Cafestol
(Synonyms: 咖啡醇) 目录号 : GC40352
Cafestol是咖啡中主要活性成分之一，是一种咖啡特异性二萜类化合物，具有ERK2抑制活性。
Cas No.:469-83-0
Sample solution is provided at 25 µL, 10mM.
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Cafestol, one of the major components of coffee, is a coffee-specific diterpene form and an inhibitor of ERK2[1]. Cafestol has elevated blood lipids[2], anti-inflammatory[1], anti-angiogenic[3] and anti-diabetic[4] activities. In addition, Cafestol induces tumor cell apoptosis and autophagy, which can be used in the study of cancer[5].
In vitro, Cafestol (0–100μM; 1–24h) dose-dependently suppressed PGE₂ production and reduced COX-2 mRNA levels in LPS-stimulated RAW 264.7 cells, while concurrently inhibiting AP-1 activation and ERK2 activity after 1h treatment[1]. Cafestol (30μM, 24h) significantly potentiated ABT-737-induced apoptosis in Mcl-1-overexpressed human renal carcinoma Caki cells, human glioma U251MG cells, and human breast carcinoma MDA-MB231 cells by downregulating Mcl-1 protein expression (via promoting protein degradation) and upregulating Bim expression, while showing no cytotoxicity in normal human skin fibroblasts[6].
In vivo, Cafestol (40–80mg/kg; i.g.; 20 days) markedly reduced tumor growth in a colon cancer xenograft mouse model[5]. Oral administration of Cafestol (5mg/kg/day for 14 days) in Wistar albino rats significantly protected against doxorubicin-induced cardiotoxicity by attenuating oxidative stress (downregulate MDA, upregulate GSH/SOD/CAT/Gpx-1), activating the Nrf2/HO-1/NQO-1 pathway (downregulate Keap1/NF-κB), suppressing inflammation (downregulate TNF-α/IL-1β), and inhibiting apoptosis (downregulate Bax/Casp3, downregulate TUNEL-positive cells), while improving cardiac biomarkers (CK-MB/LDH/ALP/ALT) and histopathology[7].
References:
[1] Shen, T., Lee, J., Lee, E., Kim, S. H., Kim, T. W., & Cho, J. Y. (2010). Cafestol, a coffee-specific diterpene, is a novel extracellular signal-regulated kinase inhibitor with AP-1-targeted inhibition of prostaglandin E2 production in lipopolysaccharide-activated macrophages. Biological & pharmaceutical bulletin, 33(1), 128–132.
[2] Urgert, R., Schulz, A. G., & Katan, M. B. (1995). Effects of cafestol and kahweol from coffee grounds on serum lipids and serum liver enzymes in humans. The American journal of clinical nutrition, 61(1), 149–154.
[3] Wang, S., Yoon, Y. C., Sung, M. J., Hur, H. J., & Park, J. H. (2012). Antiangiogenic properties of cafestol, a coffee diterpene, in human umbilical vein endothelial cells. Biochemical and biophysical research communications, 421(3), 567–571.
[4] Mellbye, F. B., Jeppesen, P. B., Shokouh, P., Laustsen, C., Hermansen, K., & Gregersen, S. (2017). Cafestol, a Bioactive Substance in Coffee, Has Antidiabetic Properties in KKAy Mice. Journal of natural products, 80(8), 2353–2359.
[5] Feng, Y., Yang, J., Wang, Y., Wang, X., Ma, Q., Li, Y., Zhang, X., Wang, S., Zhang, Q., Mi, F., Wang, Y., Zhong, D., & Yin, J. (2024). Cafestol inhibits colon cancer cell proliferation and tumor growth in xenograft mice by activating LKB1/AMPK/ULK1-dependent autophagy. The Journal of nutritional biochemistry, 129, 109623.
[6] Woo, S. M., Min, K. J., Seo, B. R., Nam, J. O., Choi, K. S., Yoo, Y. H., & Kwon, T. K. (2014). Cafestol overcomes ABT-737 resistance in Mcl-1-overexpressed renal carcinoma Caki cells through downregulation of Mcl-1 expression and upregulation of Bim expression. Cell death & disease, 5(11), e1514.
[7] Al-Kenany, S. A., & Al-Shawi, N. N. (2023). Protective effect of cafestol against doxorubicin-induced cardiotoxicity in rats by activating the Nrf2 pathway. Frontiers in pharmacology, 14, 1206782.
Cafestol是咖啡中主要活性成分之一，是一种咖啡特异性二萜类化合物，具有ERK2抑制活性[1]。Cafestol的药理作用包括升高血脂[2]、抗炎[1]、抗血管生成[3]及抗糖尿病[4]；此外，Cafestol可诱导肿瘤细胞凋亡与自噬，适用于癌症研究[5]。
体外实验中，Cafestol（0–100μM；1–24h）在脂多糖（LPS）刺激的RAW 264.7细胞中呈剂量依赖性抑制前列腺素E₂（PGE₂）生成并降低COX-2 mRNA水平，同时1小时处理即可抑制AP-1激活与ERK2活性[1]。30μM Cafestol处理24小时可通过下调Mcl-1蛋白（促进其降解）并上调Bim表达，显著增强ABT-737对Mcl-1过表达的人肾癌Caki细胞、胶质瘤U251MG细胞及乳腺癌MDA-MB231细胞的凋亡诱导作用，且对正常人皮肤成纤维细胞无毒性[6]。
体内实验中，Cafestol（40–80mg/kg；灌胃；20天）可显著抑制结肠癌异种移植小鼠模型的肿瘤生长[5]。Wistar大鼠连续14天口服Cafestol (5mg/kg/day)可通过减轻氧化应激（下调MDA，上调GSH/SOD/CAT/Gpx-1）、激活Nrf2/HO-1/NQO-1通路（下调Keap1/NF-κB）、抑制炎症（下调TNF-α/IL-1β）及凋亡（下调Bax/Casp3，下调TUNEL阳性细胞），同时改善心脏生物标志物（CK-MB/LDH/ALP/ALT）水平与组织病理损伤，显著缓解阿霉素诱导的心脏毒性[7]。
| Cell experiment [1]: | |
Cell lines | Human renal carcinoma cells (Caki), human breast carcinoma cells (MDA-MB231), human glioma cells (U251MG), human colon carcinoma cells (HCT116), human leukemia cells (U937), and human prostate carcinoma (PC3) cells |
Preparation Method | Human renal carcinoma cells (Caki), human breast carcinoma cells (MDA-MB231), human glioma cells (U251MG), human colon carcinoma cells (HCT116), human leukemia cells (U937), and human prostate carcinoma (PC3) cells were obtained from the American Type Culture Collection. All cells were cultured in Dulbecco’s Modified Eagle’s Medium containing 10% fetal bovine serum, 20mM HEPES buffer, 100U/ml penicillin, 100μg/ml streptomycin, and 100μg/ml gentamicin. A cell death detection ELISA plus kit was used for assessing apoptotic activity by detecting fragmented DNA within the nucleus in ABT-737-, cafestol-, and combination of ABT-737 and cafestol-treated cells. Briefly, cells were treated with different concentrations of cafestol(20 or 30μM) and ABT-737 alone or in combination. After 24h, each culture plate was centrifuged for 10min at 200×g, the supernatant was removed, and the pellet was lysed for 30min. After centrifuging the plate again at 200×g for 10min, the supernatant that contained the cytoplasmic histoneassociated DNA fragments was collected and incubated with an immobilized anti-histone antibody. The reaction products were incubated with a peroxidase substrate for 5min and measured by spectrophotometry at 405 and 490nm (reference wavelength) with a microplate reader. The signals in the wells containing the substrate alone were subtracted as the background. |
Reaction Conditions | 20 or 30μM; 24h |
Applications | Cafestol significantly potentiated ABT-737-induced apoptosis. |
| Animal experiment [2]: | |
Animal models | Wistar albino experimental rats |
Preparation Method | A total of 32 Wistar albino experimental rats of both sexes aged 6 weeks with an average weight of 150g were used in this study; animals were acquired and kept under controlled conditions of a light/dark cycle (12h) at a temperature of 23°C±2°C and humidity of 50% ± 5%. Experimental animals were randomly assigned into four groups (n = 8) as follows: Group I: each rat was given vehicle only (5% Tween in DDW) orally via oral gavage for 14 consecutive days. Then, a single dose of NaCl (0.9%), 10mL/kg, was injected intraperitoneally 1h after the last vehicle administration on day 14. This group served as the normal (negative control) group. Group II: each rat was orally given cafestol (5mg/kg/day) for 14 consecutive days. Group III: each rat was given vehicle only (5% Tween in DDW) via oral gavage for 14 consecutive days. Then, a single dose of doxorubicin (15mg/kg) was injected intraperitoneally 1h after the last vehicle administration on day 14 to serve as the positive control group. Group IV: each rat received cafestol (5mg/kg/day) orally for 14 consecutive days, and then, a single dose of doxorubicin (15mg/kg) was injected intraperitoneally 1h after the last cafestol treatment on day 14. 24 hours after doxorubicin dose administration (i.e., day 15), the animals were anaesthetized and samples were collected for further analysis. |
Dosage form | 5mg/kg/day for 14 days; p.o. |
Applications | Cafestol significantly protected against doxorubicin-induced cardiotoxicity by attenuating oxidative stress, activating the Nrf2/HO-1/NQO-1 pathway, suppressing inflammation, and improving cardiac biomarkers and histopathology. |
References: | |
| Cas No. | 469-83-0 | SDF | |
| 别名 | 咖啡醇 | ||
| Canonical SMILES | O[C@]1(CO)C[C@]23[C@](CC[C@]1([H])C3)([H])[C@@](CCC4=C5C=CO4)(C)[C@]5([H])CC2 | ||
| 分子式 | C20H28O3 | 分子量 | 316.4 |
| 溶解度 | DMF: 12 mg/ml,DMF:PBS (pH 7.2) (1:50): 0.02 mg/ml,DMSO: 5 mg/ml,Ethanol: 5 mg/ml | 储存条件 | 4°C, protect from light |
| 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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.1606 mL | 15.8028 mL | 31.6056 mL |
| 5 mM | 0.6321 mL | 3.1606 mL | 6.3211 mL |
| 10 mM | 0.3161 mL | 1.5803 mL | 3.1606 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。
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