LDLR-/- mice
HVC1 ameliorates hyperlipidemia and inflammation in LDLR−/− mice
... The effects of HVC1 on the mRNA expression of PPAR family members in liver tissue were examined by qRT- PCR analysis. As shown in Fig. 3, the mRNA expression of PPAR-α in the HCD group was not different from that in the ...
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Original Article Polypeptides and polyphenols in Chinese yellow wine inhibitatherosclerosis in LDLR knockout mice
... in LDLR knockout mice has been proved, which ingredients in it played the key role remained ...in LDLR-/- mice. Methods: Six weeks old LDLR-/- male mice (n=56) were randomly ...
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Original Article Fucoidan attenuates atherosclerosis in LDLR mice through inhibition of inflammation and oxidative stress
... Abstract: Background and purpose: Fucoidan is a major bioactive polysaccharide which contains substantial percent- ages of L-fucose and sulfate ester groups, mainly isolated from brown seaweed. For the past decade ...
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T Cells in Atherosclerosis in Ldlr-/- and Apoe-/- Mice
... or Ldlr- /- mice in the C57BL/6 genetic background. The LDLR is a ubiquitously expressed cell-surface receptor that recognizes apoB100 and apoE on lipoprotein particles and mediates their clearance ...
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Myricetin and Hesperidin Inhibit Cerebral Thrombogenesis and Atherogenesis in Apoe / and Ldlr / Mice
... and LDLR deficient mice were fed high fat diet (F2HFD1) alone (N = 8), F2HFD1 plus myricetin at 200 mg/kg/day (N = 8) or F2HFD1 plus G-hesperidin at 500 mg/kg/day (N = 8) for 8 weeks from the age of 8 ...of ...
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HDL is redundant for adrenal steroidogenesis in LDLR knockout mice with a human-like lipoprotein profile
... between mice and ...ed mice with a human-like lipoprotein profi ...knockout mice was associated with HDL defi ciency and a parallel increase in the level of cho- lesterol associated with nonHDL ...
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Uptake of 68gallium in atherosclerotic plaques in LDLR-/-ApoB100/100 mice
... eight LDLR -/- ApoB 100/100 mice (one sample was discarded from the analysis because of remaining blood clot inside the aorta) and 8 autoradiographs of aortic sections from six control mice were ...
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Original Article Inhibition of NOX4 prevents the development of atherosclerosis in Ldlr mice
... phages [6]. Endothelium-dependent diastolic function is significantly enhanced in patients with inherited NOX2 deficiency [6]. NOX5 pro- motes endothelium-dependent diastole in human coronary artery disease caused by ...
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The effect of ABCG1 deficiency on atherosclerotic lesion development in LDL receptor knockout mice depends on the stage of atherogenesis
... ABCG1 expression was expected to protect against atherosclero- sis. However, independent groups have shown that ABCG1 might be pro-atherogenic as well as anti-atherogenic. Previously, we reported that both total body and ...
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LDL receptor knock-out mice show impaired spatial cognition with hippocampal vulnerability to apoptosis and deficits in synapses
... of Ldlr −/− mice. These results indicate that Ldlr −/− -mediated distribution of brain cholesterol metabolism led to an increase in apop- ...tosis. Ldlr −/− -mediated reduced cellular uptake ...
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Increased Atherosclerosis in Mice Deficient in Perilipin1
... -/- mice were a gift from I Tabas (Columbia Univer- sity, NY, ...These mice are from the strain generated and described by Martinez-Botas et al [24] and are on a C57BL/6 ...background. Ldlr -/- ...
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Novel cerebrovascular pathology in mice fed a high cholesterol diet
... hypercholesterolemic LDLR-/- mice following ischemia/reperfusion injury, larger numbers of adherent leukocytes are seen in postcapillary venules and vascular permeability is increased ...C57BL/6J ...
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Hepatic insulin signaling regulates VLDL secretion and atherogenesis in mice
... crossed mice deficient for the LDL receptor (Ldlr –/– mice) with mice that express low levels of IR in the liver and lack IR in peripheral tissues (the L1 B6 mouse ...with Ldlr –/– ...
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Deficiency of cathepsin S reduces atherosclerosis in LDL receptor–deficient mice
... in mice, we characterized lesions by (a) lesion area in the abdominal aorta delin- eated by lipid staining with oil red O (Fig- ure 1), (b) quantitative morphometric measurement of intimal thickening (area between ...
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Modulation of atherosclerosis in mice by Toll like receptor 2
... tion in atherosclerosis. However, with BM transplantation, loss of TLR2 expression from BM-derived cells had no effect on disease progression. This suggested that an unknown endogenous TLR2 agonist influenced lesion ...
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Metabolomic study of the LDL receptor null mouse fed a high-fat diet reveals profound perturbations in choline metabolism that are shared with ApoE null mice
... the mice fed HFCC diet had lower plasma triglyc- eride concentrations, despite a significant increase in plasma cholesterol ...of mice fed RM1 diet did not protect either C57BL/6J or LDLR ⫺/⫺ ...
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Hepatic S1P deficiency lowers plasma cholesterol levels in apoB-containing lipoproteins when LDLR function is compromised
... transgenic mice overexpressing the nuclear form of SREBP1a in liver (SREBP1a Tg mice) [26], the mecha- nisms underlying the phenotypes are very ...Tg mice produce large lipid-rich ...the LDLR ...
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The macrophage C type lectin receptor CLEC5A (MDL 1) expression is associated with early plaque progression and promotes macrophage survival
... being an important contributor to plaque progression [32], these cells might come from neutrophils. This con- clusion was also demonstrated in our immunofluores- cent costaining of ldlr−/− mice lesional ...
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Original Article Eperythrozoon suis infection enhances atherosclerosis in low-density lipoprotein receptor-deficient mice
... C57BL/6 mice were inoculated respectively with human EP 10 times (once a day); and 20 C57BL/6 and the same number of (LDLR-/-) C57BL/6 mice were not injected with EPs as ...inoculated mice ...
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BTLA stimulation protects against atherosclerosis by regulating follicular B cells
... Given the high expression of BTLA on peripheral B cells from CVD patients and its inhibitory role, we wanted to further explore the poten- tial of BTLA as a therapeutic target to treat atherosclerosis. First, we ...
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