Malabaricone C
(Synonyms: 马拉巴酮C) 目录号 : GC46028
A diarylnonanoid with diverse biological activities
Cas No.:63335-25-1
Sample solution is provided at 25 µL, 10mM.
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Malabaricone C is a diarylnonanoid that has been found in Myristica and has diverse biological activities.1,2,3,4 It scavenges 59.9% of 2,2-diphenyl-1-picrylhydrazyl radicals when used at a concentration of 7 μg/ml.1 Malabaricone C is active against S. aureus, B. subtilis, and C. albicans in vitro (MICs = 2-32 μg/ml).2 It is cytotoxic to A549, HL-60, and MCF-7 cells (IC50s = 12.3, 46.1, and 10.8 μM, respectively).3 Malabaricone C inhibits sphingomyelin synthase 1 (SMS1) and SMS2 activity in cell lysates (IC50s = 3 and 1.5 μM, respectively).4 It decreases body weight gain, hepatic steatosis, and hepatic and plasma triglyceride levels in a mouse model of high-fat diet-induced obesity when administered at a dose of 0.1% in the diet.
|1. Patro, B.S., Bauri, A.K., Mishra, S., et al. Antioxidant activity of Myristica malabarica extracts and their constituents. J. Agric. Food Chem. 53(17), 6912-6918 (2005).|2. Orabi, K.Y., Mossa, J.S., and El-Feraly, F.S. Isolation and characterization of two antimicrobial agents from mace (Myristica fragrans). J. Nat. Prod. 54(3), 856-859 (1991).|3. Cuong, T.D., Lim, C.J., Trang, T.T.T., et al. Compounds from the seeds of Myristica fragrans and their cytotoxic activity. Nat. Prod. Sci. 18(2), 97-101 (2012).|4. Othman, M.A., Yuyama, K., Murai, Y., et al. Malabaricone C as natural sphingomyelin synthase inhibitor against diet-induced obesity and its lipid metabolism in mice. Med. Chem. Lett. 10(8), 1154-1158 (2019).
Cas No. | 63335-25-1 | SDF | |
别名 | 马拉巴酮C | ||
Canonical SMILES | OC1=C(C(CCCCCCCCC2=CC=C(O)C(O)=C2)=O)C(O)=CC=C1 | ||
分子式 | C21H26O5 | 分子量 | 358.4 |
溶解度 | DMF: 25 mg/ml,DMSO: 20 mg/ml,Ethanol: 10 mg/ml | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg |
1 mM | 2.7902 mL | 13.9509 mL | 27.9018 mL |
5 mM | 0.558 mL | 2.7902 mL | 5.5804 mL |
10 mM | 0.279 mL | 1.3951 mL | 2.7902 mL |
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Malabaricone C derived from nutmeg inhibits arachidonate 5-lipoxygenase activity and ameliorates psoriasis-like skin inflammation in mice
Free Radic Biol Med 2022 Nov 20;193(Pt 1):1-8.PMID:36183930DOI:10.1016/j.freeradbiomed.2022.09.028.
As pro-inflammatory lipid mediators, leukotrienes have pathophysiological activities in several inflammatory diseases, including psoriasis. In the biosynthesis of leukotrienes from arachidonic acid, 5-lipoxygenase catalyzes the first two steps. In the present study, we showed that nutmeg (Myristica fragrans) strongly inhibited the catalytic activity of 5-lipoxygenase. To characterize the bioactive component(s) of nutmeg, we performed 5-lipoxygenase inhibitory activity-guided fractionation of aqueous ethanol extract of nutmeg, resulting in the isolation of Malabaricone C having antioxidant activity. Malabaricone C exhibited potent competitive inhibition of 5-lipoxygenase with an IC50 value of 0.2 μM. In mice with imiquimod-induced psoriasis-like skin lesions, topical application of 2 mM Malabaricone C significantly ameliorated hyperplasia and inflammatory cell infiltration, and suppressed the expression of the psoriasis-associated genes S100a9, Krt1, Il17a, and Il22. Lipid metabolome analysis of these psoriasis-like skin lesions showed that Malabaricone C markedly decreased the level of leukotriene B4 but did not significantly increase the other pro-inflammatory lipid mediators. These findings suggest that Malabaricone C decreases LTB4 by the 5-lipoxygenase inhibition and ameliorates the symptoms of psoriasis-like skin inflammation.
Giganteone A and Malabaricone C as potential pharmacotherapy for diabetes mellitus
Nat Prod Res 2022 Mar;36(6):1581-1586.PMID:33593208DOI:10.1080/14786419.2021.1885405.
The use of antidiabetic agents which control glycemic levels in the blood and simultaneously inhibit oxidative stress is an important strategy in the prevention of Diabetes Mellitus and its complications. In our previous study, Malabaricone C (3) and its dimer, giganteone A (5) exhibited significant DPPH free radical scavenging activities which were lower than the activity of the positive control, ascorbic acid. These compounds were evaluated for their α-glucosidase inhibitory activities at different concentrations (0.02-2.5 mM) in the present study. Compounds 3 (IC50 59.61 µM) and 5 (IC50 39.52 µM) were identified as active alpha-glucosidase inhibitors, each respectively being 24 and 37 folds more potent than the standard inhibitor, acarbose. Based on the molecular docking studies, compounds 3 and 5 docked into the active site of the α-glucosidase enzyme, forming mainly hydrogen bonds in the active site.
Malabaricone C, a constituent of spice Myristica malabarica, exhibits anti-inflammatory effects via modulation of cellular redox
J Biosci 2023;48(2):9.PMID:36971326DOI:10.1007/s12038-023-00329-3.
The present study primarily focuses on the efficacy of Malabaricone C (Mal C) as an anti-inflammatory agent. Mal C inhibited mitogen-induced T-cell proliferation and cytokine secretion. Mal C significantly reduced cellular thiols in lymphocytes. N-acetyl cysteine (NAC) restored cellular thiol levels and abrogated Mal C-mediated inhibition of T-cell proliferation and cytokine secretion. Physical interaction between Mal C and NAC was evinced from HPLC and spectral analysis. Mal C treatment significantly inhibited concanavalin A-induced phosphorylation of ERK/JNK and DNA binding of NF-κB. Administration of Mal C to mice suppressed T-cell proliferation and effector functions ex vivo. Mal C treatment did not alter the homeostatic proliferation of T-cells in vivo but completely abrogated acute graft-versus-host disease (GvHD)-associated morbidity and mortality. Our studies indicate probable use of Mal C for prophylaxis and treatment of immunological disorders caused due to hyper-activation of T-cells.
Malabaricone C Attenuates Nonsteroidal Anti-Inflammatory Drug-Induced Gastric Ulceration by Decreasing Oxidative/Nitrative Stress and Inflammation and Promoting Angiogenic Autohealing
Antioxid Redox Signal 2020 Apr 10;32(11):766-784.PMID:31830804DOI:10.1089/ars.2019.7781.
Aims: Nonsteroidal anti-inflammatory drugs (NSAIDs), among the most commonly used drugs worldwide, are associated with gastrointestinal (GI) complications that severely limit the clinical utility of this essential class of pain medications. Here, we mechanistically dissect the protective impact of a natural product, Malabaricone C (Mal C), on NSAID-induced gastropathy. Results: Mal C dose dependently diminished erosion of the stomach lining and inflammation in mice treated with NSAIDs with the protective impact translating to improvement in survival. By decreasing oxidative and nitrative stress, Mal C treatment prevented NSAID-induced mitochondrial dysfunction and cell death; nuclear factor κ-light-chain enhancer of activated B cell induction, release of proinflammatory cytokines and neutrophil infiltration; and disruptions in the vascular endothelial growth factor/endostatin balance that contributes to mucosal autohealing. Importantly, Mal C failed to impact the therapeutic anti-inflammatory properties of multiple NSAIDs in a model of acute inflammation. In all assays tested, Mal C proved as or more efficacious than the current first-line therapy for NSAID-dependent GI complications, the proton pump inhibitor omeprazole. Innovation: Given that omeprazole-mediated prophylaxis is, itself, associated with a shift in NSAID-driven GI complications from the upper GI to the lower GI system, there is a clear and present need for novel therapeutics aimed at ameliorating NSAID-induced gastropathy. Mal C provided significant protection against NSAID-induced gastric ulcerations impacting multiple critical signaling cascades contributing to inflammation, cell loss, extracellular matrix degradation, and angiogenic autohealing. Conclusion: Thus, Mal C represents a viable lead compound for the development of novel gastroprotective agents.
Malabaricone C inhibits PDGF-induced proliferation and migration of aortic smooth muscle cells through induction of heme oxygenase-1
J Cell Biochem 2012 Sep;113(9):2866-76.PMID:22511233DOI:10.1002/jcb.24161.
Malabaricone C (Mal-C), isolated from nutmeg, is known to exert a variety of pharmacological activities. However, the effect of Mal-C on vascular smooth muscle cells (VSMCs) is unknown. This study examined the effect of Mal-C on proliferation and migration of primary rat aortic smooth muscle cells (RASMCs) as well as its underlying mechanisms. Treatment of RASMCs with Mal-C induced both protein and mRNA expression of heme oxygenase-1 (HO-1) in a dose- and time-dependent manner. Mal-C-mediated HO-1 induction was inhibited by treatment with actinomycin D or by cycloheximide. SB203580 (a p38 inhibitor), SP600125 (a JNK inhibitor), U0126 (a MEK inhibitor), and N-acetylcysteine (NAC, an antioxidant) did not suppress Mal-C-induced HO-1 expression. In contrast, LY294002 (a PI3K inhibitor) blocked Mal-C-induced HO-1 expression. Moreover, RASMCs treated with Mal-C exhibited activation of AKT in a dose- and time-dependent manner. Treatment of RASMCs with Mal-C increased nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2), which is a key regulator of HO-1 expression, and this translocation was also inhibited by LY294002. Consistent with the notion that HO-1 has protective effects against VSMCs, Mal-C remarkably inhibited platelet-derived growth factor (PDGF)-induced proliferation and migration of RASMCs. However, inhibition of HO-1 significantly attenuated the inhibitory effects of Mal-C on PDGF-induced proliferation and migration of RASMCs. Taken together, these findings suggest that Mal-C could suppress PDGF-induced proliferation and migration of RASMCs through Nrf2 activation and subsequent HO-1 induction via the PI3K/AKT pathway, and may be a potential HO-1 inducer for preventing or treating vascular diseases.