Campestanol
(Synonyms: 油菜甾醇) 目录号 : GC43136
A phytosterol
Cas No.:474-60-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Campestanol is a phytosterol found in vegetables, fruits, nuts, and seeds. Dietary administration of vegetable stanol esters (1% w/w) containing campestanol (30.1%) and sitostanol lower serum cholesterol, LDL, VLDL, and intermediate-density lipoprotein (IDL) cholesterol levels in an APOE*3-Leiden transgenic mouse model of atherosclerosis. This combination of campestanol with sitostanol also reduces atherosclerotic lesion area by 91% and the proportion of lesions with extensive macrophage infiltration.
| Cas No. | 474-60-2 | SDF | |
| 别名 | 油菜甾醇 | ||
| Canonical SMILES | C[C@H](CC[C@@H](C)C(C)C)[C@@]1([H])CC[C@@]2([H])[C@]3([H])CC[C@@]4([H])C[C@@H](O)CC[C@]4(C)[C@@]3([H])CC[C@@]21C | ||
| 分子式 | C28H50O | 分子量 | 402.7 |
| 溶解度 | Chloroform: slightly soluble | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.4832 mL | 12.4162 mL | 24.8324 mL |
| 5 mM | 0.4966 mL | 2.4832 mL | 4.9665 mL |
| 10 mM | 0.2483 mL | 1.2416 mL | 2.4832 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Campestanol (24-methyl-5alpha-cholestan-3beta-ol) absorption and distribution in New Zealand White rabbits: effect of dietary sitostanol
Metabolism 1999 Mar;48(3):363-8.PMID:10094114DOI:10.1016/s0026-0495(99)90086-0.
Campestanol (24-methyl-5alpha-cholestan-3beta-ol) is a naturally occurring plant stanol, structurally similar to cholesterol (5-cholesten-3beta-ol) and widely distributed in vegetable oils consumed in human diets. We measured the absorption and turnover of Campestanol by the plasma dual-isotope ratio method and mathematical analysis of specific activity versus time decay curves after simultaneous oral and intravenous pulse-labeling with [3alpha-3H]- and [23-14C]-labeled Campestanol, respectively, in New Zealand White (NZW) rabbits: six fed chow and six fed chow with 125 mg/d Campestanol and 175 mg/d sitostanol (24-ethyl-5alpha-cholestan-3beta-ol). Plasma concentrations increased insignificantly from 0.08+/-0.01 to 0.09+/-0.01 mg/dL with dietary stanols. The percent Campestanol absorption measured by the plasma dual-isotope ratio method after the rabbits were fasted for 6 hours yielded the percent absorption in the absence of competing intestinal sterols and stanols and declined insignificantly from 11.6%+/-3.5% in controls to 8.1%+/-3.7% in the treated rabbit groups. In contrast, the turnover, which measured actual absorption averaged over 24 hours, increased from 0.12+/-0.05 to 0.37+/-0.05 mg/d (P < .05) with Campestanol and sitostanol added to the diet. However, the actual percent absorption declined from 3% to 0.3% of dietary intake with the Campestanol and sitostanol-enriched diet. Campestanol pool sizes, although remaining small, increased slightly from 1.1+/-0.4 to 2.5+/-1.5 mg. The removal constant (KA) from pool A (MA) did not change significantly with added dietary Campestanol and sitostanol (KA= -0.040+/-0.005 v -0.037+/-0.007 d(-1)). The results demonstrate small Campestanol plasma concentrations and body pools even when the rabbits consumed substantial amounts because (1) intestinal absorption was limited and (2) was further reduced by competing dietary sitostanol, and (3) Campestanol was removed rapidly from the body. Thus, Campestanol, which shares the same basic structure and intestinal absorption pathway with cholesterol, does not accumulate when fed, and may be incorporated into the diet to block cholesterol absorption.
Dietary sitostanol and Campestanol: accumulation in the blood of humans with sitosterolemia and xanthomatosis and in rat tissues
Lipids 2005 Sep;40(9):919-23.PMID:16331855DOI:10.1007/s11745-005-1452-7.
Dietary sitostanol has a hypocholesterolemic effect because it decreases the absorption of cholesterol. However, its effects on the sitostanol concentrations in the blood and tissues are relatively unknown, especially in patients with sitosterolemia and xanthomatosis. These patients hyperabsorb all sterols and fail to excrete ingested sitosterol and other plant sterols as normal people do. The goal of the present study was to examine the absorbability of dietary sitostanol in humans and animals and its potential long-term effect. Two patients with sitosterolemia were fed the margarine Benecol (McNeill Nutritionals, Ft. Washington, PA), which is enriched in sitostanol and Campestanol, for 7-18 wk. Their plasma cholesterol levels decreased from 180 to 167 mg/dL and 153 to 113 mg/dL, respectively. Campesterol and sitosterol also decreased. However, their plasma sitostanol levels increased from 1.6 to 10.1 mg/dL and from 2.8 to 7.9 mg/dL, respectively. Plasma Campestanol also increased. After Benecol withdrawal, the decline in plasma of both sitostanol and Campestanol was very sluggish. In an animal study, two groups of rats were fed high-cholesterol diets with and without sitostanol for 4 wk. As expected, plasma and liver cholesterol levels decreased 18 and 53%, respectively. The sitostanol in plasma increased fourfold, and sitostanol increased threefold in skeletal muscle and twofold in heart muscle. Campestanol also increased significantly in both plasma and tissues. Our data indicate that dietary sitostanol and Campestanol are absorbed by patients with sitosterolemia and xanthomatosis and also by rats. The absorbed plant stanols were deposited in rat tissues. Once absorbed by sitosterolemic patients, the prolonged retention of sitostanol and Campestanol in plasma might increase their atherogenic potential.
Hyperabsorption and retention of Campestanol in a sitosterolemic homozygote: comparison with her mother and three control subjects
J Lipid Res 2000 Nov;41(11):1883-9.PMID:11060358doi
We measured the percent absorption, turnover, and distribution of Campestanol (24-methyl-5alpha-cholestan-3beta-ol) in a sitosterolemic homozygote, her obligate heterozygous mother, and three healthy human control subjects. For reasons relating to sterol hyperabsorption, the homozygote consumed a diet low in plant sterols that contained Campestanol at about 2 mg/day. The heterozygote and three control subjects were fed a diet supplemented with a spread that contained Campestanol at 540 mg/day and sitostanol (24-ethyl-5alpha-cholestan-3beta-ol) at 1.9 g/day as fatty acid esters. Plasma Campestanol concentrations determined by capillary gas-liquid chromatography were 0.72 +/- 0.03 mg/dl in the homozygote, 0.09 +/- 0.04 mg/dl in the heterozygote, and 0.05 +/- 0.03 mg/dl for the control mean. After simultaneous pulse labeling with [3alpha-(3)H]Campestanol intravenously and [23-(14)C]Campestanol orally, the maximum percent absorption measured by the plasma dual-isotope ratio method as a single time point was 80% in the homozygote, 14.3% in the heterozygote, and 5.5 +/- 4.3% as the mean for three control subjects. Turnover (pool size) values estimated by mathematical analysis of the specific activity versus time [3alpha-(3)H]Campestanol decay curves were as follows: 261 mg in the homozygote, 27.3 mg in the heterozygote, and 12.8 +/- 7.6 mg in the three control subjects (homogygote vs. controls, P < 0.001). The calculated production rate (mg/24 h) equivalent to actual absorption in the presence of dietary sterols and stanols was 0.67 mg/day or 31% of intake in the homozygote, 2.1 mg/day or 0.3% of intake in the heterozygote, and 0.7 +/- 0.3 mg/day or 0.1% of intake in the three control subjects. However, the excretion constant from pool A (K(A)) was prolonged markedly in the homozygote, but was 100 times more rapid in the heterozygote and three control subjects.Thus, Campestanol, like other noncholesterol sterols, is hyperabsorbed and retained in sitosterolemic homozygotes. However, Campestanol absorption was only slightly increased in the sitosterolemic heterozygote and removal was as rapid as in control subjects.
Cholesterol reduction by different plant stanol mixtures and with variable fat intake
Metabolism 1999 May;48(5):575-80.PMID:10337856DOI:10.1016/s0026-0495(99)90053-7.
Our aim was to investigate (1) whether different Campestanol/sitostanol mixtures in margarine differ in reducing serum cholesterol, and (2) whether sitostanol ester in butter decreases serum cholesterol and alters cholesterol absorption and metabolism. Twenty-three postmenopausal women replaced 25 g dietary fat with (1) sitostanol ester-rich (Campestanol to sitostanol ratio 1:11) and (2) Campestanol ester-rich (Campestanol to sitostanol ratio 1:2) rapeseed oil margarine, (3) butter, and (4) sitostanol ester-rich (Campestanol to sitostanol ratio 1:13) butter. The respective scheduled stanol intake was 3.18, 3.16, and 2.43 g/d. The 6-week margarine periods and, after an 8-week washout, 5-week butter periods were double-blind and in random order. Serum cholesterol precursor sterols (indicators of cholesterol synthesis) and plant sterols (indicators of cholesterol absorption) were quantified with gas-liquid chromatography (GLC). Low-density lipoprotein (LDL) cholesterol was reduced by 8% and 10% with the sitostanol and Campestanol ester-rich margarines versus baseline (P < .05 for both) and high-density lipoprotein (HDL) cholesterol was increased by 6% and 5% (P < .05), so the LDL/HDL cholesterol ratio was reduced by 15% (P < .05 for both). Sitostanol ester-rich butter decreased LDL cholesterol 12% and the LDL/HDL cholesterol ratio 11% (P < .05 for both) versus the butter period. The serum proportions of plant sterols and cholestanol were similarly reduced and those of cholesterol precursor sterols were similarly increased during all periods (P < .05 for all). Serum proportions of sitostanol and Campestanol were slightly increased, indicating that their absorption related to their dietary intake. During all stanol interventions, serum vitamin D and retinol concentrations and alpha-tocopherol to cholesterol ratios were unchanged, whereas those of alpha- and beta-carotenes were significantly reduced. We conclude that varying the Campestanol to sitostanol ratio from 1:13 to 1:2 in margarine and in butter similarly decreased cholesterol absorption, LDL cholesterol, and the LDL/HDL cholesterol ratio such that the serum lipids became less atherogenic.
The Protective Effect of Dietary Phytosterols on Cancer Risk: A Systematic Meta-Analysis
J Oncol 2019 Jun 23;2019:7479518.PMID:31341477DOI:10.1155/2019/7479518.
Backgrounds/aims: Many studies have explored the association between dietary phytosterols and cancer risk, but the results have been inconsistent. We aimed to provide a synopsis of the current understanding of phytosterol intake for cancer risk through a systematic evaluation of the results from previous studies. Methods: We performed a literature search of PUBMED, EMBASE, CNKI, and Wanfang, and studies published before May 2019 focusing on dietary total phytosterols, β-sitosterol, campesterol, stigmasterol, β-sitostanol, and Campestanol, as well as their relationships with cancer risk, were included in this meta-analysis. Summaries of the relative risks from 11 case-control and case-cohort studies were eventually estimated by randomized or fixed effects models. Results: The summary relative risk for the highest versus the lowest intake was 0.63 (95% confidence interval [CI] = 0.49-0.81) for total phytosterols, 0.74 (95% CI = 0.54-1.02) for β-sitosterol, 0.72 (95% CI = 0.51-1.00) for campesterol, 0.83 (95% CI = 0.60-1.16) for stigmasterol, 1.12 (95% CI = 0.96-1.32) for β-sitostanol, and 0.77 (95% CI = 0.65-0.90) for Campestanol. In a dose-response analysis, the results suggested a linear association for campesterol and a nonlinear association for total phytosterol intake. Conclusion: Our findings support the hypothesis that high phytosterol intake is inversely related to risk of cancer. Further studies with prospective designs that control for vital confounders and investigate the important anticancer effects of dietary phytosterols are warranted.