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Cholesterol

MCE China：Cholesterol

Brand：MedChemExpress (MCE)

Cat. No.HY-N0322

CAS：57-88-5

Purity：99.94%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Cholesterol is the major sterol in mammals. It is making up 20-25% of structural component of the plasma membrane. Plasma membranes are highly permeable to water but relatively impermeable to ions and protons. Cholesterol plays an important role in determining the fluidity and permeability characteristics of the membrane as well as the function of both the transporters and signaling proteins. Cholesterol is also an endogenous estrogen-related receptor α (ERRα) agonist.

In Vitro：GT1-7 hypothalamic cells subjected to Cholesterol depletion in vitro produced 20-31% reductions in cellular Cholesterol content. All Cholesterol-depleted neuron-derived cells, exhibit decreased phosphorylation/activation of IRS-1 and AKT following stimulation by insulin, insulin-like growth factor-1, or the neurotrophins (NGF and BDNF). Reduction in cellular Cholesterol also results in increased basal autophagy and impairment of induction of autophagy by glucose deprivation[1].

In Vivo：Cholesterol can be used to create models of hyperlipidemia and atherosclerosis. The metabolic half-life of Cholesterol varies from a few hours to several years, depending on its association with different lipoproteins and the specific tissues in which it is located[4]. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of Hyperlipidemia[5][6] Background Hyperlipidemia is a group of disorders characterized by elevated concentrations of circulating lipids, including cholesterol, cholesterol esters, phospholipids and triglycerides. If the intake of cholesterol is too much, and exceeds the body's metabolic capacity, it may lead to increased plasma cholesterol levels, causing hyperlipidemia. Specific Mmodeling Methods Rat: Wistar • male • 18-week-old (period: 8 weeks)Administration: 2% cholesterol; diet • 8 weeks Note (1) Rats were housed in a room maintained at a 12-h light-dark cycle and a constant temperature of 22±2 °C(2) Wistar rats were always chosen for hyperlipidemia studies since this species shows a moderate increase in serum cholesterol and triglyceride level due to a high-cholesterol diet and no substantial atherosclerosis develops; therefore, the direct myocardial effect of hyperlipidemia, independent from atherosclerosis, can be studied in this model. Modeling Indicators Molecular changes: Significant increase in total cholesterol levels in blood samples (about 20%) Correlated Product(s): / Opposite Product(s): / .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of atherosclerosis[7][8] Background High levels of cholesterol in the blood, especially low-density lipoprotein cholesterol (LDL-C), can accumulate plaque on the walls of blood vessels, a process known as atherosclerosis. Over time, these plaques can block blood flow and cause serious health problems such as myocardial ischemia or myocardial infarction. Specific Mmodeling Methods Rabbits: Oryctolagus cuniculus • male • 4–6-month-old (period: 16 weeks)Administration: 0.3% cholesterol and 3% soybean oil; diet • 16 weeks Note (1) The cholesterol-fed rabbit is a widely used model for experimental atherosclerosis research as cholesterol only cause atherosclerotic changes in the rabbit arterial intima, which was very similar to human atherosclerosis.(2) As the absorption of dietary cholesterol requires fat, you must add oil into the diet. Otherwise, rabbits will use their internal fat, which makes them lean or sick. In addition, using soybean oil, which consists of unsaturated fatty acids, can prevent the levels of plasma cholesterol from becoming too high. Other vegetable oils, such as peanut oil or corn oil, can be used because they are all unsaturated fatty acids. Animal fat (saturated fatty acids) like tallow and lard is not recommended. (3) 0.3–0.5% cholesterol diet is recommended for most experiments. Rabbits cannot tolerate a 1–2% cholesterol diet for a month as they develop severe liver dysfunction. (4) Adult rabbits at 4 months or older can consume approximately ~150 g a day. You can either feed ab libitum or restricted (100–150 g/day/adult rabbit). (5) Plasma lipids should be measured weekly, especially for the first 4 weeks, because you need to determine whether plasma levels of cholesterol are elevated in each animal. Non-responder rabbits can be excluded from the experiments if their plasma cholesterol levels do not increase after cholesterol diet feeding. (6) Plasma lipoproteins can be measured at 8 and 16 weeks when the plasma levels of cholesterol are stable. (7) The age of rabbits should be considered because young rabbits are more susceptible to aortic atherosclerosis than old rabbits even though they have similar plasma cholesterol levels. 4–6-month-old rabbits are usually used for cholesterol feeding experiments. (8) Male and female rabbits are different in terms of response to a cholesterol diet and atherosclerosis. In our experience, female rabbits develop higher hypercholesterolemia and greater aortic lesions than their counterpart male rabbits. In general, male rabbits are recommended for experiments because estrogen may influence the results. Modeling Indicators Histological changes: atherosclerosis lesions can be seen on HE stained aortic arch and thoracic aorta segments Correlated Product(s): Soybean oil (HY-108750) Opposite Product(s): /

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References：

[1]. Casaburi I, et al. Cholesterol as an Endogenous ERRα Agonist: A New Perspective to Cancer Treatment. Front Endocrinol (Lausanne). 2018 Sep 11;9:525.  [Content Brief]

[2]. Dietschy JM, et al. Thematic review series: brain Lipids. Cholesterol metabolism in the central nervous system during early development and in the mature animal. J Lipid Res. 2004 Aug;45(8):1375-97.  [Content Brief]

[3]. Fukui K, et al. Effect of Cholesterol Reduction on Receptor Signaling in Neurons. J Biol Chem. 2015 Sep 14.  [Content Brief]

[4]. Puskás LG, et al. Cholesterol diet-induced hyperlipidemia influences gene expression pattern of rat hearts: a DNA microarray study. FEBS Lett. 2004 Mar 26;562(1-3):99-104.  [Content Brief]

[5]. Onody A, et al. Hyperlipidemia induced by a cholesterol-rich diet leads to enhanced peroxynitrite formation in rat hearts. Cardiovasc Res. 2003 Jun 1;58(3):663-70.  [Content Brief]

[6]. Baumer Y, et al. Hyperlipidemia-induced cholesterol crystal production by endothelial cells promotes atherogenesis. Nat Commun. 2017 Oct 24;8(1):1129.  [Content Brief]

[7]. Finking G, et al. Nikolaj Nikolajewitsch Anitschkow (1885-1964) established the cholesterol-fed rabbit as a model for atherosclerosis research. Atherosclerosis. 1997 Nov;135(1):1-7.  [Content Brief]

[8]. Fan J, et al. Use of Rabbit Models to Study Atherosclerosis. Methods Mol Biol. 2022;2419:413-431.  [Content Brief]