Naoxintong Protects against Atherosclerosis through Lipid-lowering and Inhibiting Maturation of Dendritic Cells in LDL Receptor Knockout Mice fed a High-fat Diet

2013 ◽  
Vol 19 (33) ◽  
pp. 5891-5896 ◽  
Author(s):  
Jingjing Zhao ◽  
Hong Zhu ◽  
Shijun Wang ◽  
Xin Ma ◽  
Xiangwei Liu ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Ldl Receptor ◽  
Lipid Lowering ◽  
High Fat ◽  
Ldl Receptor Knockout Mice

scholarly journals Impaired compensatory beta-cell function and growth in response to high-fat diet in LDL receptor knockout mice

2014 ◽  
Vol 95 (4) ◽  
pp. 296-308 ◽  
Author(s):  
Ricardo B. d. Oliveira ◽  
Carolina P. d. F. Carvalho ◽  
Carla C. Polo ◽  
Gabriel d. G. Dorighello ◽  
Antônio C. Boschero ◽  
...  
Keyword(s):  
Beta Cell ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Beta Cell Function ◽  
Cell Function ◽  
Ldl Receptor ◽  
High Fat ◽  
Ldl Receptor Knockout Mice

scholarly journals A High-Fat Diet Exacerbates the Course of Experimental Trypanosoma cruzi Infection That Can Be Mitigated by Treatment with Simvastatin

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Débora Maria Soares de Souza ◽  
Guilherme de Paula Costa ◽  
Ana Luísa Junqueira Leite ◽  
Daniela Silva de Oliveira ◽  
Kelerson Mauro de Castro Pinto ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
High Fat Diet ◽  
Biochemical Parameters ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Lipid Lowering ◽  
Histopathological Analysis ◽  
High Fat ◽  
Inflammatory State

The protozoan Trypanosoma cruzi is responsible for triggering a damage immune response in the host cardiovascular system. This parasite has a high affinity for host lipoproteins and uses the low-density lipoprotein (LDL) receptor for its invasion. Assuming that the presence of LDL cholesterol in tissues could facilitate T. cruzi proliferation, dietary composition may affect the parasite-host relationship. Therefore, the aim of this study was to evaluate myocarditis in T. cruzi-infected C57BL/6 mice—acute phase—fed a high-fat diet and treated with simvastatin, a lipid-lowering medication. Animals (n=10) were infected with 5×103 cells of the VL-10 strain of T. cruzi and treated or untreated daily with 20 mg/kg simvastatin, starting 24 h after infection and fed with a normolipidic or high-fat diet. Also, uninfected mice, treated or not with simvastatin and fed with normolipidic or high-fat diet, were evaluated as control groups. Analyses to measure the production of chemokine (C-C motif) ligand 2 (CCL2), interferon- (IFN-) γ, interleukin- (IL-) 10, and tumor necrosis factor (TNF); total hepatic lipid dosage; cholesterol; and fractions, as well as histopathological analysis, were performed on day 30 using cardiac and fat tissues. Our results showed that the high-fat diet increased (i) parasite replication, (ii) fat accumulation in the liver, (iii) total cholesterol and LDL levels, and (iv) the host inflammatory state through the production of the cytokine TNF. However, simvastatin only reduced the production of CCL2 but not that of other inflammatory mediators or biochemical parameters. Together, our data suggest that the high-fat diet may have worsened the biochemical parameters of the uninfected and T. cruzi-infected animals, as well as favored the survival of circulating parasites.

scholarly journals Hypolipidemic Effects and Mechanisms of Val-Phe-Val-Arg-Asn in C57BL/6J Mice and 3T3-L1 Cell Models

2019 ◽  
Author(s):  
Shi W ◽  
He Hui ◽  
Cao Ruge ◽  
Hou Tao
Keyword(s):  
High Fat Diet ◽  
Cell Model ◽  
Regulatory Element ◽  
Fatty Acid Synthetase ◽  
Ldl Receptor ◽  
Lipid Lowering ◽  
Peroxisome Proliferator ◽  
Mice Model ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptors

Val-Phe-Val-Arg-Asn (VFVRN) has been identified and screened from lipid-lowering chickpea peptides (ChPs) by using a pharmacokinetic model in our previous experiment. The present study was conducted to investigate its effects and mechanisms on lipid metabolism. A high-fat diet C57BL/6J mice model and 3T3-L1 preadipocyte cell model were used. VFVRN was found to significantly decrease the levels of some blood lipids. The expressions of LDL receptor (LDLR), peroxisome proliferator-activated receptors (PPAR)α, liver X receptor (LXR)α, cholesterol 7α-hydroxylase (CYP7A1) and AMP-activated protein kinase (p-AMPK) in liver were up-regulated by VFVRN treatment. The expressions of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), fatty acid synthetase (FAS), 1-aminocyclopropane-1-carboxylate synthetase (ACC), sterol regulatory element-binding protein (SREBP)-1c and SREBP-2 in liver were significantly (P<0.05) down-regulated. Additionally, the expressions of PPARα and PPARγ in adipose tissues were up-regulated by VFVRN significantly (P<0.05). VFVRN might also contribute to transintestinal cholesterol efflux (TICE) by up-regulating the expressions of LXRα and ATP binding cassette G5/8 transporters (ABGC5/8). Moreover, VFVRN promoted 3T3-L1 preadipocyte apoptosis by up-regulating the expressions of BaX, cleaved Caspase-3 and down-regulating Bcl-2. VFVRN had potent effects in reversing metabolic disorders of blood and liver in a high-fat diet mice model, as well as to promote the apoptosis of 3T3-L1 preadipocytes.

The Effect of Resveratrol on Reducing Neointimal Growth after Femoral Artery Injury in AMPKα2 Knockout Mice Given High-Fat Diet

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 484-P
Author(s):  
LIWEI ZHOU ◽  
JUNE GUO ◽  
HANGJUN ZHANG ◽  
SCOTT HEXIMER ◽  
ADRIA GIACCA
Keyword(s):  
Femoral Artery ◽  
Knockout Mice ◽  
High Fat Diet ◽  
High Fat ◽  
Artery Injury
Sign in / Sign up

Export Citation Format

Share Document