scholarly journals BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Jian Wang ◽  
Chi Zhang ◽  
Zhiguo Zhang ◽  
Qiang Chen ◽  
Xuemian Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Growth Factor ◽  
Liver Damage ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Liver Weight ◽  
High Fat ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

The present study was to investigate whether amagnoliaextract, named BL153, can prevent obesity-induced liver damage and identify the possible protective mechanism. To this end, obese mice were induced by feeding with high fat diet (HFD, 60% kcal as fat) and the age-matched control mice were fed with control diet (10% kcal as fat) for 6 months. Simultaneously these mice were treated with or without BL153 daily at 3 dose levels (2.5, 5, and 10 mg/kg) by gavage. HFD feeding significantly increased the body weight and the liver weight. Administration of BL153 significantly reduced the liver weight but without effects on body weight. As a critical step of the development of NAFLD, hepatic fibrosis was induced in the mice fed with HFD, shown by upregulating the expression of connective tissue growth factor and transforming growth factor beta 1, which were significantly attenuated by BL153 in a dose-dependent manner. Mechanism study revealed that BL153 significantly suppressed HFD induced hepatic lipid accumulation and oxidative stress and slightly prevented liver inflammation. These results suggest that HFD induced fibrosis in the liver can be prevented partially by BL153, probably due to reduction of hepatic lipid accumulation, inflammation and oxidative stress.

scholarly journals Optimized Rapeseed Oils Rich in Endogenous Micronutrients Protect High Fat Diet Fed Rats from Hepatic Lipid Accumulation and Oxidative Stress

Nutrients ◽  
2015 ◽  
Vol 7 (10) ◽  
pp. 8491-8502 ◽  
Author(s):  
Jiqu Xu ◽  
Xiaoli Liu ◽  
Hui Gao ◽  
Chang Chen ◽  
Qianchun Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

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.

scholarly journals (-)-Epicatechin Mitigates High Fat Diet-induced Inflammation in the Hippocampus and Altered Recognition Memory in Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 411-411
Author(s):  
Jiye Kang ◽  
Ziwei Wang ◽  
Patricia Oteiza
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Object Recognition ◽  
Recognition Memory ◽  
High Fat Diet ◽  
High Fat ◽  
Short Term ◽  
Dietary Treatments ◽  
Metabolic Endotoxemia ◽  
And Oxidative Stress

Abstract Objectives This project investigated the capacity of dietary (-)-epicatechin (EC) to mitigate hippocampal inflammation and impaired memory in high fat diet (HFD)-fed mice. Methods Healthy 6 weeks old male C57BL/6J mice (10 mice/group) were fed for 13 weeks either: a control diet (10% total calories from fat), a high fat diet (60% total calories from lard fat), or the control and high fat diets supplemented with 20 mg EC/kg body weight. Between weeks 10 and 12 of the dietary intervention, object recognition memory was evaluated by the novel object recognition task and short-term spatial memory by the object location memory task, and the Morris Water Maze. After 13 weeks on the dietary treatments, mice were euthanized, and brain tissues and blood were collected. Hippocampus was isolated, flash-frozen in liquid nitrogen, and stored at −80°C. Metabolic endotoxemia was assessed by measuring plasma lipopolysaccharide (LPS) levels. Gene expressions related to inflammation (Toll-like receptor 4 (TLR4) and tumor necrosis factor-α (TNF-α)), activation of microglia (ionized calcium-binding adapter molecule 1 (Iba-1)), and oxidative stress (NADPH oxidase 4 (NOX4)) were analyzed in the hippocampus with RT-qPCR. Results After 13 weeks on the dietary treatments, HFD-fed mice developed obesity, endotoxemia, and showed increased parameters of hippocampal inflammation, i.e., high mRNA levels of TLR4, Iba-1, and NOX4. While not affecting body weight gain, EC supplementation prevented all other HFD-induced changes. Impaired recognition memory was observed in HFD-fed mice, which was prevented by EC supplementation. Neither HFD consumption nor EC supplementation affected mouse spatial memory. Conclusions EC supplementation prevented short-term recognition memory in HFD-induced obese mice, which could be in part due to the capacity of EC to mitigate metabolic endotoxemia and associated hippocampal inflammation and oxidative stress. Funding Sources HA Jastro Shields Award.

scholarly journals Electromagnetic Fields Ameliorate Hepatic Lipid Accumulation and Oxidative Stress by Activating the CaMKKβ/AMPK/SREBP-1c and Nrf2 Pathways in High-Fat Diet-Fed Mice

2021 ◽  
Author(s):  
Mingming Zhai ◽  
Jinxiu Cui ◽  
Chenxu Zhang ◽  
Juan Liu ◽  
Yuanzhe Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Protein Expression ◽  
Electromagnetic Fields ◽  
High Fat Diet ◽  
Lipid Deposition ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

Abstract Background: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, and is related to disturbed lipid metabolism and redox homeostasis. However, a definitive drug treatment has not been approved for this disease. Studies have found that electromagnetic fields (EMFs) can ameliorate hepatic steatosis and oxidative stress. Nevertheless, the mechanism remains unclear.Methods: NAFLD models were established by feeding mice a high-fat diet. Simultaneously, EMF exposure is performed. The effects of the EMF on hepatic lipid deposition and oxidative stress were investigated. Additionally, the AMPK and Nrf2 pathways were analysed to confirm whether they were activated by the EMF.Results: Administration of the EMF decreased the body weight, liver weight and serum triglyceride (TG) levels and restrained the excessive hepatic lipid accumulation caused by feeding the HFD. This EMF function is achieved by boosting CaMKKβ protein expression, activating AMPK phosphorylation and suppressing mature SREBP-1c protein expression. Meanwhile, the activity of GSH-Px was enhanced following an increase in nuclear Nrf2 protein expression by EMF. However, no change was observed in the activities of SOD and CAT. Consequently, EMF reduced hepatic reactive oxygen species (ROS) and MDA levels, which means that EMF relieved liver damage by oxidative stress in HFD-fed mice.Conclusions: EMF can activate the CaMKKβ/AMPK/SREBP-1c and Nrf2 pathways to control hepatic lipid deposition and oxidative stress. This investigation indicates that EMF may be a novel therapeutic method for NAFLD.

scholarly journals MagnoliaExtract (BL153) Protection of Heart from Lipid Accumulation Caused Cardiac Oxidative Damage, Inflammation, and Cell Death in High-Fat Diet Fed Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Weixia Sun ◽  
Zhiguo Zhang ◽  
Qiang Chen ◽  
Xia Yin ◽  
Yaowen Fu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Body Weight ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Tunel Staining ◽  
High Fat ◽  
Cardiac Lipid ◽  
Cell Death Pathway

Magnoliaas an herbal material obtained fromMagnolia officinalishas been found to play an important role in anti-inflammation, antioxidative stress, and antiapoptosis. This study was designed to investigate the effect ofMagnoliaextract (BL153) on obesity-associated lipid accumulation, inflammation, oxidative stress, and apoptosis in the heart. C57BL/6 mice were fed a low- (10 kcal% fat) or high-fat (60 kcal% fat) diet for 24 weeks to induce obesity. These mice fed with high-fat diet (HFD) were given a gavage of vehicle, 2.5, 5, or 10 mg/kg body weight BL153 daily. The three doses of BL153 treatment slightly ameliorated insulin resistance without decrease of body weight gain induced by HFD feeding. BL153 at 10 mg/kg slightly attenuated a mild cardiac hypertrophy and dysfunction induced by HFD feeding. Both 5 mg/kg and 10 mg/kg of BL153 treatment significantly inhibited cardiac lipid accumulation measured by Oil Red O staining and improved cardiac inflammation and oxidative stress by downregulating ICAM-1, TNF-α, PAI-1, 3-NT, and 4-HNE. TUNEL staining showed that BL153 treatment also ameliorated apoptosis induced by mitochondrial caspase-3 independent cell death pathway. This study demonstrates that BL153 attenuates HFD-associated cardiac damage through prevention of HFD-induced cardiac lipid accumulation, inflammation, oxidative stress, and apoptosis.

scholarly journals Cinnamon Polyphenol Extract Inhibits Hyperlipidemia and Inflammation by Modulation of Transcription Factors in High-Fat Diet-Fed Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Zeynep Tuzcu ◽  
Cemal Orhan ◽  
Nurhan Sahin ◽  
Vijaya Juturu ◽  
Kazim Sahin
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Lipid Profile ◽  
High Fat Diet ◽  
Elevated Serum ◽  
Liver Weight ◽  
Serum Glucose ◽  
High Fat ◽  
Normal Chow ◽  
And Oxidative Stress

We evaluated the effects of cinnamon polyphenol extract on hepatic transcription factors expressions including SREBP-1c and LXR-α in rats fed high fat diet (HFD). Twenty-eight Wistar rats were allocated into four groups: (i) normal control: animals fed with normal chow; (ii) cinnamon: animals supplemented with cinnamon polyphenol; (iii) HFD: animals fed a high-fat diet; and (iv) HFD + cinnamon: animals fed a high-fat diet and treated with cinnamon polyphenol. Obesity was linked to hyperglycemia, hyperlipidemia, and oxidative stress as imitated by elevated serum glucose, lipid profile, and serum and liver malondialdehyde (MDA) concentrations. Cinnamon polyphenol decreased body weight, visceral fat, liver weight and serum glucose and insulin concentrations, liver antioxidant enzymes, and lipid profile (P<0.05) and reduced serum and liver MDA concentration compared to HFD rats (P<0.05). Cinnamon polyphenol also suppressed the hepatic SREBP-1c, LXR-α, ACLY, FAS, and NF-κB p65 expressions and enhanced the PPAR-α, IRS-1, Nrf2, and HO-1 expressions in the HFD rat livers (P<0.05). In conclusion, cinnamon polyphenol reduces the hyperlipidemia, inflammation, and oxidative stress through activating transcription factors and antioxidative defense signaling pathway in HFD rat liver.

NF-E2-Related Factor 2 Inhibits Lipid Accumulation and Oxidative Stress in Mice Fed a High-Fat Diet

2008 ◽  
Vol 325 (2) ◽  
pp. 655-664 ◽  
Author(s):  
Yuji Tanaka ◽  
Lauren M. Aleksunes ◽  
Ronnie L. Yeager ◽  
Maxwell A. Gyamfi ◽  
Noriko Esterly ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Related Factor ◽  
High Fat ◽  
And Oxidative Stress
Sign in / Sign up

Export Citation Format

Share Document