these rats. Prevention of oxidative stress by S. alexandrina leaf supplementation in high-fat diet-fed rats is regulated by enhancing the antioxidant enzyme activity, followed by the restoration of corresponding gene expressions, such as NRF-2, HO-1, SOD, and CAT. Histological staining provides further evidence that S. alexandrina leaf supplementation prevents inflammatory cell infiltration, lipid droplet deposition, and fibrosis in the liver of high-fat diet-fed rats. Furthermore, this investigation revealed that S. alexandrina leaf supplementation controlled non-alcoholic fatty liver disease by modulating the expression of fat metabolizing enzymes in high-fat diet-fed rats. Therefore, S. alexandrina leaf supplementation inhibits fatty liver inflammation and fibrosis, suggesting its usefulness in treating non-alcoholic steatohepatitis. Thus, this natural leaf extract has potential in treatment of obesity related liver dysfunction.

scholarly journals Obesity and Breast Cancer: The Roles of Peroxisome Proliferator-Activated Receptor-γand Plasminogen Activator Inhibitor-1

PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
Jennifer C. Carter ◽  
Frank C. Church
Keyword(s):  
Breast Cancer ◽  
Plasminogen Activator ◽  
High Fat Diet ◽  
Plasminogen Activator Inhibitor ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Plasminogen Activator Inhibitor 1 ◽  
Peroxisome Proliferator Activated Receptor ◽  
Activator Inhibitor ◽  
Pai 1

Breast cancer is the most prominent cancer among females in the United States. There are a number of risk factors associated with development of breast cancer, including consumption of a high-fat diet and obesity. Plasminogen activator inhibitor-1 (PAI-1) is a cytokine upregulated in obesity whose expression is correlated with a poor prognosis in breast cancer. As a key mediator of adipogenesis and regulator of adipokine production, peroxisome proliferator-activated receptor-γ(PPAR-γ) is involved in PAI-1 expression from adipose tissue. We summarize the current knowledge linking PPAR-γand PAI-1 expression to high-fat diet and obesity in the risk of breast cancer.

scholarly journals Extraction and Hypolipidemic Activity of Low Molecular Weight Polysaccharides Isolated from Rosa Laevigata Fruits

2020 ◽  
Vol 2020 ◽  
pp. 1-20
Author(s):  
Xuejiao Zhang ◽  
Yihong Hu ◽  
Chenzhong Jin ◽  
Weiguo Wu
Keyword(s):  
Oxidative Stress ◽  
Molecular Weight ◽  
Stress Responses ◽  
High Fat Diet ◽  
Raw Material ◽  
Low Molecular Weight ◽  
Peroxisome Proliferator ◽  
Extraction Temperature ◽  
High Fat ◽  
Chinese Medicinal Herb

Three novel low molecular weight polysaccharides (RLP-1a, RLP-2a, and RLP-3a) with 9004, 8761, and 7571 Da were first obtained by purifying the crude polysaccharides from the fruits of a traditional Chinese medicinal herb Rosae Laevigatae. The conditions for polysaccharides from the R. Laevigatae fruit (RLP) extraction were optimized by the response surface methodology, and the optimal conditions were as follows: extraction temperature, 93°C; extraction time, 2.8 h; water to raw material ratio, 22; extraction frequency, 3. Structural characterization showed that RLP-1a consisted of rhamnose, arabinose, xylose, glucose, and galactose with the ratio of 3.14 : 8.21 : 1 : 1.37 : 4.90, whereas RLP-2a was composed of rhamnose, mannose, glucose, and galactose with the ratio of 1.70 : 1 : 93.59 : 2.73, and RLP-3a was composed of rhamnose, arabinose, xylose, mannose, glucose, and galactose with the ratio of 6.04 : 26.51 : 2.05 : 1 : 3.17 : 31.77. The NMR analyses revealed that RLP-1a, RLP-2a, and RLP-3a contained 6, 4, and 6 types of glycosidic linkages, respectively. RLP-1a and RLP-3a exhibited distinct antioxidant abilities on the superoxide anions, 1,1-diphenyl-2-picrylhydrazyl (DPPH), and hydroxyl radicals in vitro. RLPs could decrease the serum lipid levels, elevate the serum high-density lipoprotein cholesterol levels, enhance the antioxidant enzymes levels, and upregulate of FADS2, ACOX3, and SCD-1 which involved in the lipid metabolic processes and oxidative stress in the high-fat diet-induced rats. These results suggested that RLPs ameliorated the high-fat diet- (HFD-) induced lipid metabolism disturbance in the rat liver through the peroxisome proliferator-activated receptor (PPAR) signaling pathway. Low molecular weight polysaccharides of RLP could be served as a novel potential functional food for improving hyperlipidemia and liver oxidative stress responses.

scholarly journals Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jinlei Liu ◽  
Yao Sun ◽  
Hongwei Zheng ◽  
Jing Wang ◽  
Lili Liu ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
High Fat Diet ◽  
Cell Damage ◽  
Kidney Tissue ◽  
Kidney Damage ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Ppar Γ ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Objective. Secretion of glucagon-like peptide 1 (GLP-1) and its effect on target organs were impaired in individuals with obesity. However, its mechanism needs to be further studied. We aim to explore the roles of the receptor of GLP-1 (GLP-1R) involved in high-fat-diet- (HFD-) induced kidney damage improved by emodin. Methods. Male C57bl/6 mice were fed with HFD diet and therapied by emodin. NRK-52E cells were cultured and treated with palmitic acid or low-density lipoprotein cholesterol (LDL-C). Emodin was used to remedy the NRK-52E cell damage. GW9662 was administrated to block the function of peroxisome proliferator-activated receptor γ (PPAR-γ). GLP-1 in the plasma was measured by ELISA. PPAR-γ and GLP-1R in the kidney and NRK-52E cells were detected by western blotting. The interaction between PPAR-γ protein and GLP-1R promoter regions was observed by chromatin immunoprecipitation (ChIP). Results. Postprandial GLP-1 levels in plasma, as well as PPAR-γ and GLP-1R, decreased in kidney tissue of HFD mice, while they were reserved by emodin treatment. Although PPAR-γ and GLP-1R were not downregulated by LDL-C, they were suppressed by palmitic acid. Interestingly, GLP-1R mRNA was detected by PCR in the mixture pulled down with PPAR-γ antibody. Additionally, downregulation of PPAR-γ and GLP-1R by palmitic acid was remanded by emodin. Moreover, GW9662, an inhibitor of PPAR-γ, abolished the protective effect of emodin. Conclusion. The kidney damage of HFD mice seems to be alleviated by emodin via the upregulation of GLP-1R in kidney tissue.

scholarly journals ACE Reduces Metabolic Abnormalities in a High-Fat Diet Mouse Model

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Seong-Jong Lee ◽  
Jong-Min Han ◽  
Jin-Seok Lee ◽  
Chang-Gue Son ◽  
Hwi-Jin Im ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Serum Lipid ◽  
Peroxisome Proliferator ◽  
Metabolic Abnormalities ◽  
Oxidative Stress Markers ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Stress Markers ◽  
And Oxidative Stress

The medicinal plantsArtemisia iwayomogi(A. iwayomogi) andCurcuma longa(C. longa) radix have been used to treat metabolic abnormalities in traditional Korean medicine and traditional Chinese medicine (TKM and TCM). In this study we evaluated the effect of the water extract of a mixture ofA. iwayomogiandC. longa(ACE) on high-fat diet-induced metabolic syndrome in a mouse model. Four groups of C57BL/6N male mice (except for the naive group) were fed a high-fat diet freely for 10 weeks. Among these, three groups (except the control group) were administered a high-fat diet supplemented with ACE (100 or 200 mg/kg) or curcumin (50 mg/kg). Body weight, accumulation of adipose tissues in abdomen and size of adipocytes, serum lipid profiles, hepatic steatosis, and oxidative stress markers were analyzed. ACE significantly reduced the body and peritoneal adipose tissue weights, serum lipid profiles (total cholesterol and triglycerides), glucose levels, hepatic lipid accumulation, and oxidative stress markers. ACE normalized lipid synthesis-associated gene expressions (peroxisome proliferator-activated receptor gamma, PPARγ; fatty acid synthase, FAS; sterol regulatory element-binding transcription factor-1c, SREBP-1c; and peroxisome proliferator-activated receptor alpha, PPARα). The results from this study suggest that ACE has the pharmaceutical potential reducing the metabolic abnormalities in an animal model.

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