Nerve growth factor protects against palmitic acid- induced injury in retinal ganglion cells

Accumulating evidence supports an important role for nerve growth factor （NGF） in diabetic retinopathy. We hypothesized that NGF has a protective effect on rat retinal ganglion RGC-5 cells injured by palmitic acid （PA）, a metabolic factor implicated in the development of dia- betes and its complications. Our results show that PA exposure caused apoptosis of RGC-5 cells, while NGF protected against PA insult in a concentration-dependent manner. Additionally, NGF significantly attenuated the levels of reactive oxygen species （ROS） and malondialde- hyde （MDA） in RGC-5 cells. Pathway inhibitor tests showed that the protective effect of NGF was completely reversed by LY294002 （PI3K inhibitor）, Akt VIII inhibitor, and PD98059 （ERK1/2 inhibitor）. Western blot analysis revealed that NGF induced the phosphorylation of Akt/FoxO1 and ERK1/2 and reversed the PA-evoked reduction in the levels of these proteins. These results indicate that NGF protects RGC-5 cells against PA-induced injury through anti-oxidation and inhibition of apoptosis by modulation of the PI3K/Akt and ERK1/2 signaling pathways.

Eicosane, pentadecane and palmitic acid: The effects in in vitro wound healing studies

Objective: To examine the wound healing properties of eicosane, pentadecane and palmitic acid by evaluating in term of anti-microbial, anti-inflammatory, proliferation, migration and collagen synthesis. Methods: Anti-microbial activities of Staphylococcus aureus, Bacillus subtilis, Escherichia coli and Pseudomonas aeruginosa were evaluated by carrying out disk diffusion and agar well diffusion methods. Growth rate of tested bacteria was also evaluated for 8 h in conjunction with the sample drugs. Besides, U937 cell lines were used as model study for realtime mRNA genes expression studies of TNF-毩 and IL-12 under the treatment. Proliferation, migration and collagen content synthesis were carried out on human dermal fibroblast. Results: None of the sample drugs possessed significant inhibition of bacteria tested in this study both in disk diffusion and agar well diffusion methods. In contrary, significantly low expressed mRNA gene expression levels of TNF-毩 and IL-12 were found under the treatment of respective drugs. Meanwhile in proliferation, migration and hydroxyproline content analysis, all the sample drugs showed no significant positive stimulation. Conclusions: This study therefore explains that apart from their potential in downregulating pro-inflammatory cytokines, these three compounds which were examined individually may not be good candidates in promoting wound healing.

Cannabidiol (CBD) Prevents Palmitic Acid-Induced Drop in Mitochondrial Membrane Potential

Exposure of macrophages and microglia cells to the saturated palmitic acid (PA) leads to reduction in the mitochondrial membrane potential (), shrinkage of the cells and apoptosis. Here we show that the Cannabis component Cannabidiol (CBD) rescues both macrophages and microglia cells from the detrimental effects of PA. CBD prevents the shrinkage in cell size and the reduction incaused by PA. The protective effect of CBD on the macrophage mitochondria is important for sustaining the macrophage population even under the immunosuppressed conditions caused by this drug. To a similar extent, the antagonistic effect of CBD on PA-mediated microglia cytotoxicity is important for its role in neuroprotection.

血清LncRNA UCA1、NPASDP4水平与急性脑梗死患者神经功能缺损的关系及对预后的预测价值

目的探讨血清长链非编码核糖核酸尿路上皮癌胚抗原1(LncRNA UCA1)、神经元PAS结构域蛋白4(NPASDP4)水平与急性脑梗死(ACI)患者神经功能缺损的关系及对预后的预测价值。方法选取2021年1月—2023年6月南京大学医学院附属鼓楼医院急诊科收治的ACI患者163例(ACI组),根据美国国立卫生研究院卒中量表(NIHSS)评分分为轻度(n=32)、中度(n=73)、重度缺损亚组(n=58),另选取同期健康体检者65例作为健康对照组。根据ACI患者90 d预后分为不良预后亚组52例、良好预后亚组111例。采用实时荧光定量聚合酶链式反应与酶联免疫吸附法,检测血清LncRNA UCA1与NPASDP4水平。Spearman相关性分析血清LncRNA UCA1、NPASDP4水平与ACI患者NIHSS评分的相关性。多因素Logistic回归分析ACI患者不良预后的因素,受试者工作特征(ROC)曲线分析血清LncRNA UCA1、NPASDP4预测ACI患者不良预后的价值。结果与健康对照组比较,ACI组血清LncRNA UCA1、NPASDP4水平升高(t/P=20.114/<0.001、15.711/<0.001)。血清LncRNA UCA1、NPASDP4水平重度缺损亚组>中度缺损亚组>轻度缺损亚组(F/P=187.914/<0.001、195.031/<0.001)。ACI患者血清LncRNA UCA1、NPASDP4水平与NIHSS评分呈正相关(r/P=0.759/<0.001、0.773/<0.001)。随访90 d,与良好预后亚组比较,不良预后亚组血清LncRNA UCA1、NPASDP4水平升高(t/P=6.963/<0.001、6.515/<0.001)。年龄大、NIHSS评分增加、LncRNA UCA1和NPASDP4升高为ACI患者不良预后的独立危险因素[OR(95%CI)=1.107(1.043~1.176)、1.098(1.049~1.150)、3.479(1.941~6.235)、1.959(1.398~2.745)]。血清LncRNA UCA1、NPASDP4及二者联合预测不良预后的AUC分别为0.777、0.789、0.870,二者联合大于血清LncRNA UCA1、NPASDP4单独预测的AUC(Z/P=3.312/0.001、2.721/0.007)。结论血清LncRNA UCA1表达、NPASDP4水平升高与ACI患者神经功能缺损加重和不良预后密切相关,血清LncRNA UCA1联合NPASDP4水平预测ACI患者不良预后的效能较高。

Palmitic acid reduces the methylation of the FOXO1 promoter to suppress the development of diffuse large B-cell lymphoma via modulating the miR-429/DNMT3A axis

Diffuse large B-cell lymphoma(DLBCL)is characterized by significant treatment resistance.Palmitic acid(PA)has shown promising antitumor properties.This study aims to elucidate the molecular mechanisms by which PA influences DLBCL progression.We quantified the expression levels of microRNAs(miRNAs),Forkhead box protein O1(FOXO1),and DNA methyltransferase 3A(DNMT3A)in both untreated and PA-treated DLBCL tumors and cell lines.Assessments were made of cell viability,apoptosis,and autophagy-related protein expression following PA administration.Interaction analyses among miR-429,DNMT3A,and FOXO1 were conducted using luciferase reporter assays and methylation-specific(MSP)Polymerase chain reaction(PCR).After transfecting the miR-429 inhibitor,negative control(NC)inhibitor,shRNA against DNMT3A(sh-DNMT3A),shRNA negative control(sh-NC),over-expression vector for DNMT3A(oe-DNMT3A),or overexpression negative control(oe-NC),we evaluated the effects of miR-429 and DNMT3A on cell viability,mortality,and autophagy-related protein expression in PA-treated DLBCL cell lines.The efficacy of PA was also tested in vivo using DLBCL tumor-bearing mouse models.MiR-429 and FOXO1 expression levels were downregulated,whereas DNMT3A was upregulated in DLBCL compared to the control group.PA treatment was associated with enhanced autophagy,mediated by the upregulation of miR-429 and downregulation of DNMT3A.The luciferase reporter assay and MSP confirmed that miR-429 directly inhibits DNMT3A,thereby reducing FOXO1 methylation.Subsequent experiments demonstrated that PA promotes autophagy and inhibits DLBCL progression by upregulating miR-429 and modulating the DNMT3A/FOXO1 axis.In vivo PA signific-antly reduced the growth of xenografted tumors through its regulatory impact on the miR-429/DNMT3A/FOXO1 axis.Palmitic acid may modulate autophagy and inhibit DLBCL progression by targeting the miR-429/DNMT3A/FOXO1 signaling pathway,suggesting a novel therapeutic target for DLBCL management.

Lipase-Catalyzed Synthesis of Sn-2 Palmitate: A Review

Human milk fat(HMF)is an important source of nutrients and energy for infants.Triacylglycerols(TAGs)account for about 98%of HMF and have a unique molecular structure.HMF is highly enriched in palmitic acid(PA)at the sn-2 position of the glycerol backbone(more than 70%)and in unsaturated fatty acids at the sn-1,3 position.The specific TAG structure in HMF plays a valuable function in infant growth.Sn-2 palmitate(mainly 1,3-dioleoyl-2-palmitoyl-glycerol)is one of the structured TAGs that is commonly supplemented into infant formula in order to enable it to present a similar structure to HMF.In this review,the development of the lipase-catalyzed synthesis of sn-2 palmitate over the last 25 years are summarized,with a focus on reaction schemes in a laboratory setting.Particular attention is also paid to the commercialized sn-1,3 regioselective lipases that are used in structured TAGs synthesis,to general methods of TAG analysis,and to successfully developed sn-2 palmitate products on the market.Prospects for the lipase-catalyzed synthesis of sn-2 palmitate are discussed.

Lipase-catalyzed regioselective synthesis of palmitolyglucose ester in ionic liquids

Candida antarctica lipase B (CAL-B) was used as a catalyst in the synthesis of palmitolyglucose ester in the ionic liquids, 1-butyl-3-methylimidazolium triflu- oromethanesulfonate ([Bmim][TfO]), with glucose as a substrates and palmitic acid vinyl ester as the acyl donor. The effect of substrate ratio, lipase content, and temperature on the activity and stability of lipase was studied. The reaction conditions in [Bmim][TfO] re- sulting in the highest yield of the sugar ester were a temperature of 50?C, enzyme concentration of 50 mg/ mL, and a molar ratio of glucose/vinyl palmitate of 1:3. The major reaction product was purified and char- acterized by FT-IR, HPLC, MS and NMR, as being 6-O-palmitolyglucose ester. The advantages of ionic liquid vs. organic solvent were noted.

Reaction kinetics of isopropyl palmitate synthesis

In this study, the kinetics of isopropyl palmitate synthesis including the reaction mechanism was studied based on the two-step noncatalytic method. The liquid-phase diffusion effect on the reaction process was eliminated by adjusting the stirring rate. The results showed that the two-step reaction followed a tetrahedral mechanism and conformed to second-order reaction kinetics. Nucleophilic attack on the carbonyl carbon afforded an intermediate, containing a tetrahedral carbon center. The intermediate ultimately decomposed by elimination of the leaving group, affording isopropyl palmitate. The experimental data were analyzed at different temperatures by the integral method. The kinetic equations of the each step were deduced, and the activation energy and frequency factor were obtained. Experiments were performed to verify the feasibility of kinetic equations, and the result showed that the kinetic equations were reliable. This study could be very signi ficant to both industrial application and determining the continuous production of isopropyl palmitate.

基于DGKα-PA信号轴探讨扶正祛邪方对人肺癌H292细胞增殖、迁移的影响

目的探讨扶正祛邪方调节DGKα-PA信号轴对人肺癌H292细胞增殖、迁移的影响及可能机制。方法将H292细胞分为对照组和扶正祛邪方低、中、高浓度组,扶正祛邪方低、中、高浓度组分别予3、6、12 mg/mL扶正祛邪方干预48 h,对照组予等体积培养基常规培养。克隆形成实验观察H292细胞增殖情况,细胞划痕实验、Transwell实验观察细胞迁移和侵袭情况,ELISA检测细胞磷脂酸(PA)含量,Western blot检测细胞二酰甘油激酶α(DGKα)、蛋白激酶B(AKT)、p-AKT和雷帕霉素机械靶蛋白(mTOR)表达。结果与对照组比较,扶正祛邪方低、中、高浓度组细胞克隆形成数明显减少(P<0.05,P<0.01),细胞迁移率明显降低(P<0.01),侵袭细胞数明显减少(P<0.05,P<0.01),细胞PA含量明显减少(P<0.01),DGKα、p-AKT、mTOR蛋白表达明显降低(P<0.05,P<0.01),且以扶正祛邪方高浓度组抑制作用最明显(P<0.01)。结论扶正祛邪方可能通过DGKα-PA信号轴抑制人肺癌H292细胞增殖、迁移,其机制与抑制下游AKT/mTOR信号通路有关。

Dihydroartemisinin ameliorates palmitate-induced apoptosis in cardiomyocytes via regulation on miR-133b/Sirt1 axis

Excessive fat ectopically deposited in the non-adipose tissues is considered as one of the leading causes of myopathy.The aim of this study was to investigate the role of Dihydroartemisinin(DHA)in palmitate(PAL)-incubated H9c2 cells(lipotoxicity-induced cell injury model).Cell viability of PAL-treated cells was determined by MTT assay,and apoptotic regulators were examined by qRT-PCR and western blot analysis,in the absence or in the presence of DHA,respectively.Expression levels of miR-133b and Sirt1 were also evaluated by qRT-PCR and western blotting examination.PAL decreased the viability of H9c2 cells and enhanced the expression of apoptotic genes.DHA reversed the effect of PAL on cell viability and lowed the level of Caspase3 and Bax.It also lowered the expression of miR-133b,while enhanced the expression of Bcl-2.Sirt1 was revealed as target of miR-133b through transcriptional regulation and the process was affected by DHA.DHA partially protected against the PAL-induced lipotoxicity by influencing the expression of miR-133b that hindered the activity of Sirt1.DHA may be used as a potential treatment in clinical management for lipotoxicity induced heart complications.

棕榈酸定形复合相变材料研究进展

棕榈酸因存在热导率低和物态相变时易泄漏的缺点,限制了其在诸多领域的发展和应用。棕榈酸定形复合相变材料以支撑材料为基体,将棕榈酸分散在基体材料中,不仅有效解决棕榈酸的泄漏问题,而且基体材料的加入还能提高复合相变材料的热导率。综述了基于不同基体材料的棕榈酸定形复合相变材料的研究进展,指出了棕榈酸定形复合相变材料的不足之处,并展望了其未来研究方向。

鸢尾素缓解棕榈酸对骨髓间充质干细胞的成骨抑制

背景:鸢尾素是肌肉细胞在运动时从跨膜蛋白FNDC5中分离出来的肌因子,具有诱导白色脂肪组织褐变的功能,但是其对脂毒性引起的成骨分化的影响及机制尚不清楚。目的:探究鸢尾素对棕榈酸诱导的骨髓间充质干细胞成骨能力的影响及作用机制。方法:CCK-8检测不同浓度棕榈酸对小鼠骨髓间充质干细胞增殖的影响,以及鸢尾素对棕榈酸存在条件下骨髓间充质干细胞增殖的影响;鸢尾素和棕榈酸预处理24 h后,对小鼠骨髓间充质干细胞成骨诱导分化,在成骨诱导培养第7天进行碱性磷酸酶染色,qRT-PCR检测成骨相关基因的表达,Western blot检测AMPK/BMP2/SMAD信号通路相关蛋白的表达,第21天进行茜素红染色,检测成骨差异。结果与结论:①CCK-8结果提示骨髓间充质干细胞的扩增与棕榈酸的浓度呈反比,但在0.02 mmol/L浓度时,棕榈酸对骨髓间充质干细胞扩增无显著影响,鸢尾素质量浓度在0.1-20μg/L范围内时,不影响骨髓间充质干细胞增殖;②碱性磷酸酶染色及茜素红染色结果显示,棕榈酸抑制骨髓间充质干细胞成骨分化能力,鸢尾素能改善棕榈酸诱导的骨髓间充质干细胞成骨抑制,qRT-PCR结果显示,棕榈酸可以引起成骨相关基因下调,而鸢尾素可以抑制这一趋势;③Western bolt结果显示,相较于单纯棕榈酸干预组,鸢尾素处理后增强了骨髓间充质干细胞中AMPK/BMP2/SMAD信号通路传导。该研究发现了鸢尾素能够改善棕榈酸预处理骨髓间充质干细胞的成骨分化能力并提出了具体的机制可能是由AMPK/BMP/SMAD信号通路介导的。

基于IP联合蛋白质组学探讨ENG互作蛋白在bEnd.3细胞中的作用

目的本研究拟筛选并验证在脑微血管内皮细胞(bEnd.3)中Endoglin(ENG)的互作蛋白及其作用。方法采用蛋白质组学和生物信息学技术鉴定并富集ENG互作蛋白,对这些互作蛋白进行亚细胞定位、GO功能注释、IPR注释和蛋白互作网络等分析。将以上分析筛选出的ENG互作蛋白,采用免疫共沉淀(IP)实验、细胞免疫荧光(IF)和蛋白免疫印迹(WB)技术进行验证和对比,探究ENG互作蛋白在棕榈酸(PA)、基因沉默和过表达ENG处理bEnd.3细胞中的表达变化及作用。结果通过蛋白质组学分析,bEnd.3细胞中ENG互作蛋白在亚细胞定位分析中细胞骨架相关成分呈现出较高的占比;通过GO注释和IPR注释进一步发现,是细胞骨架中的中间纤维和微丝蛋白呈现较高的富集状态。ENG与细胞骨架蛋白互作热力图结果显示,与对照组相比,PA处理的bEnd.3细胞中微丝蛋白Filamin B(Flnb)数值显著降低。IP和IF结果显示,bEnd.3细胞中ENG与Flnb存在蛋白互作和共定位情况。WB结果显示,bEnd.3细胞在PA处理条件下,ENG和Flnb蛋白表达均下降;在ENG沉默条件下,Flnb蛋白随ENG表达的减少而降低;在ENG过表达条件下,Flnb蛋白随ENG表达的增加而升高。结论ENG互作蛋白广泛参与到多种相关的生物途径以及信号通路之中,ENG在bEnd.3细胞中与Flnb蛋白存在相互作用且二者具有共定位现象,ENG还能够调控PA处理的bEnd.3细胞Flnb蛋白表达水平。

褪黑素通过改善线粒体动力学缓解棕榈酸诱导的牛子宫内膜上皮细胞损伤

旨在探究褪黑素对棕榈酸(palmitic acid,PA)诱导的牛子宫内膜上皮细胞(bovine endometrial epithelial cells,BEECs)线粒体动力学的影响及机制。本试验以BEECs为研究对象,分为3组:对照组、PA组和褪黑素组,其中,对照组添加0.2 mmol·L^(-1)BSA溶剂,PA组添加0.2 mmol·L^(-1)PA,褪黑素组同时添加0.2 mmol·L^(-1)PA和100 nmol·L^(-1)褪黑素。本研究通过CCK8法(n=4)和Annexin V-FITC/PI双染法(n=3)检测细胞活力和凋亡情况;利用细胞流式术检测细胞线粒体内的ROS水平(n=3);进一步使用Seahorse XFe96细胞代谢呼吸动态分析仪检测耗氧率、基础呼吸值、ATP合成能力等线粒体呼吸功能的相关指标(n=4);qRT-PCR法检测线粒体动力学相关基因MFN1、DRP 1和PGC1-α的mRNA表达变化量(n=3);最后通过Western-Blot法检测线粒体动力学相关蛋白MFN1、p-DRP1、DRP1和PGC1-α的表达变化量(n=3)。结果显示:与PA组相比,1)添加褪黑素能显著降低BEECs线粒体ROS水平(P<0.05),并显著提高BEECs活力和显著降低BEECs凋亡率(P<0.05);2)Seahorse结果提示,添加褪黑素能显著提高线粒体基础呼吸值、ATP产量和最大耗氧量(P<0.05),此结果表明褪黑素能改善线粒体功能,促进线粒体有氧呼吸,增加ATP产量;3)qRT-PCR结果表明,添加褪黑素能显著降低MFN1、DRP 1的mRNA表达量,显著提高PGC1-α的mRNA表达量(P<0.05);4)Western-Blot检测发现褪黑素组中MFN1蛋白表达量显著下降(P<0.05),p-DRP1/DRP1和PGC1-α蛋白表达量显著上升(P<0.05)。综上,本研究表明褪黑素可能通过改善BEECs线粒体动力学功能,从而缓解PA诱导下的线粒体氧化应激和提高线粒体呼吸功能,最终增强BEECs活力和降低BEECs凋亡;本研究初步探究了褪黑素对PA诱导BEECs损伤的作用机制,为提高严重NEB奶牛低繁殖力提供了理论依据。

柚皮苷通过抑制ERK1/2活化和DRP1表达减轻棕榈酸处理后脂肪细胞炎症

目的探讨柚皮苷(Nar)对棕榈酸(PA)处理后成熟脂肪细胞炎症反应的影响及机制。方法3T3-L1前脂肪细胞经成脂化诱导为成熟脂肪细胞后采用不同浓度(0、25、50、100、200μmol·L^(-1))PA处理细胞48 h,CCK-8检测细胞活力,ELISA检测细胞上清IL-6水平,确定后续实验最佳PA浓度。不同浓度(0、12.5、25、50、100μmol·L^(-1))Nar处理成熟脂肪细胞,CCK-8检测细胞活力,确定后续实验最佳Nar浓度。单独PA处理实验分为2组:Ctrl组、PA组;联合Nar处理实验分为4组:Ctrl组、PA组、Nar组、PA+Nar组;western blotting法检测各组p-ERK1/2和DRP1蛋白表达水平。联合线粒体裂变抑制剂Mdivi-1处理实验分为7组:Ctrl组、PA组、Nar组、Mdivi-1组、PA+Nar组、PA+Mdivi-1组、PA+Nar+Mdivi-1组,ELISA和western blotting法分别检测7组细胞上清IL-6水平和p-ERK1/2、DRP1蛋白表达水平。结果后续实验PA和Nar分别选择50和25μmol·L^(-1)。与Ctrl组比较,PA组p-ERK1/2和DRP1表达水平均升高(P<0.001)。与PA组比较,PA+Nar组、PA+Mdivi-1组、PA+Nar+Mdivi-1组IL-6水平、p-ERK1/2和DRP1表达均更低(P<0.05);与PA+Nar组比较,PA+Nar+Mdivi-1组IL-6水平差异无统计学意义(P>0.05),但p-ERK1/2和DRP1表达水平均降低(P<0.05)。结论Nar可减轻PA处理后成熟脂肪细胞的炎症反应,其机制是通过抑制ERK1/2激活和DRP1表达实现的。

棕榈酸诱导斑马鱼脂毒性损伤骨形成抑制模型的建立

目的 建立棕榈酸诱导的斑马鱼脂毒性损伤骨形成抑制模型。方法 将AB品系斑马鱼胚胎分为对照组、棕榈酸组(PA组)和辛伐他汀组(SIM组)。从3 dpf(days post fertilization, dpf)开始,PA组、SIM组给予PA造模。从5 dpf开始,SIM组给予SIM连续给药4 d。9 dpf通过钙黄绿素染色法、尼罗红染色法、甘油三酯及总胆固醇含量测定、q-PCR判断模型是否成功建立。结果 PA显著减少斑马鱼椎骨骨节数目、促进脂质堆积、增加甘油三酯及总胆固醇含量、促进成脂相关基因PPARγ、c/EBPα的表达并抑制成骨相关基因ALP、RUNX2的表达。SIM可以改善PA对斑马鱼的骨形成抑制效应。结论 采用PA给药的方法可成功造成与骨质疏松症(osteoporosis, OP)病理过程相似的脂毒性损伤骨形成抑制模型,该方法简便、灵敏、可控,可用于OP及相关疾病的药物筛选。

固定化脂肪酶ANL-MARE催化酸解合成1-油酸-2-棕榈酸-3-亚油酸甘油三酯

1-油酸-2-棕榈酸-3-亚油酸甘油三酯(OPL)是人乳中主要的脂质组成,为满足婴幼儿配方食品母乳化需求,该试验探究了新型固定化脂肪酶ANL-MARE催化制备OPL的方法。试验成功制备和表征了固定化酶ANLMARE,并以ANL-MARE为生物催化剂,建立了一种用三棕榈酸甘油三酯(PPP)、油酸(OA)和亚油酸(LA)高效酶催化制备富含OPL结构脂的方法。经单因素和响应面试验优化,获得OPL最优合成工艺为:PPP与总脂肪酸的摩尔比1:14.27,OA与LA摩尔比为1:0.76,脂肪酶添加量12.70%,反应温度50℃,反应4 h,此条件下产物中OPL相对含量为47.93%,2位棕榈酸(sn-2 PA)占总棕榈酸(PA)的质量分数(sn-2 PA相对含量)为71.69%。此外,固定化酶ANL-MARE与商业脂肪酶相比,表现出较好的催化合成OPL的活性。综上所述,固定化酶ANL-MARE具有催化制备OPL结构脂的重大潜力,为人乳脂替代脂的高效制备提供了新策略和理论基础。

直接法合成棕榈酰基甲基牛磺酸钠的催化剂筛选和反应动力学

N-酰基氨基酸型表面活性剂具有优良的表面活性、安全性和生物降解性,广泛应用于日化、医药和食品等领域。以棕榈酸和N-甲基牛磺酸钠为原料经直接法合成棕榈酰基甲基牛磺酸钠,对比分析了金属氧化物、金属氯化物和硼酸系催化剂对棕榈酰基甲基牛磺酸钠合成反应的影响,筛选出适宜的催化剂,并进行反应动力学研究。结果表明,2-氯苯硼酸可有效催化棕榈酰基甲基牛磺酸钠的合成反应,当2-氯苯硼酸质量为棕榈酸质量的4%时,棕榈酰基甲基牛磺酸钠的收率达到97.5%,选择性达到98.4%。在棕榈酸过量的情况下,反应活化能为68.0 kJ/mol,指前因子为1.6×10^(10 )h^(−1)。

立方形纳米碳酸钙改性及其在油墨中的应用

纳米碳酸钙作为添加剂可以提升油墨的光泽、改善填料的分散性和降低生产成本。本研究以立方形纳米碳酸钙(CNCC)为原料,硬脂酸钠(SS)和棕榈酸(PA)为复合改性剂(SS/PA),采用湿法制备了油墨用改性纳米碳酸钙(SS/PA/CNCC)。考察了SS/PA复配比例、添加量、反应温度等因素对SS/PA/CNCC性能的影响,当SS/PA复配比例为1∶1、质量分数为3%、反应温度为70℃时,SS/PA/CNCC平均粒径为60 nm、吸油值为35 g/100 g,满足油墨填料使用要求。采用扫描电镜(SEM)、红外光谱(FT-IR)分析和热失重(TG)分析等表征手段,对SS/PA改性纳米碳酸钙微观形貌进行分析表征。上述SS/PA/CNCC应用在油墨中,当SS/PA/CNCC在油墨中添加9份时,油墨细度为12.5μm、流动度为32 mm、光泽度为64.5 GU,所制备的油墨性能良好。

膨胀蛭石基复合相变储热材料的制备及性能研究

文章以癸酸-棕榈酸(CA-PA)二元共晶物作为相变材料,膨胀蛭石(EVM)作为支撑材料,采用真空浸渍法制备癸酸-棕榈酸/膨胀蛭石复合相变储热材料(CA-PA/EVM)。通过FT-IR,DSC,TG,热循环等测试方法对癸酸-棕榈酸/膨胀蛭石复合相变储热材料的化学兼容性、储热性能、热稳定性及可靠性进行系统研究。结果表明:膨胀蛭石通过物理作用吸附癸酸-棕榈酸二元共晶物至其层状孔隙结构,且二者化学兼容性良好;癸酸-棕榈酸/膨胀蛭石复合相变储热材料的融化和凝固相变温度分别23.61,20.41℃,熔化和凝固相变潜热分别为67.22,64.87 J/g;膨胀蛭石中癸酸-棕榈酸的封装量可达52.22%,在工作温度下具有良好的热稳定性;癸酸-棕榈酸/膨胀蛭石复合相变储热材料经过100次热循环后仍保持良好的热可靠性,在建筑节能领域具有广阔的应用前景。