scholarly journals Exogenous IGF-1 improves cognitive function in rats with high-fat diet consumption

2020 ◽  
Vol 64 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Feng Wang ◽  
Lu Wang ◽  
Yifeng Wang ◽  
Dai Li ◽  
Tianpeng Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Western Blot ◽  
Blot Analysis ◽  
High Fat Diet ◽  
Western Blot Analysis ◽  
High Fat ◽  
Anxiety Behavior ◽  
And Oxidative Stress ◽  
Creb Pathway

Insulin-like growth factor-1 (IGF-1) improves cognitive function, but its mechanism has not been elucidated. The aim of the study was to explore whether IGF-1 exerted its protective effect on cognitive function and anxiety behavior through the activation of PI3K/Akt/CREB pathway in high-fat diet rats. Neuronal cells HT22 were treated with nothing, IGF-1, IGF-1 + LY294002 or IGF-1 + 666-15. Expressions of p-PI3K, p-Akt and p-CREB were measured using Western blot analysis. Thirty C57BL/6J rats were used. After feeding with high-fat diet, normal saline, PEG-IGF-1, PEG-IGF-1 + LY294002 or PEG-IGF-1 + 666-15 was treated. Cognitive function and anxiety behavior were assessed by Morris water maze and open field test. Several inflammation and oxidative stress biomarkers were measured using recognized methods. Expressions of p-PI3K and p-CREB were also measured using Western blot analysis. After IGF-1 treatment in cells, expressions of p-PI3K, p-Akt and p-CREB were increased. Furthermore, LY294002 downregulated the expressions of these three proteins, but 666-15 only inhibited the expression of CREB in the cells. Compared with the control rats, we found abnormalities of cognitive function and anxiety behavior, inhibition of PI3K/Akt/CREB pathway and increase of oxidative stress and inflammation in high-fat diet rats. After PEG-IGF-1 treatment, the changes in high-fat diet rats were reversed. Then, we blocked the pathway and found that these blockers attenuated the protective effects of PEG-IGF-1. In conclusion, IGF-1 improved cognitive function and anxiety behavior in high-fat diet rats and inhibited inflammation and oxidative stress in hippocampus tissue through the activation of PI3K/Akt/CREB pathway.

scholarly journals Kaempferol and Kaempferide Attenuate Oleic Acid-Induced Lipid Accumulation and Oxidative Stress in HepG2 Cells

2021 ◽  
Vol 22 (16) ◽  
pp. 8847
Author(s):  
Fangfang Tie ◽  
Jin Ding ◽  
Na Hu ◽  
Qi Dong ◽  
Zhi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oleic Acid ◽  
Lipid Metabolism ◽  
Western Blot ◽  
Blot Analysis ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Western Blot Analysis ◽  
Heme Oxygenase 1 ◽  
And Oxidative Stress

Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases which lacks ideal treatment options. Kaempferol and kaempferide, two natural flavonol compounds isolated from Hippophae rhamnoides L., were reported to exhibit a strong regulatory effect on lipid metabolism, for which the mechanism is largely unknown. In the present study, we investigated the effects of kaempferol and kaempferide on oleic acid (OA)-treated HepG2 cells, a widely used in vitro model of NAFLD. The results indicated an increased accumulation of lipid droplets and triacylglycerol (TG) by OA, which was attenuated by kaempferol and kaempferide (5, 10 and 20 μM). Western blot analysis demonstrated that kaempferol and kaempferide reduced expression of lipogenesis-related proteins, including sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD-1). Expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer binding proteins β (C/EBPβ), two adipogenic transcription factors, was also decreased by kaempferol and kaempferide treatment. In addition, western blot analysis also demonstrated that kaempferol and kaempferide reduced expression of heme oxygenase-1 (HO-1) and nuclear transcription factor-erythroid 2-related factor 2 (Nrf2). Molecular docking was performed to identify the direct molecular targets of kaempferol and kaempferide, and their binding to SCD-1, a critical regulator in lipid metabolism, was revealed. Taken together, our findings demonstrate that kaempferol and kaempferide could attenuate OA-induced lipid accumulation and oxidative stress in HepG2 cells, which might benefit the treatment of NAFLD.

scholarly journals Differential expression of liver proteins between obesity-prone and obesity-resistant rats in response to a high-fat diet

2011 ◽  
Vol 106 (4) ◽  
pp. 612-626 ◽  
Author(s):  
Xia Wang ◽  
Jung-Won Choi ◽  
Jeong In Joo ◽  
Dong Hyun Kim ◽  
Tae Seok Oh ◽  
...  
Keyword(s):  
Western Blot ◽  
Blot Analysis ◽  
High Fat Diet ◽  
Western Blot Analysis ◽  
Statistical Significance ◽  
Differentially Expressed ◽  
High Fat ◽  
Two Dimensional Gel Electrophoresis ◽  
Or Groups ◽  
Proteomic Study

Rodents respond to a chronic high-fat diet (HFD) in two ways: some readily become obese (obesity prone, OP) and others do not (obesity resistant, OR). Although several hypotheses have been proposed, the mechanisms underlying the inter-individual susceptibility to diet-induced obesity remain to be fully defined. In the present study, two-dimensional gel electrophoresis (2-DE) combined with matrix-assisted laser desorption ionisation time-of-flight MS was carried out for identification of differentially expressed liver proteins in OP and OR rats fed a HFD, in an attempt to discover marker proteins involved in susceptibility and/or resistance to obesity in rat liver. The 2-DE analysis demonstrated that forty spots from 380 visualised spots were differentially regulated between the groups. Among these forty spots, twelve were differentially expressed proteins between OP and OR rats, reaching statistical significance. Of these, five proteins have already been linked to obesity; however, seven proteins involved in obesity susceptibility or resistance were identified for the first time in the present study. In order to validate the proteomic results and gain insight into the metabolic changes between the OP and OR groups, we further confirmed the expression pattern of some proteins of interest by Western blot analysis. Combined results of proteomic analysis with Western blot analysis revealed that reduced lipogenesis and increased fat oxidation were achieved in the livers of OR rats. In conclusion, the present proteomic study is an important advance over the previous steps required for identification of OP and OR rats, and should prove valuable in the search for the pathogenesis of obesity in humans.

scholarly journals Silencing ferritin alleviates atherosclerosis in mice via regulating the expression levels of matrix metalloproteinases and interleukins

2021 ◽  
Author(s):  
Mei Zheng ◽  
Lizhuo Li ◽  
Yuqian Liu ◽  
Yun Liang ◽  
Xiaoyong Qi
Keyword(s):  
Matrix Metalloproteinases ◽  
Western Blot ◽  
Knockout Mice ◽  
Blot Analysis ◽  
High Fat Diet ◽  
Western Blot Analysis ◽  
High Fat ◽  
Expression Levels ◽  
Atherosclerotic Lesions ◽  
Apoe Knockout Mice

This study was conducted to investigate the roles of ferritin in atherosclerosis. The mouse model of atherosclerosis was established by feeding ApoE knockout mice with a high-fat diet. The mice were then treated with ferritin-overexpressing and -silencing constructs, and assessed for interleukins (ILs) and matrix metalloproteinases (MMPs) levels using ELISA and Western blot analysis. After being fed with a high-fat diet, the ApoE knockout mice developed pro-atherogenic lipid profiles with elevated total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C). They also showed increased atherosclerotic lesions including narrowed lumen diameter, reduced lumen area, and increased plaque size. Following injection of the overexpression and silencing constructs, mRNA levels of ferritin were increased and decreased, respectively, and at the same time the atherosclerotic lesions were aggravated and alleviated, respectively. Further analysis indicated that silencing of ferritin gene reduced IL-1β and IL-10 levels while overexpressing ferritin increased them. On other hand, the TNF-α levels showed an opposite trend. MMP8, MMP12 and MMP13 levels were increased or decreased significantly after the mice were injected with ferritin over-expression or silencing vectors, respectively. Western blot analysis showed that compared to the control, overexpressing ferritin resulted in increased expression of p-JNK while silencing ferritin decreased the expression. Meanwhile, the levels of pc-Jun remained unchanged. Our work demonstrates that ferritin can regulate the progress of atherosclerosis via regulating the expression levels of MMPs and interleukins. Silencing ferritin inhibits the development of atherosclerosis and is, therefore, worth being further investigated as a potential therapeutic approach for this disease.

scholarly journals Mitochondrial-Targeting Antioxidant SS-31 Suppresses Airway Inflammation and Oxidative Stress Induced by Cigarette Smoke

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
De-qing Yang ◽  
Qiu-nan Zuo ◽  
Tao Wang ◽  
Dan Xu ◽  
Liu Lian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Airway Inflammation ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Mapk Signaling ◽  
Tnf Α ◽  
And Oxidative Stress

This study investigated whether the mitochondrial-targeted peptide SS-31 can protect against cigarette smoke- (CS-) induced airway inflammation and oxidative stress in vitro and in vivo. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure. Pathologic changes and oxidative stress in lung tissue, inflammatory cell counts, and proinflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) were examined. The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues. SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF. SS-31 also attenuated CS-induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD). It also reversed CS-induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol. Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression. RNA sequencing and western blot analysis showed that SS-31 inhibited CS-induced activation of the mitogen-activated protein kinase (MAPK) signaling pathway in vitro and in vivo. Thus, SS-31 alleviates CS-induced airway inflammation and oxidative stress via modulation of mitochondrial function and regulation of MAPK signaling and thus has therapeutic potential for the treatment of airway disorders caused by smoking.

Improvement for High Fat Diet-Induced Hepatic Injuries and Oxidative Stress by Flavonoid-Enriched Extract from Nelumbo nucifera Leaf

2009 ◽  
Vol 57 (13) ◽  
pp. 5925-5932 ◽  
Author(s):  
Ming-Cheng Lin ◽  
Shao-Hsuan Kao ◽  
Pei-Jun Chung ◽  
Kuei-Chuan Chan ◽  
Mon-Yuan Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Nelumbo Nucifera ◽  
High Fat ◽  
Hepatic Injuries ◽  
And Oxidative Stress

scholarly journals Effects of a Mixed Limosilactobacillus fermentum Formulation with Claimed Probiotic Properties on Cardiometabolic Variables, Biomarkers of Inflammation and Oxidative Stress in Male Rats Fed a High-Fat Diet

Foods ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2202
Author(s):  
Micaelle Oliveira de Luna Freire ◽  
Luciana Caroline Paulino do Nascimento ◽  
Kataryne Árabe Rimá de Oliveira ◽  
Alisson Macário de Oliveira ◽  
Thiago Henrique Napoleão ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Control Diet ◽  
Male Rats ◽  
Control Group ◽  
Low Grade ◽  
Probiotic Properties ◽  
High Fat ◽  
Low Grade Inflammation ◽  
And Oxidative Stress

High-fat diet (HFD) consumption has been linked to dyslipidemia, low-grade inflammation and oxidative stress. This study investigated the effects of a mixed formulation with Limosilactobacillusfermentum 139, L. fermentum 263 and L. fermentum 296 on cardiometabolic parameters, fecal short-chain fatty acid (SCFA) contents and biomarkers of inflammation and oxidative stress in colon and heart tissues of male rats fed an HFD. Male Wistar rats were grouped into control diet (CTL, n = 6), HFD (n = 6) and HFD with L. fermentum formulation (HFD-Lf, n = 6) groups. The L.fermentum formulation (1 × 109 CFU/mL of each strain) was administered twice a day for 4 weeks. After a 4-week follow-up, biochemical parameters, fecal SCFA, cytokines and oxidative stress variables were evaluated. HFD consumption caused hyperlipidemia, hyperglycemia, low-grade inflammation, reduced fecal acetate and propionate contents and increased biomarkers of oxidative stress in colon and heart tissues when compared to the CTL group. Rats receiving the L. fermentum formulation had reduced hyperlipidemia and hyperglycemia, but similar SCFA contents in comparison with the HFD group (p < 0.05). Rats receiving the L. fermentum formulation had increased antioxidant capacity throughout the colon and heart tissues when compared with the control group. Administration of a mixed L. fermentum formulation prevented hyperlipidemia, inflammation and oxidative stress in colon and heart tissues induced by HFD consumption.

Aromatic aldehyde compound cuminaldehyde protects nonalcoholic fatty liver disease in rats feeding high fat diet

2019 ◽  
Vol 38 (7) ◽  
pp. 823-832 ◽  
Author(s):  
MR Haque ◽  
SH Ansari
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Liver Enzymes ◽  
Liver Weight ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
And Oxidative Stress

Nonalcoholic fatty liver disease (NAFLD) is caused by fat accumulation and is related with obesity and oxidative stress. In this study, we investigated the effect of cuminaldehyde on NAFLD in rats fed a high fat diet (HFD). Male Wistar rats were fed a HFD for 42 days to induce NAFLD. The progression of NAFLD was evaluated by histology and measuring liver enzymes (alanine transaminase and aspartate transaminase), serum and hepatic lipids (total triglycerides and total cholesterol), and oxidative stress markers (thiobarbituric acid reactive substances, glutathione, superoxide dismutase, and catalase). The HFD feeding increased the liver weight and caused NAFLD, liver steatosis, hyperlipidemia, oxidative stress, and elevated liver enzymes. Administration of cuminaldehyde ameliorated the changes in hepatic morphology and liver weight, decreased levels of liver enzymes, and inhibited lipogenesis. Our findings suggest that cuminaldehyde could improve HFD-induced NAFLD via abolishment of hepatic oxidative damage and hyperlipidemia. Cuminaldehyde might be considered as a potential aromatic compound in the treatment of NAFLD and obesity through the modulation of lipid metabolism.

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