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Cycloartenyl ferulate Sale

(Synonyms: 环木菠萝烯醇阿魏酸酯; Cycloartenol ferulate; Cycloartenol ferulic acid ester) 目录号 : GC64799

Cycloartenyl ferulate (Cycloartenol ferulate) 是一种典型的三萜醇,具有抗氧化活性、抗过敏活性、抗炎活性和抗癌活性等多种生物活性。

Cycloartenyl ferulate Chemical Structure

Cas No.:21238-33-5

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产品描述

Cycloartenyl ferulate (Cycloartenol ferulate) is one of the typical triterpene alcohols and possesses several biological activities including anti-oxidative activity, antiallergic activity, anti-inflammatory and anticancer activities[1].

[1]. Guang-Liang Hong, et al. The reversal of paraquat-induced mitochondria-mediated apoptosis by cycloartenyl ferulate, the important role of Nrf2 pathway. Exp Cell Res. 2013 Nov 1;319(18):2845-55.
[2]. T Oka, et al. Cycloartenyl ferulate, a component of rice bran oil-derived gamma-oryzanol, attenuates mast cell degranulation.Phytomedicine. 2010 Feb;17(2):152-6.

Chemical Properties

Cas No. 21238-33-5 SDF Download SDF
别名 环木菠萝烯醇阿魏酸酯; Cycloartenol ferulate; Cycloartenol ferulic acid ester
分子式 C40H58O4 分子量 602.89
溶解度 储存条件 4°C, protect from light
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1 mM 1.6587 mL 8.2934 mL 16.5868 mL
5 mM 0.3317 mL 1.6587 mL 3.3174 mL
10 mM 0.1659 mL 0.8293 mL 1.6587 mL
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Research Update

Cycloartenyl ferulate and β-Sitosteryl Ferulate - Steryl Ferulates of γ-Oryzanol - Suppress Intracellular Reactive Oxygen Species in Cell-based System

J Oleo Sci 2019 Aug 1;68(8):765-768.PMID:31292340DOI:10.5650/jos.ess19054.

γ-Oryzanol is a naturally occurring component of rice bran and consists of various steryl ferulates. The antioxidant activities of γ-oryzanol have mostly been demonstrated in cell-free systems. Therefore, we determined whether steryl ferulate of γ-oryzanol suppress spontaneous intracellular reactive oxygen species (ROS) in cell-based systems. We found that Cycloartenyl ferulate and β-sitosteryl ferulate suppressed spontaneous intracellular ROS in a similar way to N-acetylcysteine and α-tocopherol.

Cycloartenyl ferulate Inhibits Paraquat-Induced Apoptosis in HK-2 Cells With the Involvement of ABCC1

J Cell Biochem 2016 Apr;117(4):872-80.PMID:26358524DOI:10.1002/jcb.25370.

Nephrotoxicity induced by chemicals such as paraquat (PQ) is a common clinical phenomenon; therefore, searching for drugs with renal protective effect is of a great practical significance. Our previous investigation found that Cycloartenyl ferulate (CF) can antagonize the cytotoxic effect of PQ, and recent studies also revealed a variety of bioactivities of CF. However, specific molecular mechanisms underlying the protective effect of CF have not been explored yet. HPLC detection of PQ content indicated that CF reduced PQ accumulation in HK-2 cells and thereby improved cell survival. Western blot results showed that both PQ and CF did not affect the expression of ABCB1; however, while PQ suppressed the expression of ABCC1, CF upregulated ABCC1 expression and thereby reversed the inhibitory effect of PQ on ABCC1 expression. Meanwhile, HK-2 cells did not express ABCG2. When the expression of ABCC1 was knocked down with siRNA, the inhibitory effect of CF on intracellular PQ accumulation was blocked. Further flow cytometric analysis showed that while PQ significantly induced the appearance of sub-G1 apoptotic peak in cells, CF evidently inhibited apoptosis. TUNEL-DAPI double-staining also detected that PQ significantly induced the occurrence of DNA fragmentation in cells, whereas CF effectively inhibited the effect of PQ. Further results showed that ABCC1 siRNA effectively abolished the protective effect of CF on PQ-induced apoptosis. Taken together, these data demonstrated that in HK-2 cells, CF could antagonize PQ-induced toxicity with the involvement of regulatiion of ABCC1 protein expression, which provides a new strategy for treatments of nephrotoxicity.

Cycloartenyl ferulate Is the Predominant Compound in Brown Rice Conferring Cytoprotective Potential against Oxidative Stress-Induced Cytotoxicity

Int J Mol Sci 2023 Jan 3;24(1):822.PMID:36614263DOI:10.3390/ijms24010822.

Since brown rice extract is a rich source of biologically active compounds, the present study is aimed to quantify the major compounds in brown rice and to compare their cytoprotective potential against oxidative stress. The content of the main hydrophobic compounds in brown rice followed the order of Cycloartenyl ferulate (CAF) (89.00 ± 8.07 nmol/g) >> α-tocopherol (αT) (19.73 ± 2.28 nmol/g) > γ-tocotrienol (γT3) (18.24 ± 1.41 nmol/g) > α-tocotrienol (αT3) (16.02 ± 1.29 nmol/g) > γ-tocopherol (γT) (3.81 ± 0.40 nmol/g). However, the percent contribution of CAF to the radical scavenging activity of one gram of whole brown rice was similar to those of αT, αT3, and γT3 because of its weaker antioxidant activity. The CAF pretreatment displayed a significant cytoprotective effect on the hydrogen peroxide-induced cytotoxicity from 10 µM, which is lower than the minimal concentrations of αT and γT required for a significant protection. CAF also enhanced the nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation coincided with the enhancement of the heme oxygenase-1 (HO-1) mRNA level. An HO-1 inhibitor, tin protoporphyrin IX (SnPP), significantly impaired the cytoprotection of CAF. The cytoprotective potential of CAF is attributable to its cycloartenyl moiety besides the ferulyl moiety. These results suggested that CAF is the predominant cytoprotector in brown rice against hydrogen peroxide-induced cytotoxicity.

Cycloartenyl ferulate, a component of rice bran oil-derived gamma-oryzanol, attenuates mast cell degranulation

Phytomedicine 2010 Feb;17(2):152-6.PMID:19577449DOI:10.1016/j.phymed.2009.05.013.

IgE-targeting therapy could provide significant progress in the treatment of allergic inflammation. In this study, we examined the effect of Cycloartenyl ferulate (cycloartenol ferulic acid ester; CAF), a natural product from rice bran oil-derived gamma-oryzanol, on allergic reaction. When CAF and gamma-oryzanol were injected intradermally with anti-DNP IgE into the dorsal skin of rats, the passive cutaneous anaphylaxis reaction induced by DNP-HSA was attenuated. CAF and gamma-oryzanol also inhibited the degranulation of DNP-IgE sensitized RBL-2H3 mast cells stimulated with anti-DNP-HSA. IgE conjugated with CAF could not be detected by anti-IgE antibody in the ELISA analysis. Although incubation of IgE with CAF did not decrease the amount of IgE, it was possible to precipitate IgE by centrifugation. These results demonstrate that CAF captures IgE, prevents it from binding to FcepsilonRI, and attenuates mast cell degranulation.

The reversal of paraquat-induced mitochondria-mediated apoptosis by Cycloartenyl ferulate, the important role of Nrf2 pathway

Exp Cell Res 2013 Nov 1;319(18):2845-55.PMID:23954820DOI:10.1016/j.yexcr.2013.08.005.

In this study, we demonstrate the protective effects of Cycloartenyl ferulate (CF) against Paraquat (PQ)-induced cytotoxicity and elucidate the underlying molecular mechanisms. The results show that, CF could reverse the PQ-induced growth inhibition and release of lactate dehydrogenase in HK-2 human proximal tubular cells. Treatment with PQ induced apoptosis in HK-2 cells, as evidenced by accumulation of sub-G1 cell population, chromatin condensation, DNA fragmentation, and translocation of phosphatidylserine, which were significantly attenuated by co-incubation with CF. Mitochondria-mediated apoptosis pathway contributed importantly to PQ-induced apoptosis, as revealed by the activation of caspase-3/-9, cleavage of PARP, depletion of mitochondrial membrane potential regulated by Bcl-2 family members, and overproduction of reactive oxygen species, which were also effectively blocked by CF. Moreover, treatments of PQ strongly inhibited the expression of Nrf2 and the downstream effectors, HO1 and NQO1. However, co-treatment with CF effectively reversed this action of PQ. Furthermore, silencing of Nrf2 by the siRNA technique significantly blocked the cytoprotective effects of CF against PQ-induced apoptosis, which suggest the important role of Nrf2 signaling pathway an cell apoptosis induced by PQ. Taken together, this study provides a novel strategy for molecular intervention against PQ-induced nephrotoxicity by using phytochemicals.