Direct Electrochemistry of Cytochrome C on the Glassy Carbon Electrode Modified with 1-Pyrenebutyric Acid/MWNTs

With 1-Pymnebutyric acid （PBA） and multiwalled carbon nanotubes （MWNTs）, glassy carbon electrode modified was successfully prepared. In phosphate buffer solution （pH 7,0）, the direct electrochemistry of cytochrome C （Cyt C） was realized. In the cyclic voltammetry experiment two pairs of redox peaks ofCyt C were observed at 0.018 V and -0.314 V （vs. SCE）, respectively. The redox reaction at 0.018 V was diffusion controlled, while the redox reaction at -0.314 V was adsorption controlled.

P-aminobenzoic acid promotes retinal regeneration through activation of Ascl1a in zebrafish

The retina of zebrafish can regenerate completely after injury.M ultiple studies have demonstrated that metabolic alte rations occur during retinal damage;however to date no study has identified a link between metabolites and retinal regeneration of zebrafish.Here,we performed an unbiased metabolome sequencing in the N-methyl-D-aspartic acid-damaged retinas of zebrafish to demonstrate the metabolomic mechanism of retinal regeneration.Among the differentially-ex pressed metabolites,we found a significant decrease in p-aminobenzoic acid in the N-methyl-D-aspartic acid-damaged retinas of zebrafish.Then,we investigated the role of p-aminobenzoic acid in retinal regeneration in adult zebrafish.Impo rtantly,p-aminobenzoic acid activated Achaetescute complex-like 1a expression,thereby promoting Müller glia reprogramming and division,as well as Müller glia-derived progenitor cell proliferation.Finally,we eliminated folic acid and inflammation as downstream effectors of PABA and demonstrated that PABA had little effect on Müller glia distribution.Taken together,these findings show that PABA contributes to retinal regeneration through activation of Achaetescute complex-like 1a expression in the N-methyl-Daspartic acid-damaged retinas of zebrafish.

FaSnRK1a mediates salicylic acid pathways to enhance strawberry resistance to Botrytis cinerea

Strawberry is a major fruit crop worldwide because its nutritional and health benefits to human health,but its productivity is limited by Botrytis cinerea.Sucrose nonfermentation 1-related protein kinase 1(SnRK1)has a defense function against pathogens,but the function of SnRK1 in the defense response to B.cinerea in plants is still unclear.In this study,FaSnRK1a-OE and RNAi fruits were constructed and then inoculated with B.cinerea.The result reveals a positive role of Fa SnRK1a in the regulation of resistance to gray mold.FaSnRK1a affects SA content by regulating FaPAL1 and FaPAL2 expressions.The genes related to the SA signaling pathway(FaTGA1 and FaTGA2.1)were significantly increased/decreased in FaSnRK1a-OE or FaSnRK1a-RNAi fruit,respectively.FaSnRK1a interacted with the FaWRKY33.2 protein and negatively regulated FaWRKY33.2 expression,and FaWRKY33.2 acts as a repressor of disease resistance to B.cinerea.Finally,FaSnRK1a regulates the expression of six PR genes and the activities of antioxidant enzymes to boost defense response after B.cinerea inoculation.Our findings showed that FaSnRK1a increases the resistance of strawberry fruit to B.cinerea via SA signaling pathway and interaction with the FaWRKY33.2 transcription factor.

Phosphotungstic acid immobilized on amino-functionalized TS-1 zeolite as a solid acid catalyst for the synthesis of tributyl citrate

The amino-functionalization of TS-1 zeolite followed by immobilization of phosphotungstic acid(HPW)was presented to prepare a strong solid acid catalyst for the synthesis of bio-based tributyl citrate from the esterification of citric acid and n-butanol.γ-Aminopropyltriethoxysilane(APTES)was first grafted on the TS-1 zeolite via the condensation reactions with surface hydroxyl groups,and subsequently the HPW was immobilized via the reaction between the amino groups and the protons from HPW-forming strong ionic bonding.The Keggin structure of HPW and MFI topology of TS-1 zeolite were well maintained after the modifications.The amino-functionalization generated abundant uniformly distributed active sites on TS-1 for HPW immobilization,which promoted the dispersity,abundance,as well as the stability of the acid sites.The tetrahedrally coordinated framework titanium and non-framework titania behaved as weak Lewis acid sites,and the protons from the immobilized HPW acted as the moderate or strong Brønsted acid sites.An optimized TBC yield of 96.2%(mol)with a conversion of-COOH of 98.1%(mol)was achieved at 150℃for 6 h over the HPW immobilized on amino-functionalized TS-1.The catalyst exhibited good stability after four consecutive reaction runs,where the activity leveled off at still a relatively high level after somewhat deactivation possibly caused by the leaching of a small portion of weakly anchored APTES or HPW.

Ganoderic acid A ameliorates renalfibrosis by suppressing the expression of NPC1L1

Objective: The study aimed to explore the protective mechanism of Ganoderic acid A (GAA) in renal fibrosisand to verify that GAA can ameliorate renal fibrosis by regulating the Niemann-pick C1-like 1 (NPC1L1) gene. Methods:Transforming growth factor beta1 (TGF-β1) was used to treat Human Kidney-2 (HK-2) cells to establish a renal fibrosismodel. The differentially expressed genes in the control (CTRL) group, TGF-β1 group, and TGF-β1 + GAA group werescreened via transcriptome sequencing technology and verified by qPCR and Western blot experiments. The NPC1L1gene overexpression plasmid was constructed. The expression levels of N-cad, E-cad, and Slug-related proteins inCTRL, TGF-β1, TGF-β1+GAA (25 μg/mL), and TGF-β1+GAA (25 μg/mL) + NPC1L1 Overexpression (OE) groupswere detected by qPCR and Western blot analysis. Western blot analysis was used to identify the extracellular matrixassociated proteins Tenascin-C, α-SMA, and fibrosis-related protein Collagen I. Fibrosis marker protein Fibronectinwas detected and quantified by immunofluorescence. Results: Transcriptomic sequencing revealed that TGF-β1stimulation led to 267 differentially regulated genes, with 118 up-regulated and 149 down-regulated, while furthermodulation of 213 genes, comprising 112 up-regulated and 101 down-regulated genes, was observed in the GAAintervention group. The target gene in these processes was found to be NPC1L1 by investigations using GeneOntology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). qPCR and Western blot resultsconfirmed that TGF-β1 increased NPC1L1 expression, which was attenuated by GAA. Additionally, TGF-β1upregulated N-cad and Slug. However, GAA reversed this effect and NPC1L1 overexpression partially rescued theGAA effect. TGF-β1 also decreased E-cad expression, reversed by GAA, and NPC1L1 overexpression antagonized thisreversal. Furthermore, TGF-β1 promoted Collagen I, α-SMA, and Tenascin-C expression, and GAA reduced theselevels, effects that were reversed by NPC1L1 overexpression. Immunofluorescence results showed that TGF-β1increased fibronectin expression, which was decreased by GAA, and increased by NPC1L1 overexpression.Conclusion: GAA ameliorates renal fibrosis by antagonizing NPC1L1 gene expression inhibiting epithelialmesenchymal transition and reducing extracellular matrix formation.

Glycyrrhizic acid alleviates lung injury in sepsis through SIRT1/HMGB1 pathway

Objectives:This study explores the protective effects of glycyrrhizic acid(GA)on sepsis-induced cellular damage and inflammation in acute lung injury(ALI),specifically through the modulation of the sirtuin 1(SIRT1)and high mobility group box 1(HMGB1)pathway.Methods:The study employed two experimental models:lipopolysaccharide(LPS)-induced BEAS-2B human lung epithelial cells and cecal ligation and puncture(CLP)rats,to simulate sepsis conditions.The cell model involved treatments with LPS,GA,control siRNA(si-NC),and SIRT1-specific siRNA(si-SIRT1).Evaluations included cell viability,apoptosis,and cytokine production.In the rat model,treatments included GA and the SIRT1 inhibitor EX527,with assessments on lung tissue damage,inflammation,and protein expression using Western blot and co-immunoprecipitation(Co-IP)analysis.Results:LPS exposure significantly reduced SIRT1 mRNA levels and cell viability in BEAS-2B cells,which effects were reversed by cotreatment with GA and si-NC but negated by si-SIRT1.LPS also induced apoptosis and increased pro-inflammatory cytokines and HMGB1 expression,which were mitigated by GA and si-NC and exacerbated by si-SIRT1.In CLP rats,GA treatment decreased lung tissue damage,inflammatory cytokines,and HMGB1 expression,and enhanced SIRT1 levels.However,these protective effects were reversed when GA was combined with EX527.Conclusion:GA demonstrates significant protective effects against LPS-induced damage and inflammation in lung cells and tissue by modulating the SIRT1-HMGB1 pathway.This suggests that GA could be a potential therapeutic strategy for treating sepsis and related inflammatory conditions.

Overexpression of PbrGA2ox1 enhances pear drought tolerance through the regulation of GA_(3)-inhibited reactive oxygen species detoxification and abscisic acid signaling

Drought stress is a devastating natural disaster driven by the continuing intensification of global warming,which seriously threatens the productivity and quality of several horticultural crops,including pear.Gibberellins(GAs)play crucial roles in plant growth,development,and responses to drought stress.Previous studies have shown significant reductions of GA levels in plants under drought stress;however,our understanding of the intrinsic regulation mechanisms of GA-mediated drought stress in pear remains very limited.Here,we show that drought stress can impair the accumulation of bioactive GAs(BGAs),and subsequently identified PbrGA2ox1 as a chloroplast-localized GA deactivation gene.This gene was significantly induced by drought stress and abscisic acid(ABA)treatment,but was suppressed by GA_(3)treatment.PbrGA2ox1-overexpressing transgenic tobacco plants(Nicotiana benthamiana)exhibited enhanced tolerance to dehydration and drought stresses,whereas knock-down of PbrGA2ox1 in pear(Pyrus betulaefolia)by virus-induced gene silencing led to elevated drought sensitivity.Transgenic plants were hypersensitive to ABA,and had a lower BGAs content,enhanced reactive oxygen species(ROS)scavenging ability,and augmented ABA accumulation and signaling under drought stress compared to wild-type plants.However,the opposite effects were observed with PbrGA2ox1 silencing in pear.Moreover,exogenous GA_(3)treatment aggravated the ROS toxic effect and restrained ABA synthesis and signaling,resulting in the compromised drought tolerance of pear.In summary,our results shed light on the mechanism by which BGAs are eliminated in pear leaves under drought stress,providing further insights into the mechanism regulating the effects of GA on the drought tolerance of plants.

Mepiquat chloride increases the Cry1Ac protein content of Bt cotton under high temperature and drought stress by regulating carbon and amino acid metabolism

The effects of mepiquat chloride(DPC)on the Cry1Ac protein content in Bacillus thuringiensis(Bt)cotton boll shells under high temperature and drought stress were investigated to provide a theoretical reference for Bt cotton breeding and high-yield and-efficiency cotton cultivation.This study was conducted using Bt cotton cultivar‘Sikang 3'during the 2020 and 2021 growing seasons at Yangzhou University Farm,Yangzhou,Jiangsu Province,China.Potted cotton plants were exposed to high temperature and drought stress,and sprayed with either 20 mg L^(-1)DPC or water(CK).Seven days after treatment,the Cry1Ac protein content,α-ketoglutarate content,pyruvic acid content,glutamate synthase activity,glutamic oxaloacetic transaminase activity,soluble protein content,and amino acid content were measured,and transcriptome sequencing was performed.DESeq was used for differential gene analysis.Under the DPC treatment,the Cry1Ac protein content increased by 4.7-11.9% compared to CK.Theα-ketoglutarate content,pyruvic acid content,glutamate synthase activity,glutamic oxaloacetic transaminase activity,soluble protein content,and amino acid content all increased.Transcriptome analysis revealed 7,542 upregulated genes and 10,449 downregulated genes for DPC vs.CK.Gene ontology(GO)and Kyoto Encyclopedia of Gene and Genomes(KEGG)analyses showed that the differentially expressed genes were mainly involved in biological processes,such as carbon and amino acid metabolism.For example,genes encoding 6-phosphofructokinase,pyruvate kinase,glutamic pyruvate transaminase,pyruvate dehydrogenase,citrate synthase,isocitrate dehydrogenase,2-oxoglutarate dehydrogenase,glutamate synthase,1-pyrroline-5-carboxylate dehydrogenase,glutamic oxaloacetic transaminase,amino-acid N-acetyltransferase,and acetylornithine deacetylase were all significantly upregulated.The DPC treatment increased pyruvate,α-ketoglutarate,and oxaloacetate by increasing the operational rate of the glycolytic pathway of the citric acid cycle.It also significantly upregulated the genes encoding glutamate synthase,pyrrolidine-5-carboxylic acid dehydrogenase,glutamate oxaloacetate transaminase,and N-acetylglutamate synthetase,while it downregulated the genes encoding glutamine synthetase.Therefore,the synthesis of aspartic acid,glutamic acid,pyruvate,and arginine increased after treatment with DPC,and the Cry1Ac protein content was increased by regulating carbon and amino acid metabolism.

Hepatic protein phosphatase 1 regulatory subunit 3G alleviates obesity and liver steatosis by regulating the gut microbiota and bile acid metabolism

Intestinal dysbiosis and disrupted bile acid(BA)homeostasis are associated with obesity,but the precise mechanisms remain insufficiently explored.Hepatic protein phosphatase 1 regulatory subunit 3G(PPP1R3G)plays a pivotal role in regulating glycolipid metabolism;nevertheless,its obesity-combatting potency remains unclear.In this study,a substantial reduction was observed in serum PPP1R3G levels in high-body mass index(BMI)and high-fat diet(HFD)-exposed mice,establishing a positive correlation between PPP1R3G and non-12a-hydroxylated(non-12-OH)BA content.Additionally,hepatocyte-specific overexpression of Ppp1r3g(PPP1R3G HOE)mitigated HFD-induced obesity as evidenced by reduced weight,fat mass,and an improved serum lipid profile;hepatic steatosis alleviation was confirmed by normalized liver enzymes and histology.PPP1R3G HOE considerably impacted systemic BA homeostasis,which notably increased the non-12-OH BAs ratio,particularly lithocholic acid(LCA).16S ribosomal DNA(16S rDNA)sequencing assay indicated that PPP1R3G HOE reversed HFD-induced gut dysbiosis by reducing the Firmicutes/Bacteroidetes ratio and Lactobacillus population,and elevating the relative abundance of Blautia,which exhibited a positive correlation with serum LCA levels.A fecal microbiome transplantation test confirmed that the anti-obesity effect of hepatic PPP1R3G was gut microbiotadependent.Mechanistically,PPP1R3G HOE markedly suppressed hepatic cholesterol 7a-hydroxylase(CYP7A1)and sterol-12a-hydroxylase(CYP8B1),and concurrently upregulated oxysterol 7-a hydroxylase and Takeda G protein-coupled BA receptor 5(TGR5)expression under HFD conditions.Furthermore,LCA administration significantly mitigated the HFD-induced obesity phenotype and elevated non-12-OH BA levels.These findings emphasize the significance of hepatic PPP1R3G in ameliorating diet-induced adiposity and hepatic steatosis through the gut microbiota-BA axis,which may serve as potential therapeutic targets for obesity-related disorders.

Ferulic acid reduces inflammatory response induced by radiation through Sirt1-NLRP3 pathway

Objective:A model of inflammatory damage was induced by radiation to investigate whether ferulic acid(FA)can reduce the inflammatory response through the Sirt1-NLRP3 inflammatory pathway.This will help discover radiation-protective drugs and elucidate the molecular mechanisms related to radiation-induced inflammatory damage.Methods:A mouse model of radiation-induced immunoinflammatory injury was established to verify the anti-inflammatory effects of FA in vivo.C57BL/6J mice were randomly divided into six groups,and 5 Gy whole-body irradiation was used for modeling.Mice were administered a gastric solvent,amifostine,or 25,50,or 100 mg/kg FA daily for 12 days,consecutively,before irradiation.The serum of mice was collected 24 hour after irradiation to observe the content of inflammatory factors interleukin(IL)-1β,IL-18,IL-6,and tumor necrosis factor(TNF)-α.The spleen and thymus tissues of mice were weighed and the organ index was calculated for pathological testing and immunofluorescence detection.Results:FA reduced the radiation-induced decrease in the spleen and thymus indices.FA significantly reduced the secretion of inflammatory factors in the serum and reversed the radiation-induced reduction in lymphocytes in the spleen and thymus of mice.FA activated Sirt1 and inhibited the expression of the NLRP3 inflammasome to alleviate the inflammatory response.Conclusions:FA reduced radiation-induced inflammation in animals,possibly by activating Sirt1 and reducing nucleotide oligomerization domain(NOD)-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome expression,thereby reducing the secretion of inflammatory factors.

Targeting CXCR4 and EDN1 for the treatment of recurrent miscarriage using stearic acid from traditional Chinese medicine

Background:Recurrent miscarriage(RM)affects an estimated 1-3%of couples attempting to conceive,and its molecular components stay ineffectively caught on.This study aims to explore potential therapeutic targets for RM by examining gene expression patterns and biological pathways in both mouse and human RM models.Meanwhile,explore relevant traditional Chinese medicine(TCM)components targeting potential therapeutic targets.Methods:We utilized the GSE211251 mouse and the GSE26787 human datasets,employing gene set enrichment analysis and gene metaphysics analysis to examine differentially expressed genes and enriched pathways.Single-cell RNA analysis uncovered cellular heterogeneity and arranged pharmacology-mapped potential drug-target intelligence.We employed molecular docking strategies to assess the affinity of TCM components for key proteins.Results:In the mouse model,genes such as Ly6f1 and Gpr26 were upregulated,while Stc5a and Galca exhibited downregulation.Gene set enrichment analysis identified key pathways,including the tumor necrosis factor-mediated signaling pathway.In human samples,Gene Ontology analysis highlighted processes such as apoptosis and cell adhesion.Single-cell RNA analysis revealed distinct cellular populations between normal and RM samples.Systems pharmacology identified C-X-C motif chemokine receptor 4(CXCR4)and endothelin 1(EDN1)as potential key targets,and molecular docking confirmed that stearic acid from TCM appears to regulate these proteins.Conclusion:This study presents a comprehensive analysis of the genetic and cellular underpinnings of RM,identifying CXCR4 and EDN1 as promising therapeutic targets.Stearic acid from TCM could provide targeted treatment by modulating these key proteins,paving the way for new RM treatment strategies.

Pachymic acid exerts antitumor activities by modulating the Wnt/β-catenin signaling pathway via targeting PTP1B

Objective:To determine the inhibitory effects of pachymic acid on lung adenocarcinoma(LUAD)cells and elucidate its underlying mechanism.Methods:CCK-8,wound healing,Transwell,Western blot,tube formation,and immunofluorescence assays were carried out to measure the effects of various concentrations of pachymic acid on LUAD cell proliferation,metastasis,angiogenesis as well as autophagy.Subsequently,molecular docking technology was used to detect the potential targeted binding association between pachymic acid and protein tyrosine phosphatase 1B(PTP1B).Moreover,PTP1B was overexpressed in A549 cells to detect the specific mechanisms of pachymic acid.Results:Pachymic acid suppressed LUAD cell viability,metastasis as well as angiogenesis while inducing cell autophagy.It also targeted PTP1B and lowered PTP1B expression.However,PTP1B overexpression reversed the effects of pachymic acid on metastasis,angiogenesis,and autophagy as well as the expression of Wnt3a andβ-catenin in LUAD cells.Conclusions:Pachymic acid inhibits metastasis and angiogenesis,and promotes autophagy in LUAD cells by modulating the Wnt/β-catenin signaling pathway via targeting PTP1B.

青年缺血性脑卒中病人血清miR-218-5p、LASP1水平及其应用价值

目的探究青年缺血性脑卒中(IS)病人血清微RNA-218-5p(miR-218-5p)、LIM和SH3蛋白1(LASP1)水平及其应用价值。方法选取2020年6月至2022年6月山东中医药大学附属医院收治的青年IS病人96例为IS组,对所有IS病人进行为期3个月的随访,按照改良Rankin量表(mRS)评分进行分组,预后良好组68例(mRS评分≤2分)和预后不良组28例(mRS评分>2分)。选择同期在该院进行体检的健康志愿者96例为对照组。血清miR-218-5p、LASP1 mRNA水平检测采用实时荧光定量PCR(qRT-PCR);Pearson相关性分析血清miR-218-5p与LASP1 mRNA表达水平的关系。采用受试者操作特征曲线(ROC曲线)分析血清中miR-218-5p、LASP1 mRNA表达水平对IS预后评估的价值。结果与对照组相比,IS组白细胞计数、总胆固醇、三酰甘油、低密度脂蛋白胆固醇水平显著升高,高密度脂蛋白胆固醇水平显著降低(P<0.05);与对照组(1.03±0.11、1.01±0.11)相比,IS组血清中miR-218-5p水平0.88±0.09显著降低,LASP1 mRNA(1.12±0.12)水平显著升高(P<0.05)。IS病人血清miR-218-5p与LASP1 mRNA呈负相关(r=−0.73,P<0.001)。与预后良好组(0.94±0.10、1.05±0.11)相比,预后不良组血清中miR-218-5p(0.74±0.08)水平显著降低,LASP1 mRNA(1.28±0.13)水平显著升高(P<0.05)。ROC曲线显示,二者联合评估IS预后不良的AUC高于miR-218-5p、LASP1 mRNA单独预测的AUC值(Z=12.35,P<0.001;Z=6.60,P=0.010)。结论青年IS病人血清miR-218-5p较低,LASP1 mRNA较高,可用于评估青年IS病人的预后。

Gossypol acetic acid regulates leukemia stem cells by degrading LRPPRC via inhibiting IL-6/JAK1/STAT3 signaling or resulting mitochondrial dysfunction

BACKGROUND Leukemia stem cells(LSCs)are found to be one of the main factors contributing to poor therapeutic effects in acute myeloid leukemia(AML),as they are protected by the bone marrow microenvironment(BMM)against conventional therapies.Gossypol acetic acid(GAA),which is extracted from the seeds of cotton plants,exerts anti-tumor roles in several types of cancer and has been reported to induce apoptosis of LSCs by inhibiting Bcl2.AIM To investigate the exact roles of GAA in regulating LSCs under different microenvironments and the exact mechanism.METHODS In this study,LSCs were magnetically sorted from AML cell lines and the CD34+CD38-population was obtained.The expression of leucine-rich pentatricopeptide repeat-containing protein(LRPPRC)and forkhead box M1(FOXM1)was evaluated in LSCs,and the effects of GAA on malignancies and mitochondrial RESULTS LRPPRC was found to be upregulated,and GAA inhibited cell proliferation by degrading LRPPRC.GAA induced LRPPRC degradation and inhibited the activation of interleukin 6(IL-6)/janus kinase(JAK)1/signal transducer and activator of transcription(STAT)3 signaling,enhancing chemosensitivity in LSCs against conventional chemotherapies,including L-Asparaginase,Dexamethasone,and cytarabine.GAA was also found to downregulate FOXM1 indirectly by regulating LRPPRC.Furthermore,GAA induced reactive oxygen species accumulation,disturbed mitochondrial homeostasis,and caused mitochondrial dysfunction.By inhibiting IL-6/JAK1/STAT3 signaling via degrading LRPPRC,GAA resulted in the elimination of LSCs.Meanwhile,GAA induced oxidative stress and subsequent cell damage by causing mitochondrial damage.CONCLUSION Taken together,the results indicate that GAA might overcome the BMM protective effect and be considered as a novel and effective combination therapy for AML.

Enhanced autophagic clearance of amyloid-βvia histone deacetylase 6-mediated V-ATPase assembly and lysosomal acidification protects against Alzheimer's disease in vitro and in vivo

Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.

基质细胞衍生因子1修饰左旋聚乳酸多孔微球促进软骨细胞增殖和组织形成

背景:二维培养条件下的软骨细胞增殖及表型维持受限,多孔微球作为支架材料可提供三维培养环境,以更好地模拟体内生长条件。基质细胞衍生因子1是有强趋化效力的稳态细胞因子,能够促进细胞的黏附与增殖。目的:明确接枝基质细胞衍生因子1左旋聚乳酸多孔微球对软骨细胞生物学特性及软骨组织形成的影响。方法:(1)体外验证不同质量浓度基质细胞衍生因子1对兔软骨细胞增殖、迁移、表型维持的影响。(2)采用复乳法制备左旋聚乳酸多孔微球,利用碳二亚胺法将基质细胞衍生因子1接枝于左旋聚乳酸多孔微球上,通过酶联免疫吸附实验及孵育基质细胞衍生因子1特异荧光抗体验证接枝情况。(3)将兔软骨细胞分别接种于左旋聚乳酸多孔微球、接枝基质细胞衍生因子1左旋聚乳酸多孔微球上,检测细胞增殖与黏附。(4)在裸鼠背部皮下分别植入甲基丙烯酰胺基明胶-软骨细胞复合体(对照组)、左旋聚乳酸多孔微球-甲基丙烯酰胺基明胶-软骨细胞复合体(多孔微球组)、接枝基质细胞衍生因子1左旋聚乳酸多孔微球-甲基丙烯酰胺基明胶-软骨细胞复合体(多孔微球修饰组),8周后取材,分别进行组织学染色与成软骨相关基因qRT-PCR检测。结果与结论:(1)相较于0,1 000 ng/mL基质细胞衍生因子1,500 ng/mL基质细胞衍生因子1可促进软骨细胞的增殖与迁移,提升软骨细胞内Ⅱ型胶原、弹性蛋白、增殖细胞核抗原、Bcl-2 mRNA表达;(2)基质细胞衍生因子1成功接枝于左旋聚乳酸多孔微球上,接枝率为93.75%;(3)相较于左旋聚乳酸多孔微球,接枝基质细胞衍生因子1左旋聚乳酸多孔微球可促进软骨细胞的增殖、黏附;(4)裸鼠皮下植入8周后,相较于对照组、多孔微球组,多孔微球修饰组具有更明显的软骨陷窝结构、更丰富的软骨特异性基质和Ⅱ型胶原沉积,弹性蛋白、Ⅱ型胶原、增殖细胞核抗原、Bcl-2 mRNA表达升高。结果表明:接枝基质细胞衍生因子1左旋聚乳酸多孔微球有利于软骨细胞的黏附、增殖、表型维持以及体内软骨组织形成。

Flotation behavior and adsorption mechanism of(1-hydroxy-2-methyl-2-octenyl) phosphonic acid to cassiterite

The flotation behavior and adsorption mechanism of novel（1-hydroxy-2-methyl-2-octenyl） phosphonic acid（HEPA） to cassiterite were investigated by micro-flotation tests, zeta potential measurements, FTIR determination and density functional theory（DFT） calculation. The flotation results demonstrated that HEPA exhibited superior collecting performance compared with styrene phosphonic acid（SPA）. The cassiterite recovery maintained above 90% over a wide pH range of 2-9 with 50 mg/L HEPA. The results of zeta potential measurement and FTIR detection indicated that the adsorption of HEPA onto cassiterite was mainly attributed to the chemisorption between HEPA monoanions and Sn species on mineral surfaces. The DFT calculation results demonstrated that HEPA monoanions owned higher HOMO energy and exhibited a better affinity to cassiterite than SPA, which provided very clear evidence for the stronger collecting power of HEPA presented in floatation test and zeta potential measurement.

Research on Expression of LeWRKY1 in Tomato Induced by Jasmonic Acid and Other Two Factors

[Objective]The aim was to explore the molecular mechanism of plant resistance to various stress response.[Method]The expression of LeWRKY1 in tomato seedlings under treatment with B.cinerea,exogenous JA and SA were explored by real time quantitative RT-PCR technology.[Result]JA induced the expression of LeWRKY1,but SA did not.LeWRKY1 expression was up-regulated under B.cinerea infection.[Conclusion]LeWRKY1 might be involved in the tomato defense response to B.cinerea through JA dependent but SA independent signal pathway.

One-pot synthesis of a hierarchical microporous-mesoporous phosphotungstic acid-HKUST-1 catalyst and its application in the selective oxidation of cyclopentene to glutaraldehyde

A hierarchical microporous-mesoporous metal-organic framework of HKUST-l（Cu）-encapsulated phosphotungstic acid （HPW） material, referred to as HPWs@Meso-HKUST-1, is prepared by a one-pot synthesis method using cetyltrimethylammonium bromide as the supramolecular template. The addition of HPWs to the synthesis mixture of hierarchical porous HKUST-1 results in the direct encapsulation of HPWs inside the mesopores of the HKUST-1 structure, with a homogeneous distribution over the HKUST-1 crystals, which is confirmed by XRD, FT-IR, N2 adsorption, UV-Vis DRS, and TEM. FT-IR-CO adsorption experiments indicated that additional Lewis acid sites were present in the HPWs@Meso-HKUST-1 sample. The novel heterogeneous catalyst demonstrates excellent catalytic performance for the selective oxidation of cyclopentene （CPE） to glutaraldehyde CGA） using tert-butyl hydroperoxide and acetonitrile （MeCN） as the oxidant and solvent, respectively. The high activity of the catalyst is attributed to the mesostructure of the catalyst and the nature and appropriate abundance of the HPWs--being highly dispersed with the addition of Lewis sites. After a reaction for 36 h, the 30% wt% HPWs@Meso-HKUST-1 catalyst exhibits a CPE conversion of 92.5% and a high GA yield of 73%. Furthermore, the HPWs@Meso-HKUST-1 material is sufficiently stable to prevent the leaching of HPWs, and behaves as a true heterogeneous catalyst that can be repeatedly recycled without sustaining a loss of activity and selectivity in the selective oxidation of CPE.

1-甲基环丙烯结合水杨酸处理维持百香果甲基环丙烯结合水杨酸处理维持百香果果实贮藏品质

为延长百香果的贮藏期并保持贮藏过程中的品质,对比研究2 mmol/L水杨酸(salicylic acid,SA)、1 mmol/L 1-甲基环丙烯(1-methylcyclopropene,1-MCP)、1-MCP结合SA处理对紫色百香果果实采后贮藏期间品质、活性氧、抗氧化酶指标的影响。百香果果实经SA、1-MCP和1-MCP结合SA处理后,一定程度抑制乙烯的释放和脂氧合酶(li-poxygenase,LOX)活性,促进几丁质酶(chitinase,CHI)和β-1,3-葡聚糖酶(β-1,3-glucanase,GLU)的活性,增强抗氧化和抗病性作用,降低腐烂率。但因SA可以增强呼吸,故导致凹陷和失重,加快总酸流失;1-MCP抑制呼吸作用,增强超氧化物歧化酶(superoxide dismutase,SOD)活性,有利于控制失重和凹陷,但其对过氧化物酶(peroxidase,POD)活性的影响不利于控制衰老。1-MCP结合SA对POD活性,CHI活性以及GLU活性的正向影响强于单独使用1-MCP或SA处理。因此,1-MCP结合SA通过提高百香果果实的抗氧化能力和抗病能力,降低百香果果实的凹陷、失重和腐烂率,且可有效避免单独使用1-MCP或SA处理的不良作用,协同维持百香果果实采后贮藏品质。