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Molecules.2015, 20(11):20014-30Arch Pharm Res.2015, 38(6):1080-9Oncol Rep.2016, 35(3):1356-64Free Radic Biol Med.2017, 112:191-199Nat Prod Commun.2017, 12(5):771-778Evid Based Complement Alternat Me...2018...Life Sci.2018, 209:498-506Pak J Pharm Sci.2018, 31:311-315
Phytomedicine.2018, 41:62-66Front Pharmacol.2018, 9:236BMC Complement Altern Med....2019...Molecules.2019, 24(2):329Molecules.2019, 24(23):E4303Nat Prod Sci.2019, 25(3):238Chemistry of Natural Compounds...2019...Phytomedicine.2019, 62:152962
Saudi Pharm J2020, 10.1016Pharmacological Reports2020, 1-9Front Pharmacol.2020, 11:683.JABS2020, 14:2(2020)Biomed Sci Letters.2020, 26:319-326J Food Biochem.2020, 44(6):e13198. Horticulturae2021, 7(1),5.
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Phytomedicine.2018, 40:37-47The Korea Society of Pha.2014, 300-314Asian J Beauty Cosmetol2016, 14(3):249-257J Food Biochem.2020, 44(6):e13198. Ind Crops Prod.2014, 62:173-178Antimicrob Agents Chemother.2020, AAC.01921-20.J Biomed Sci.2020, 27(1):60.Oncotarget.2016, 8(51):88386-88400J Nat Med.2018, 72(3):734-744Natural Product Communications2020, doi: 10.1177.
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||Sesamin has antifibrotic, cholesterol-lowering, anti-cancer, antioxidative, neuroprotective, anti-atherosclerosis, anti-inflammatory properties, it also might be beneficial in the prevention of hypertension and stroke. Sesamin attenuates intercellular cell adhesion molecule-1 expression in vitro in TNF-α-treated human aortic endothelial cells and in vivo in apolipoprotein-E-deficient mice.Sesamin also can protect β-cells from damage caused by AGEs through suppressing NADPH oxidase-mediated oxidative stress.
||ROS | NADPH-oxidase | NO | TNF-α | NOS | TGF-β/Smad | HMG-CoA Reductase | P450 (e.g. CYP17) | COX | Bcl-2/Bax | MMP(e.g.TIMP) | VEGFR | IL Receptor | p38MAPK | NF-kB | ERK | p65 | Caspase|
|Int Immunopharmacol. 2014 Sep;22(1):141-50. |
|The effect of sesamin on airway fibrosis in vitro and in vivo.[Pubmed: 24978608]|
|Airway fibrosis, which is a crucial pathological condition occurring in various types of pulmonary disorders, is characterized by accumulation and activation of fibroblast cells, deposition of extracellular matrix (ECM) proteins, and increase of airway basement membrane. Transforming growth factor beta 1 (TGF-β1) is the principal profibrogenic cytokine that is responsible for fibrotic responses. In the present study, we aimed to investigate the antifibrotic effects of the natural polyphenolic compound, Sesamin, on TGF-β1-induced fibroblast proliferation and activation, epithelial-mesenchymal transition (EMT), and ovalbumin (OVA)-induced airway fibrosis in vivo. |
METHODS AND RESULTS:
We found that Sesamin attenuated TGF-β1-induced proliferation of cultured lung fibroblasts. Sesamin inhibited TGF-β1-stimulated expression of alpha smooth muscle actin (α-SMA), suggesting that Sesamin plays an inhibitory role in fibroblast activation. Sesamin blocked upregulation of the mesenchymal markers (fibronectin and vimentin) and downregulation of the epithelial marker (E-cadherin), indicating an inhibitory effect on TGF-β1-induced EMT in A549 cells. TGF-β1-induced Smad3 phosphorylation was also significantly reduced by Sesamin in both cultured fibroblast and A549 cells. In the airway fibrosis induced by OVA in mice, Sesamin inhibited the accumulation of α-SMA-positive cells and expression of collagen I in the airway.
Histological studies revealed that Sesamin protected against subepithelial fibrosis by reducing myofibroblast activation and collagen accumulation in the ECM. OVA-induced thickening of basement membrane was significantly alleviated in animals receiving Sesamin treatments. These results suggest a therapeutic potential of Sesamin as an antifibrotic agent.
|Mol Nutr Food Res. 2010 Sep;54(9):1340-50. |
|Sesamin attenuates intercellular cell adhesion molecule-1 expression in vitro in TNF-alpha-treated human aortic endothelial cells and in vivo in apolipoprotein-E-deficient mice.[Pubmed: 20306475 ]|
|Sesame lignans have antioxidative and anti-inflammatory properties. |
METHODS AND RESULTS:
We focused on the effects of the lignans Sesamin and sesamol on the expression of endothelial-leukocyte adhesion molecules in tumor necrosis factor-alpha (TNF-alpha)-treated human aortic endothelial cells (HAECs). When HAECs were pretreated with Sesamin (10 or 100 microM), the TNF-alpha-induced expression of intercellular cell adhesion molecule-1 (ICAM-1) was significantly reduced (35 or 70% decrease, respectively) by Western blotting. Sesamol was less effective at inhibiting ICAM-1 expression (30% decrease at 100 microM). Sesamin and sesamol reduced the marked TNF-alpha-induced increase in human antigen R (HuR) translocation and the interaction between HuR and the 3'UTR of ICAM-1 mRNA. Both significantly reduced the binding of monocytes to TNF-alpha-stimulated HAECs. Sesamin significantly attenuated TNF-alpha-induced ICAM-1 expression and cell adhesion by downregulation of extracellular signal-regulated kinase 1/2 and p38. Furthermore, in vivo, Sesamin attenuated intimal thickening and ICAM-1 expression seen in aortas of apolipoprotein-E-deficient mice.
Taken together, these data suggest that Sesamin inhibits TNF-alpha-induced extracellular signal-regulated kinase/p38 phosphorylation, nuclear translocation of NF-kappaB p65, cytoplasmic translocalization of HuR and thereby suppresses ICAM-1 expression, resulting in reduced adhesion of leukocytes. These results also suggest that Sesamin may prevent the development of atherosclerosis and inflammatory responses.
|Nutrients. 2015 Jun 9;7(6):4689-704. |
|Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic β-Cell Dysfunction and Apoptosis.[Pubmed: 26066015]|
|Advanced glycation end products (AGEs), the direct modulators of β-cells, have been shown to cause insulin-producing β-cell dysfunction and apoptosis through increase of intracellular reactive oxygen species (ROS) production. Sesamin has been demonstrated to possess antioxidative activity.|
METHODS AND RESULTS:
This study was designed to investigate whether Sesamin protects against AGEs-evoked β-cell damage via its antioxidant property. The effects of Sesamin were examined in C57BL/6J mice and MIN6 cell line. In in vivo studies, mice were intraperitoneally injected with AGEs (120 mg/kg) and orally treated with Sesamin (160 mg/kg) for four weeks. Intraperitoneal glucose tolerance and insulin releasing tests were performed. Insulin content, ROS generation and β-cell apoptosis in pancreatic islets were also measured. In in vitro studies, MIN6 cells were pretreated with Sesamin (50 or 100 μM) and then exposed to AGEs (200 mg/L) for 24 h. Insulin secretion, β-cell death, ROS production as well as expression and activity of NADPH oxidase were determined. Sesamin treatment obviously ameliorated AGE-induced β-cell dysfunction and apoptosis both in vivo and in vitro. These effects were associated with decreased ROS production, down-regulated expression of p67(phox) and p22(phox), and reduced NADPH oxidase activity.
These results suggest that Sesamin protects β-cells from damage caused by AGEs through suppressing NADPH oxidase-mediated oxidative stress.
|Ther Adv Cardiovasc Dis. 2015 Jun 2. |
|Sesamin enhances nitric oxide bioactivity in aortas of spontaneously hypertensive rats.[Pubmed: 26037786]|
|The blood pressure lowering effect of Sesamin has been demonstrated to be associated with the increase in vascular nitric oxide (NO) biological activity by our previous studies and others. The present study was designed to explore the underlying mechanisms involved in the effect of Sesamin on aortic NO bioactivity in spontaneously hypertensive rats (SHRs).
METHODS AND RESULTS:
Sesamin was orally administered for 8 consecutive weeks in SHRs. Systolic blood pressure (SBP) was measured using the tail-cuff method. The aortas were isolated and in vitro vascular reactivity studies were performed. Superoxide anion production in carotid arteries was assessed by dihydroethidium fluorescence staining. The protein expression of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (P-eNOS), dihydrofolate reductase (DHFR), nicotinamide adenine dinucleotide phosphate oxidase subunit p47phox, and copper, zinc superoxide dismutase (Cu/Zn-SOD) in aortas was detected by Western blotting. The dimeric form of eNOS in aortas was determined by low-temperature sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Aortic level of nitrotyrosine and activities of antioxidant enzymes, namely, total SOD (T-SOD), glutathione peroxidase (GPx) and catalase were also detected.
In SHRs, Sesamin treatment reduced SBP, improved vascular relaxation induced by acetylcholine and enhanced aortic NO bioactivity. Sesamin treatment enhanced NO biosynthesis in SHR aortas was due to upregulated P-eNOS and suppressed eNOS uncoupling, and the latter effect might be attributed to decreased nitrotyrosine and upregulated DHFR. Sesamin also reduced the NO oxidative inactivation and decreased the superoxide anion production through downregulation of p47(phox) and amelioration of eNOS uncoupling. In addition, Sesamin treatment did not alter the levels of GPx and catalase activity but obviously reduced the compensatory elevated T-SOD activity and Cu/Zn-SOD protein expression.
Chronic treatment with Sesamin could reduce hypertension and improve endothelial dysfunction through enhancement of NO bioactivity in SHR aortas.
|Neurotoxicology. 2014 Dec;45:100-10. |
|Sesamin attenuates neurotoxicity in mouse model of ischemic brain stroke.[Pubmed: 25316624 ]|
|Stroke is a severe neurological disorder characterized by the abrupt loss of blood circulation into the brain resulting into wide ranging brain and behavior abnormalities. |
METHODS AND RESULTS:
The present study was designed to evaluate molecular mechanism by which Sesamin (SES) induces neuroprotection in mouse model of ischemic stroke. The results of this study demonstrate that SES treatment (30 mg/kg bwt) significantly reduced infarction volume, lipid per-oxidation, cleaved-caspase-3 activation, and increased GSH activity following MCAO in adult male mouse. SES treatment also diminished iNOS and COX-2 protein expression, and significantly restored SOD activity and protein expression level in the ischemic cortex of the MCAO animals. Furthermore, SES treatment also significantly reduced inflammatory and oxidative stress markers including Iba1, Nox-2, Cox-2, peroxynitrite compared to placebo MCAO animals. Superoxide radical production, as studied by DHE staining method, was also significantly reduced in the ischemic cortex of SES treated compared to placebo MCAO animals. Likewise, downstream effects of superoxide free radicals i.e. MAPK/ERK and P38 activation was also significantly attenuated in SES treated compared to placebo MCAO animals.
In conclusion, these results suggest that SES induces significant neuroprotection, by ameliorating many signaling pathways activated/deactivated following cerebral ischemia in adult mouse.
||The seeds of Sesamum indicum.
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||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
ChemFaces New Products and Compounds
Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)PMID: 29328914
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)PMID: 32004475
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)PMID: 29149595
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)PMID: 29553709
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)PMID: 28005066
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)PMID: 30417089
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|Oncol Rep. 2015 Jun;33(6):3117-23. |
|Sesamin inhibits lipopolysaccharide-induced proliferation and invasion through the p38-MAPK and NF-κB signaling pathways in prostate cancer cells.[Pubmed: 25845399]|
|Sesamin, a lipid-soluble lignan, is one of the major constituents of sesame. Previous studies have reported that Sesamin induces growth inhibition in human cancer cells, particularly prostate cancer cells. |
METHODS AND RESULTS:
In the present study, we mainly explored the mechanism underlying the protective effect of Sesamin on prostate cancer cell proliferation and invasion induced by lipopolysaccharide (LPS). We found that the proliferation of PC3 cells, as determined using the MTT assay, and the expression of cyclin D1, COX-2, Bcl-2 and survivin proteins elevated by LPS were distinctly inhibited by Sesamin in a dose-dependent manner. Meanwhile, the ability of PC3 cell invasion, as determined using the Transwell assay and the expression of matrix metalloproteinase 9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1) and vascular endothelial growth factor (VEGF) proteins increased by LPS were obviously reduced by Sesamin in a dose-dependent manner. In addition, the accumulation of TGF-α and interleukin-6 (IL-6) production induced by LPS in the culture supernatant was found to be decreased dose-dependently with Sesamin pretreatment in PC3 cells using the enzyme-linked immunosorbent assay (ELISA) kit. Furthermore, phosphorylation of the p38 protein and nuclear factor (NF)-κB activity in the PC3 cells were enhanced by LPS and further inhibited with Sesamin, SB203580 pretreatment or p38-siRNA transfection, respectively. Sesamin or SB203580 pretreatment obviously inhibited PC3 cells-derived tumor growth induced by LPS in vivo.
Taken together, these results suggest that the potential ability of Sesamin to downregulate the secretion of cytokines and the expression of cell proliferative- and invasive-related gene products induced by LPS was shown to be via the p38 mitogen-activated protein kinase (p38-MAPK) and NF-κB signaling pathways, which may be one of the mechanisms of the anticancer activity of this Sesamin agent in prostate cancer cells.
|Lipids. 1991 Jul;26(7):512-6. |
|Sesamin is a potent and specific inhibitor of delta 5 desaturase in polyunsaturated fatty acid biosynthesis.[Pubmed: 1943494]|
|Incubation with sesame oil increases the mycelial dihomo-gamma-linolenic acid content of an arachidonic acid-producing fungus, Mortierella alpina, but decreases its arachidonic acid content [Shimizu, S., K. Akimoto, H. Kawashima, Y. Shinmen and H. Yamada (1989) J. Am. Oil Chem. Soc. 66, 237-241]. The factor causing these effects was isolated and identified to be (+)-Sesamin. |
METHODS AND RESULTS:
The results obtained in experiments with both a cell-free extract of the fungus and with rat liver microsomes demonstrated that (+)-Sesamin specifically inhibits delta 5 desaturase at low concentrations, but does not inhibit delta 6, delta 9 and delta 12 desaturases. Kinetic analysis showed that (+)-Sesamin is a noncompetitive inhibitor (Ki for rat liver delta 5 desaturase, 155 microM). (+)-Sesamolin, (+)-Sesaminol and (+)-epiSesamin also inhibited only delta 5 desaturases of the fungus and liver.
These results demonstrate that (+)-Sesamin and related lignan compounds present in sesame seeds or its oil are specific inhibitors of delta 5 desaturase in polyunsaturated fatty acid biosynthesis in both microorganisms and animals.
|J Agric Food Chem. 2015 Mar 25;63(11):2963-9. |
|Cholesterol-lowering activity of sesamin is associated with down-regulation on genes of sterol transporters involved in cholesterol absorption.[Pubmed: 25745846]|
|Sesame seed is rich in Sesamin. The present study was to (i) investigate the plasma cholesterol-lowering activity of dietary Sesamin and (ii) examine the interaction of dietary Sesamin with the gene expression of sterol transporters, enzymes, receptors, and proteins involved in cholesterol metabolism. |
METHODS AND RESULTS:
Thirty hamsters were divided into three groups fed the control diet (CON) or one of two experimental diets containing 0.2% (SL) and 0.5% (SH) Sesamin, respectively, for 6 weeks. Plasma total cholesterol (TC) levels in hamsters given the CON, SL, and SH diets were 6.62 ± 0.40, 5.32 ± 0.40, and 5.00 ± 0.44 mmol/L, respectively, indicating dietary Sesamin could reduce plasma TC in a dose-dependent manner. Similarly, the excretion of total fecal neutral sterols was dose-dependently increased with the amounts of Sesamin in diets (CON, 2.65 ± 0.57; SL, 4.30 ± 0.65; and SH, 5.84 ± 1.27 μmol/day). Addition of Sesamin into diets was associated with down-regulation of mRNA of intestinal Niemann-Pick C1 like 1 protein (NPC1L1), acyl-CoA:cholesterol acyltransferase 2 (ACAT2), microsomal triacylglycerol transport protein (MTP), and ATP-binding cassette transporters subfamily G members 5 and 8 (ABCG5 and ABCG8). Results also showed that dietary Sesamin could up-regulate hepatic cholesterol-7α-hydroxylase (CYP7A1), whereas it down-regulated hepatic 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase and liver X receptor alpha (LXRα).
It was concluded that the cholesterol-lowering activity of Sesamin was mediated by promoting the fecal excretion of sterols and modulating the genes involved in cholesterol absorption and metabolism.
|Hypertens Res. 2001 Nov;24(6):735-42. |
|Effects of vitamin E and sesamin on hypertension and cerebral thrombogenesis in stroke-prone spontaneously hypertensive rats.[Pubmed: 11768736]|
|The preventive effects of Sesamin, a lignan from sesame oil, and vitamin E on hypertension and thrombosis were examined using stroke-prone spontaneously hypertensive rats (SHRSP). |
METHODS AND RESULTS:
At 5 weeks of age the animals were separated into four groups: (i) a control group; (ii) a vitamin E group, which was given a 1,000 mg alpha-tocopherol/kg diet; (iii) a Sesamin group, given a 1,000 mg Sesamin/kg diet; and (iv) a vitamin E plus Sesamin group, given a 1,000 mg alpha-tocopherol plus 1,000 mg Sesamin/kg diet for 5 weeks from 5 to 10 weeks of age. Resting blood pressure was measured by the tail-cuff method once weekly. A closed cranial window was created and platelet-rich thrombi were induced in vivo using a helium-neon laser technique. The number of laser pulses required for formation of an occlusive thrombus was used as an index of thrombotic tendency. In control rats, systolic blood pressure and the amount of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) became significantly elevated with age. However, the elevation in blood pressure and 8-OHdG were significantly suppressed in rats administrated vitamin E, Sesamin, or vitamin E plus Sesamin. At 10 weeks, the number of laser pulses required to induce an occlusive thrombus in arterioles of the control group was significantly lower than in the other groups (p<0.05).
These results indicate that chronic ingestion of vitamin E and Sesamin attenuated each of elevation in blood pressure, oxidative stress and thrombotic tendency, suggesting that these treatments might be beneficial in the prevention of hypertension and stroke.