Sesamin

CAS# 607-80-7

Sesamin

Catalog No. BCN4123----Order now to get a substantial discount!

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Quality Control of Sesamin

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Chemical structure

Sesamin

3D structure

Chemical Properties of Sesamin

Cas No. 607-80-7 SDF Download SDF
PubChem ID 72307 Appearance White powder
Formula C20H18O6 M.Wt 354.4
Type of Compound Lignans Storage Desiccate at -20°C
Synonyms Fagarol
Solubility Soluble to 70 mg/mL warmed (197.54 mM) in DMSO
Chemical Name 5-[(3S,3aR,6S,6aR)-3-(1,3-benzodioxol-5-yl)-1,3,3a,4,6,6a-hexahydrofuro[3,4-c]furan-6-yl]-1,3-benzodioxole
SMILES C1C2C(COC2C3=CC4=C(C=C3)OCO4)C(O1)C5=CC6=C(C=C5)OCO6
Standard InChIKey PEYUIKBAABKQKQ-AFHBHXEDSA-N
Standard InChI InChI=1S/C20H18O6/c1-3-15-17(25-9-23-15)5-11(1)19-13-7-22-20(14(13)8-21-19)12-2-4-16-18(6-12)26-10-24-16/h1-6,13-14,19-20H,7-10H2/t13-,14-,19+,20+/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Sesamin

1 Artemisia sp. 2 Commiphora sp. 3 Daphne sp. 4 Dendranthema sp. 5 Drimys sp. 6 Eleutherococcus sp. 7 Ginkgo sp. 8 Magnolia sp. 9 Piper sp. 10 Sassafras sp. 11 Sesamum sp. 12 Tanacetum sp. 13 Zanthoxylum sp.

Biological Activity of Sesamin

DescriptionSesamin 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.
TargetsROS | 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
In vitro

The effect of sesamin on airway fibrosis in vitro and in vivo.[Pubmed: 24978608]

Int Immunopharmacol. 2014 Sep;22(1):141-50.

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.
CONCLUSIONS:
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.

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 ]

Mol Nutr Food Res. 2010 Sep;54(9):1340-50.

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.
CONCLUSIONS:
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.

In vivo

Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic β-Cell Dysfunction and Apoptosis.[Pubmed: 26066015]

Nutrients. 2015 Jun 9;7(6):4689-704.

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.
CONCLUSIONS:
These results suggest that Sesamin protects β-cells from damage caused by AGEs through suppressing NADPH oxidase-mediated oxidative stress.

Sesamin enhances nitric oxide bioactivity in aortas of spontaneously hypertensive rats.[Pubmed: 26037786]

Ther Adv Cardiovasc Dis. 2015 Jun 2.

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.
CONCLUSIONS:
Chronic treatment with Sesamin could reduce hypertension and improve endothelial dysfunction through enhancement of NO bioactivity in SHR aortas.

Sesamin attenuates neurotoxicity in mouse model of ischemic brain stroke.[Pubmed: 25316624 ]

Neurotoxicology. 2014 Dec;45:100-10.

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.
CONCLUSIONS:
In conclusion, these results suggest that SES induces significant neuroprotection, by ameliorating many signaling pathways activated/deactivated following cerebral ischemia in adult mouse.

Protocol of Sesamin

Kinase Assay

Sesamin is a potent and specific inhibitor of delta 5 desaturase in polyunsaturated fatty acid biosynthesis.[Pubmed: 1943494]

Sesamin inhibits lipopolysaccharide-induced proliferation and invasion through the p38-MAPK and NF-κB signaling pathways in prostate cancer cells.[Pubmed: 25845399]

Oncol Rep. 2015 Jun;33(6):3117-23.

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.
CONCLUSIONS:
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.

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.
CONCLUSIONS:
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.

Animal Research

Effects of vitamin E and sesamin on hypertension and cerebral thrombogenesis in stroke-prone spontaneously hypertensive rats.[Pubmed: 11768736]

Cholesterol-lowering activity of sesamin is associated with down-regulation on genes of sterol transporters involved in cholesterol absorption.[Pubmed: 25745846]

J Agric Food Chem. 2015 Mar 25;63(11):2963-9.

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).
CONCLUSIONS:
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.

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).
CONCLUSIONS:
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.

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Preparing Stock Solutions of Sesamin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.8217 mL 14.1084 mL 28.2167 mL 56.4334 mL 70.5418 mL
5 mM 0.5643 mL 2.8217 mL 5.6433 mL 11.2867 mL 14.1084 mL
10 mM 0.2822 mL 1.4108 mL 2.8217 mL 5.6433 mL 7.0542 mL
50 mM 0.0564 mL 0.2822 mL 0.5643 mL 1.1287 mL 1.4108 mL
100 mM 0.0282 mL 0.1411 mL 0.2822 mL 0.5643 mL 0.7054 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Sesamin

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]

Mol Nutr Food Res. 2010 Sep;54(9):1340-50.

Sesame lignans have antioxidative and anti-inflammatory properties. 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.

Sesamin enhances nitric oxide bioactivity in aortas of spontaneously hypertensive rats.[Pubmed:26037786]

Ther Adv Cardiovasc Dis. 2015 Oct;9(5):314-24.

BACKGROUND: 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: 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. RESULTS: 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. CONCLUSION: Chronic treatment with Sesamin could reduce hypertension and improve endothelial dysfunction through enhancement of NO bioactivity in SHR aortas.

Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic beta-Cell Dysfunction and Apoptosis.[Pubmed:26066015]

Nutrients. 2015 Jun 9;7(6):4689-704.

Advanced glycation end products (AGEs), the direct modulators of beta-cells, have been shown to cause insulin-producing beta-cell dysfunction and apoptosis through increase of intracellular reactive oxygen species (ROS) production. Sesamin has been demonstrated to possess antioxidative activity. This study was designed to investigate whether Sesamin protects against AGEs-evoked beta-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 beta-cell apoptosis in pancreatic islets were also measured. In in vitro studies, MIN6 cells were pretreated with Sesamin (50 or 100 muM) and then exposed to AGEs (200 mg/L) for 24 h. Insulin secretion, beta-cell death, ROS production as well as expression and activity of NADPH oxidase were determined. Sesamin treatment obviously ameliorated AGE-induced beta-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 beta-cells from damage caused by AGEs through suppressing NADPH oxidase-mediated oxidative stress.

Sesamin attenuates neurotoxicity in mouse model of ischemic brain stroke.[Pubmed:25316624]

Neurotoxicology. 2014 Dec;45:100-10.

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. 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.

Effects of vitamin E and sesamin on hypertension and cerebral thrombogenesis in stroke-prone spontaneously hypertensive rats.[Pubmed:11768736]

Hypertens Res. 2001 Nov;24(6):735-42.

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). 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.

Cholesterol-lowering activity of sesamin is associated with down-regulation on genes of sterol transporters involved in cholesterol absorption.[Pubmed:25745846]

J Agric Food Chem. 2015 Mar 25;63(11):2963-9.

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. 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 mumol/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-7alpha-hydroxylase (CYP7A1), whereas it down-regulated hepatic 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase and liver X receptor alpha (LXRalpha). 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.

The effect of sesamin on airway fibrosis in vitro and in vivo.[Pubmed:24978608]

Int Immunopharmacol. 2014 Sep;22(1):141-50.

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-beta1) 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-beta1-induced fibroblast proliferation and activation, epithelial-mesenchymal transition (EMT), and ovalbumin (OVA)-induced airway fibrosis in vivo. We found that Sesamin attenuated TGF-beta1-induced proliferation of cultured lung fibroblasts. Sesamin inhibited TGF-beta1-stimulated expression of alpha smooth muscle actin (alpha-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-beta1-induced EMT in A549 cells. TGF-beta1-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 alpha-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.

Sesamin inhibits lipopolysaccharide-induced proliferation and invasion through the p38-MAPK and NF-kappaB signaling pathways in prostate cancer cells.[Pubmed:25845399]

Oncol Rep. 2015 Jun;33(6):3117-23.

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. 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-alpha 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)-kappaB 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-kappaB signaling pathways, which may be one of the mechanisms of the anticancer activity of this Sesamin agent in prostate cancer cells.

Sesamin is a potent and specific inhibitor of delta 5 desaturase in polyunsaturated fatty acid biosynthesis.[Pubmed:1943494]

Lipids. 1991 Jul;26(7):512-6.

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. 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.

Description

Sesamin, abundant lignan found in sesame oil, is a potent and selective delta 5 desaturase inhibitor in polyunsaturated fatty acid biosynthesis. Sesamin exerts effective neuroprotection against cerbral ischemia.

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