Inhibition of two stages of melanin synthesis by sesamol,sesamin and sesamolin

Objective: To investigate the antimelanogenesis properties of three sesame compoundssesamol, sesamin and sesamolin via two stages of melanin synthesis vis-à-vis sunscreen function and enzyme inhibition in melanoma cell line in order to search for alternative depigmenting agents.Methods: Antimelanogenic effects of sesame lignans were assessed in SK-MEL2 compared with the reference depigmenting agents, kojic acid and b-arbutin, in order to evaluate:(a) the sunscreen function of sesamol, sesamin and sesamolin by measurement of UV absorbtion property;(b) the inhibition of tyrosinase activity through mushroom and cellular tyrosinase; and(c) the effect on melanin content and melanogenic protein expression(tyrosinase, TRP-1 and TRP-2) by Western blot analysis; and(d) the toxicity of sesamol, sesamin and sesamolin to cells using cell cytotoxicity assay.Results: The results showed that sesamin, sesamolin and sesamol exerted satisfiable sunscreen function by absorbed UVB at 290 nm. Sesamol exhibited the highest inhibition of mushroom tyrosinase activity, but lipophilic sesamolin exhibited the highest cellular tyrosinase inhibition(IC_(50) of 1.6 μM) followed by sesamin, sesamol, and kojic acid,respectively. The order from high to low inhibition of melanin pigment was detected in the SK-MEL2 treated with sesamolin, sesamin, sesamol, kojic acid, and b-arbutin,respectively. Sesamolin and sesamin successfully inhibited cellular tyrosinase activity and respectively decreased TRP-1/TRP-2(36%/15%) and TRP-1 levels(16%), thereby inhibiting melanogenesis via antityrosinase activity. No cytotoxicity to SK-MEL2 or Vero(normal) cell lines was observed at the lignan concentrations that exerted an antimelanogenic effect.Conclusions: Three sesame lignans prevent melanin synthesis through 2 stages:(a) by blocking melanin-induction and(b) by interrupting melanogenic enzyme production. This study provides evidence that sesamol, sesamin and sesamolin are potential for antimelanogenesis agents.

Sesamol Alleviates the Cytotoxic Effect of Cyclophosphamide on Normal Human Lung WI-38 Cells via Suppressing RAGE/NF-κB/Autophagy Signaling

Cyclophosphamide(CYL)is a chemotherapeutic medication commonly used in managing various malignancies like breast cancer or leukemia.Though,CYL has been documented to induce lung toxicity.Mechanism of CYL toxicity is through oxidative stress and the release of damage-associated molecular patterns(DAMPs).Sesamol(SES)is a natural antioxidant isolated from Sesamum indicum and its effect against CYL-induced lung toxicity is not studied yet.This study aims to inves-tigate whether SES could prevent any deleterious effects induced by CYL on lung using normal human lung cells,WI-38 cell line,without suppressing its efficacy.Cells were pretreated with SES and/or CYL for 24 h,then cell viability was estimated by MTS and trypan blue assays.The mode of cell death was determined by AO/EB staining.Additionally,caspase-3 level,oxidative stress,and inflammatory markers were evaluated by colorimetric and ELISA techniques.qRT-PCR was performed to evaluate RAGE,NF-κB,and Beclin-1 mRNA-expression.CYL-treated WI-38 cells developed a significantly increased cell death with enhanced oxidative and RAGE/NF-κb/Autophagy signaling,which were all attenuated after pretreatment with SES.Thus,we concluded that SES offered a protective role against CYL-induced lung injury via suppressing oxidative stress and RAGE/NF-κB/Autophagy signaling,which is a natural safe therapeutic option against CYL toxicities.

Antioxidant Activity of Sesamol Derivatives and Their Drug Delivery via C60 Nanocage: a Theoretical Study

The antioxidant activity of sesamol derivatives and their drug delivery via fullerene were investigated. Fullerene can interact with sesamol derivatives, and their adsorptions were possible from the energetic viewpoint. Adding the NH_2 group to sesamol can improve the sensitivity of sesamol toward fullerene surface. The NH_2 and OMe substitutions increase the antioxidant activity of sesamol. The results can also be used to select novel sesamol derivatives with higher antioxidant activity and higher drug delivery ability.

Sesamol inhibits atherogenic LDL-induced endothelial cell senescence in vivo and in vitro

OBJECTIVE Highly electronegative L5 low-density lipoprotein(LDL),an atherogenic LDL,induces endothelial cell(EC)senescence and has been implicated in the progression of atherosclerosis.We examine whether sesamol,a natural organic compound and component of sesame oil,prevents EC senescence induced by electronegative LDL(L5)and to investigate the underlying mechanisms.METHODS Syrian hamsters,which have a LDL profile similar to that of humans,were fed a normal chow diet(control),a high-fat diet(HFD),or a HFD supplemented with the administration of 50 or 100mg·kg-1 sesamol via oral gavage(HFD+sesamol)for 16 weeks(n=10 per group).Among these groups,we compared plasma L5 levels and aortic endothelial senescence in the aortic arch.In vitro,we examined the effects of sesamol on human aortic endothelial cell(HAEC)senescence and signaling pathways induced by L5.RESULTS Hamsters in the HFD group had higher plasma L5 levels than did the HFD+sesamol groups or control group.Betagalactosidase(gal)staining showed that aortic endothelial senescence was markedly increased in the aortic arch of the HFD group but not in that of the HFD+sesamol groups when compared with the control group.In vitro,treatment of HAECs with sesamol(1-3mol·L-1)blocked L5-induced EC senescence in a dose-dependent manner.Sesamol also markedly inhibited the L5-induced phosphorylation of p38 MAPK and p53 activation and increased Mdm2 and phosphorylation of Akt.CONCLUSION The critical findings of this study suggest that sesamol may provide protection against atherosclerosis and the development of cardiovascular disease in humans.

Biomolecular changes and DNA targeting effect of sesamol in human lung adenocarcinoma (SK-LU-1) cells by FTIR microscopy

Objective: To investigate biomolecular alteration of sesamol on human lung adenocarcinoma(SK-LU-1) cells compared with cisplatin using Fourier transform infrared microscopy(FTIR). Methods: Cytotoxicity of sesamol was investigated against SK-LU-1 cells by using neutral red. DNA fragmentation and the cell cycle analysis were determined by agarose gel electrophoresis and flow cytometry, respectively. The FTIR microscopy technique was applied to explore the changes in cellular biochemical compositions in cells treated with sesamol that the biochemical and biological assays cannot cover. The alkylating property was determined by 4-(4-nitrobenzyl)pyridine assay. Results: Sesamol and cisplatin exerted an antiproliferative effect at 48 h with respective IC50 values of 2.7 and 0.07 m M. Both induced apoptosis by causing DNA damage and accumulation of cell populations at sub-G1. FTIR microscopy and Principle Component Analysis clearly discriminated the sesamol-and cisplatin-treated cells from the untreated cells or control. A significant increase of total lipid content was found in cisplatin-treated cells. Conformational changes in the proteins secondary structure from the β-helix to the β-sheet were found in both sesamol-and cisplatin-treated cells, as well as significant reductions in relative DNA content of both compared to the control were observed, suggesting DNA damage. A shift in the peak position of DNA region provides insight on the DNA interactions. Conclusions: The non-alkylating effect of sesamol based on the nitrobenzyl pyridine assay delineates the non-covalent binding mode of sesamol on DNA. Hydrogen bonding is the binding mode of sesamol on DNA, while for cisplatin it was covalent and hydrogen bonding.

New fluorimetric assay of horseradish peroxidase using sesamol as substrate and its application to EIA

Horseradish peroxidase (HRP) is generally used as a label enzyme in enzyme immunoassay (EIA).The procedure used for HRP detection in EIA is critical for sensitivity and precision.This paper describes a novel fluorimetric assay for horseradish peroxidase (HRP) using sesamol as substrate.The principle of the assay is as follow:sesamol (3,4-methylenedioxy phenol) is reacted enzymatically in the presence of hydrogen peroxide to produce dimeric sesamol.The dimer is fluorescent and can be detected sensitively at ex.347 nm,em.427 nm.The measurable range of HRP was 1.0×10-18 to 1.0×10-15 mol/assay,with a detection limit of 1.0×10-18 mol/assay.The coefficient of variation (CV,n=8) was examined at each point on the standard curve,with a mean CV percentage of 3.8%.This assay system was applied to thyroid stimulating hormone (TSH) EIA using HRP as the label enzyme.

高温条件下芝麻林素转化为芝麻酚的规律及其反应机制

本实验探究不同因素对高温条件下芝麻林素转化为芝麻酚的影响及其转化动力学,并通过液相色谱-串联质谱(liquid chromatography-tandem mass spectrometry,LC-MS/MS)分析相关转化路径。结果表明:丙三醇是芝麻林素转化为芝麻酚的理想介质,反应温度和反应时间对芝麻酚生成率影响显著;在160~200℃范围内,芝麻林素的转化符合一级动力学方程特征,且反应速率常数与温度呈正相关,半衰期和十分之一衰期与温度呈负相关,通过阿伦尼乌斯方程计算出该反应活化能为(104.50±4.32)kJ/mol;LC-MS/MS分析结果表明以芝麻林素为底物的反应系统包括芝麻酚的生成和转化两条转化路径。

量子化学计算白藜芦醇与芝麻酚在油脂中的抗氧化协同作用

目的:研究白藜芦醇与芝麻酚间的抗氧化协同机理。方法:通过DPPH和氢过氧化物分别检测葵花子油中自由基和过氧自由基的含量变化,并结合诱导期的测定,优化组合白藜芦醇与芝麻酚二者比例,并采用量子化学计算模拟反应过程。结果:在180℃加热2 h,添加白藜芦醇与芝麻酚的葵花籽油中,总自由基含量分别为(0.08±0.03),(0.20±0.03)mol/L,相比于空白[(0.44±0.01)mol/L],白藜芦醇具有最佳抑制效率,且芝麻酚清除过氧自由基的能力最强。二者在纯化的葵花籽油中发生协同作用的最佳添加量为1400,200 mg/kg,且在180℃降解速率下,白藜芦醇具有保护芝麻酚的作用。结论:利用量子化学的手段发现二者存在动态平衡的过程,由于白藜芦醇的添加量是芝麻酚的7倍,所以反应更倾向于白藜芦醇向芝麻酚自由基供H。

芝麻酚抗肝损伤作用研究进展

肝脏是人体重要的器官之一,具有多种生理功能,包括生物转化、代谢、合成及解毒等,容易受到内部或外部因素的刺激影响而导致肝脏损伤。饮食、化合物、药物、重金属等是导致肝脏损伤的常见因素。芝麻酚是芝麻中的一种有效成分,在减轻氧化应激、抗炎以及改善代谢等方面具有显著的作用,对肝损伤表现出明显的保护作用。通过对国内外相关文献分析,系统地对芝麻酚在保肝活性方面的相关研究进展进行了总结,以期为芝麻酚的进一步研究提供参考。

HPLC测定芝麻油中木脂素类化合物含量研究

建立了HPLC同时测定芝麻油中芝麻素、芝麻林素、芝麻酚和芝麻素酚4种木脂素化合物含量的方法。首先确定了HPLC法分离和测定这4种物质的色谱条件,色谱柱为ODS-C18(250 mm×4.6 mm,5μm);检测波长:芝麻素和芝麻林素为287 nm,芝麻酚和芝麻素酚为293 nm;柱温30℃;流速0.8 mL/min,流动相为甲醇(A)和水(B)进行梯度洗脱,梯度为0 min(A,60%)→6 min(A,60%)→9 min(A,75%)→24min(A,70%)→27 min(A,60%)→32 min(A,60%)。同时比较筛选了皂化法、氧化铝柱层析法和薄层层析法3种去除脂肪类成分的前处理方法,确定薄层层析法为最有效的前处理方法。

抗氧剂芝麻酚制备技术及抗氧化活性评述

芝麻酚是一种优良的抗氧剂和重要药物中间体。本文详细介绍了芝麻酚的植物提取技术、以黄樟油素为原料的半合成技术、从邻苯二酚出发的全合成技术 ,分析了各种技术合成芝麻酚产品的技术优势和工业化研究的重点 ,提出了优先发展半合成技术 ,努力开发全合成技术的发展思路 。

芝麻素的研究及开发

阐述了芝麻素的主要来源 ,开发的意义 ,芝麻素的研究现状 ,存在问题及其发展趋势。并认为芝麻素的产业化在我国具有可行性。

芝麻酚对猪精液冷冻保存效果的影响

为了探究芝麻酚对猪精液冷冻保存效果的影响,用手握法采集成年杜洛克公猪精液,预处理后添加不同浓度芝麻酚(0,0.05,0.10,0.15,0.20和0.25g/L)的冷冻稀释液进行稀释,冷冻-解冻后检测猪精子活率、质膜完整性(低渗肿胀试验)、线粒体活性、顶体完整性、DNA完整性以及超氧化歧化酶(superoxide dismutase,SOD)、过氧化氢酶(catalase,CAT)和谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活性等。结果显示:当芝麻酚添加浓度为0.20g/L时,解冻后精子活率、线粒体活性、质膜完整率和顶体完整率为最高,相比较于对照组,分别提高了12.67%、19.07%、18.78%和14.09%(P<0.05);MDA含量最低为2.04nmol/mL(P<0.05);SOD和GSH-Px酶活最高为73.04U/mL和237.59U/I(P<0.05)。当芝麻酚添加浓度为0.25g/L时,DNA完整性最高为72.46%(P<0.05)。当芝麻酚添加浓度为0.15g/L时,CAT酶活最高为3.44U/mL(P<0.05)。结果表明:与对照组相比较,在猪精液冷冻稀释液中添加适当浓度的芝麻酚能显著提高解冻后猪精子活率、功能完整性和抗氧化能力(P<0.05),且当芝麻酚的浓度为0.2g/L时对猪精子冷冻保存效果最好。研究结果表明,芝麻酚作为一种天然抗氧化剂,对猪精子冷冻保存具有良好的效果。

芝麻酚清除O_2^-·自由基的活性研究

通过改良邻苯三酚自氧化法(简称325nm法)测定芝麻酚清除自由基能力。试验表明:在等质量浓度条件下,芝麻酚对超氧阴离子自由基(O2-·)的清除效率高于BHT及VE,当芝麻酚的质量浓度为0.8g/L时,对O2-·自由基的清除率达到80.68%,高于BHT的77.12%及VE的55.65%。因此,芝麻酚具有较强的清除O2-·自由基的能力。

超高效液相色谱法测定芝麻油中芝麻酚含量

目的:建立芝麻油样品中芝麻酚含量的超高效液相色谱(UPLC)测定方法。方法:样品经90%乙腈水提取后,用水定容,进行UPLC定量分析。实验采用BEH C18色谱柱,以水和乙腈为流动相。结果:方法测定低限为5.0mg/kg,在5.0～500.0mg/kg添加水平范围内,芝麻酚回收率为81.5%～90.9%,相对标准偏差为1.8%～3.5%。结论:方法准确度和稳定性较好,操作简单快捷,样品净化效果好,测定低限能够满足限量要求。

芝麻及芝麻油中主要抗氧化物质的研究进展

芝麻及芝麻油都含有抗氧化物质,其中起着抗氧化作用的主要是酚类物质。主要介绍芝麻及芝麻油中的主要抗氧化物质、生理功能和它们的提取方法。

芝麻酚对茶油抗氧化活性研究

以茶油为底物,以过氧化值为指标,研究了芝麻酚对油脂的抗氧化性能。结果表明,芝麻酚对茶油具有显著的抗氧化活性;在茶油中添加浓度为0.01%、0.02%、0.04%、0.06%、0.08%、0.1%(质量分数)6个油样中,样品均表现出较强的抗氧化活性,经过10d强化处理的茶油样品(空白对照)的POV值达到32.16mmol/kg,而添加0.10%(质量分数)芝麻酚的样品的POV值仅为7.94mmol/kg。芝麻酚的抗氧化效果与同浓度的BHT相当,强于同浓度的VE。

3,4-亚甲二氧基苯酚的合成

3,4-亚甲二氧基苯酚是一种优良的抗氧剂和药物合成的重要中间体。以邻苯二酚、二氯甲烷为原料经环合得到1,2-亚甲二氧基苯,然后与乙酰氯经Friedel-Crafts反应得到3,4-亚甲二氧基苯乙酮,最后经双氧水/乙酸氧化、水解得到目标产物,总收率20.2%。

高温下芝麻林素对大豆油的抗氧化及其作用机理初探

以无抗氧化剂大豆油为介质,研究在加热过程中芝麻林素对大豆油的抗氧化性,并采用薄层色谱和HPLC色谱相结合的方法探讨加热过程中芝麻林素的转化过程和作用机理。结果表明:0.2%芝麻林素对大豆油经高温诱导的脂质过氧化具有良好的抑制作用,其抗氧化效果与同浓度的BHT相当并强于同浓度的维生素E,且芝麻林素与增效剂磷酸复配使用时抗氧化效果显著;加热(180℃)条件下,芝麻林素会裂解为芝麻酚,磷酸的存在会促使芝麻林素水解为芝麻酚并部分转化重排成芝麻素酚,进而发挥其抗氧化作用。

紫外光谱法测定芝麻素与芝麻林素含量

本实验采用紫外分光光度法测定芝麻油中木酚素类物质芝麻素与芝麻林素的含量。根据木酚素类化合物在200-400nm紫外区有特征吸收,利用其吸收的强弱,以芝麻油中含量最高的芝麻素为对照品, 通过标准曲线的绘制和假设检验,得到芝麻素的浓度与吸光度之间的显著的线性关系,由回归方程计算芝麻素的最低检测极限为1．95μg/mL,平均加样回收率为99．31％,RSD为1．87％;在提取后的40分钟内进行稳定性试验,RsD(％)为0．3％。重现性试验结果RSD为2．85％,精密度试验结果RSD为0．22％。