Cedrol
(Synonyms: 柏木脑,(+)-Cedrol; α-Cedrol) 目录号 : GC38681A sesquiterpene alcohol
Cas No.:77-53-2
Sample solution is provided at 25 µL, 10mM.
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- Purity: >98.00%
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(+)-Cedrol is a sesquiterpene alcohol that has been used in Cannabis testing and has diverse biological activities.1 It inhibits the growth of L. sulphureus, G. trabeum, L. betulina, and T. versicolor wood decay fungi when used at a concentration of 100 μg/ml.2 (+)-Cedrol inhibits the cytochrome P450 (CYP) isoforms CYP2B6 and CYP3A4 (Kis = 0.9 and 3.4 μM, respectively).3 In vivo, (+)-cedrol (200 mg/kg) prevents hair follicle dystrophy and reduces hair loss in a mouse model of alopecia induced by cyclophosphamide .4 (+)-Cedrol-loaded nanostructured lipid particles reduce peritoneal mast cell degranulation, a component of the type I anaphylactic response, induced by compound 48/80 in mice.5
1.Fischedick, J.T.Identification of terpenoid chemotypes among high (–)-trans-Δ9-tetrahydrocannabinol-producing Cannabis sativa L. cultivarsCannabis Cannabinoid Res.2(1)34-47(2017) 2.Cheng, S.S., Chung, M.J., Lin, C.Y., et al.Phytochemicals from Cunninghamia konishii Hayata act as antifungal agentsJ. Agric. Food Chem.60(1)124-128(2012) 3.Jeong, H.U., Kwon, S.S., Kong, T.Y., et al.Inhibitory effects of cedrol, β-cedrene, and thujopsene on cytochrome P450 enzyme activities in human liver microsomesJ. Toxicol. Environ. Health A77(22-24)1522-1532(2014) 4.Chen, S.S., Zhang, Y., Lu, Q.L., et al.Preventive effects of cedrol against alopecia in cyclophosphamide-treated miceEnviron. Toxicol. Pharmacol.46270-276(2016) 5.Chakraborty, S., Kar, N., Kumari, L., et al.Inhibitory effect of a new orally active cedrol-loaded nanostructured lipid carrier on compound 48/80-induced mast cell degranulation and anaphylactic shock in miceInt. J. Nanomedicine124849-4868(2017)
Cas No. | 77-53-2 | SDF | |
别名 | 柏木脑,(+)-Cedrol; α-Cedrol | ||
Canonical SMILES | O[C@]1(C)CC[C@]23[C@H](C)CC[C@@]2([H])C(C)(C)[C@@]1([H])C3 | ||
分子式 | C15H26O | 分子量 | 222.37 |
溶解度 | DMSO : 110 mg/mL (494.67 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble) | 储存条件 | 4°C, protect from light |
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1 mg | 5 mg | 10 mg | |
1 mM | 4.497 mL | 22.485 mL | 44.9701 mL |
5 mM | 0.8994 mL | 4.497 mL | 8.994 mL |
10 mM | 0.4497 mL | 2.2485 mL | 4.497 mL |
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2.
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Cedrol, a Sesquiterpene Isolated from Juniperus chinensis, Inhibits Human Colorectal Tumor Growth associated through Downregulation of Minichromosome Maintenance Proteins
J Cancer Prev 2022 Dec 31;27(4):221-228.PMID:36713942DOI:10.15430/JCP.2022.27.4.221.
Cedrol, a sesquiterpene alcohol, isolated from Juniperus chinensis has been reported to inhibit minichromosome maintenance (MCM) proteins as cancer biomarkers in human lung cancer in vitro. In the present study, we investigated the anti-cancer activity of Cedrol in vitro and in vivo using human colorectal cancer HT29 cells and a human colorectal tumor xenograft model. Cedrol inhibited MCM protein expression and cell growth in HT29 cells, which are associated with G1 arrest and the induction of apoptosis. We demonstrated that Cedrol effectively reduced HT29 tumor growth without apparent weight loss in a human tumor xenograft model. Compared with vehicle- and adriamycin-treated tumor tissues, Cedrol induced changes in the tumor tissue structure, resulting in a reduced cell density within the tumor parenchyma and reduced vascularization. Moreover, the expression of MCM7, an important subunit of MCM helicase, was significantly suppressed by Cedrol in tumor tissue. Collectively, these results suggest that Cedrol may act as a potential anti-cancer agent for colorectal cancer by inhibiting MCM protein expression and tumor growth.
Cedrol restricts the growth of colorectal cancer in vitro and in vivo by inducing cell cycle arrest and caspase-dependent apoptotic cell death
Int J Med Sci 2022 Oct 31;19(13):1953-1964.PMID:36438926DOI:10.7150/ijms.77719.
Background: Cedrol is a natural sesquiterpene alcohol found in Cedrus atlantica, which has been proven to have a broad spectrum of biological activities, such as antimicrobial, anti-inflammatory, analgesic, anxiolytic, and anti-cancer effects. However, the underlying anticancer mechanisms and in vivo inhibitory effects of Cedrol on colorectal cancer (CRC) have not been elucidated. In the present study, we investigated the anti-CRC potential of Cedrol using in vitro and in vivo models. Methods: The effects of Cedrol on cell viability, cell cycle progression, and apoptosis of HT-29 and CT-26 cells were detected by MTT, flow cytometry, and TUNEL assays. Western blotting was used to measure protein expression for molecular signaling analyses. Results: Cedrol inhibited HT-29 and CT-26 cell proliferation in a time- and dose-dependent manner, with IC50 values of 138.91 and 92.46 µM, respectively. Furthermore, Cedrol induced cell cycle arrest at the G0/G1 phase by regulating the expression of cell cycle regulators, such as CDK4 and cyclin D1, and triggered apoptosis through extrinsic (FasL/caspase-8) and intrinsic (Bax/caspase-9) pathways. In addition, Cedrol in combination with the clinical drug 5-fluorouracil exhibited synergistic inhibitory effects on CRC cell growth. Importantly, Cedrol treatment suppressed the progression of CRC and improved the survival rate of animals at a well-tolerated dose. Conclusion: These results suggest that Cedrol has an anti-cancer potential via induction of cell cycle arrest and apoptosis, and it could be considered as an effective agent for CRC therapy.
Cedrol alleviates the apoptosis and inflammatory response of IL-1β-treated chondrocytes by promoting miR-542-5p expression
In Vitro Cell Dev Biol Anim 2021 Dec;57(10):962-972.PMID:34893958DOI:10.1007/s11626-021-00620-3.
Cedrol has been shown to exert anti-tumor, anti-inflammatory, and anti-oxidative effects, but its role in osteoarthritis (OA) is unclear. This study aimed to explore the effect of Cedrol in OA. Chondrocytes were isolated from newborn rats and cultured in Dulbecco's modified Eagle's medium (DMEM). Then, Alcian blue staining was used to identify the chondrocytes. IL-1β and Cedrol were used to treat chondrocytes. Cell viability and apoptosis were measured by MTT and flow cytometry assays, respectively. The expressions of miR-542-5p, miR-26b-5p, miR-572, miR-138-5p, miR-328-3p, miR-1254, Bcl-2, Bax, iNOS, COX-2, and MMP-13 were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. NO and PGE2 levels were detected by ELISA. All the cells extracted from the newborn rats were dyed blue, indicating that the cells were chondrocytes. IL-1β could reduce the viability and promote apoptosis and inflammatory response of chondrocytes, while Cedrol could reverse the effect of IL-1β. In addition, Cedrol could significantly increase the expression of miR-542-5p in IL-1β-treated chondrocytes. Moreover, miR-542-5p inhibitor could partly reverse the effect of Cedrol in the apoptosis and inflammation response of chondrocytes. Cedrol alleviated IL-1β-induced apoptosis and inflammatory response of chondrocytes by promoting miR-542-5p expression.
Cedrol suppresses glioblastoma progression by triggering DNA damage and blocking nuclear translocation of the androgen receptor
Cancer Lett 2020 Dec 28;495:180-190.PMID:32987140DOI:10.1016/j.canlet.2020.09.007.
Glioblastoma (GBM) is the most common and aggressive primary brain tumor with great invasiveness and resistance to chemotherapy, which presents a treatment challenge. In this study, we investigated the antitumor effect of Cedrol, a sesquiterpene alcohol isolated from Cedrus atlantica, against GBM cells in vitro and in vivo. Cedrol was found to potently inhibit cell growth and induce intracellular ROS generation and DNA damage response. In addition, Cedrol induced significant G0/G1 cell cycle arrest and cell apoptosis via the extrinsic (Fas/FasL/Caspase-8) and intrinsic (Bax/Bcl-2/Caspase-9) pathways. In addition, Cedrol had a synergistic effect with temozolomide (TMZ) and reduced drug resistance by blockage of the AKT/mTOR pathway. Cedrol suppressed tumor growth in both orthotopic and xenograft GBM animal models with low or no short-term acute toxicity or long-term accumulative toxicity. In a molecular docking study, Cedrol targeted the androgen receptor (AR), and reduced DHT-mediated AR nuclear translocation, downstream gene KLK3/TMPRSS2 expression and cell proliferation. Our study demonstrates that Cedrol may be a potential candidate for drug development for single or combination treatment with TMZ in GBM therapy.
Fragrance material review on Cedrol
Food Chem Toxicol 2008 Nov;46 Suppl 11:S100-2.PMID:18640184DOI:10.1016/j.fct.2008.06.038.
A toxicologic and dermatologic review of Cedrol when used as a fragrance ingredient is presented.