Ti^(3+)/C/N-TiO_(2)@NGQDs纳米复合光催化剂的制备及其可见光催化性能研究

采用两步水热法制备了Ti^(3+)、C和N共掺杂TiO_(2)@氮掺杂石墨烯量子点(Ti^(3+)/C/N-TiO_(2)@NGQDs)纳米复合光催化剂,通过X射线衍射、透射电子显微镜、X射线光电子能谱和紫外可见漫反射光谱对其进行了详细表征,且通过降解甲基橙溶液研究了其可见光催化性能。结果表明,Ti^(3+)、C和N成功地共掺杂了TiO_(2),纳米NGQDs附着在共掺杂的TiO_(2)上;Ti^(3+)/C/N-TiO_(2)@NGQDs降解甲基橙的动力学一阶速率常数分别是纯TiO_(2)、C/N-TiO_(2)和C/N-TiO_(2)@NGQDs的25.7倍、4.7倍和1.7倍,提升的可见光催化性能归因于其具有更强的可见光吸收、更快的光生电荷传输和分离效率。超氧自由基和光生空穴是Ti^(3+)/C/N-TiO_(2)@NGQDs可见光降解甲基橙过程中的主要活性物质。此外,Ti^(3+)/C/N-TiO_(2)@NGQDs具有非常高的稳定性。这种TiO_(2)基的复合光催化剂可适用于实际废水处理过程。

CdS纳米颗粒修饰黑色Ti^(3+)/TiO_(2)纳米管用于高效光催化制氢研究

使用高效分级的半导体光催化剂进行光催化分解水产氢是解决目前面临的能源和环境危机的一个很有前景的策略。在这项工作中,通过阳极氧化法和NaBH 4氢化还原TiO_(2)纳米管阵列以及溶热法设计并制备立方稳态闪锌矿CdS NPs修饰于黑色Ti^(3+)/TiO_(2)纳米管的三元复合光催化剂。从扫描电镜(SEM)、透射电镜(TEM)的分析结果中可以确认CdS NPs在Ti^(3+)/TiO_(2)纳米管中的负载情况。样品BTC-1∶1表现出较高的催化性能(氢气生成率为2.77mmol/(g·h),明显高于B-TiO_(2)和CdS,分别约13倍和3.6倍)。构建异质结可以拓宽可见光的响应范围,也可以分离电子-空穴对,同时保留较高的电子-空穴氧化还原电位用于光催化反应。该研究为制备高效光解水产氢材料提供了合理的设计。

Ti^(3+)-TiO_(2)@NGQDs纳米复合光催化剂的制备及其可见光降解双酚A的研究

通过两步水热法合成了Ti^(3+)自掺杂TiO_(2)负载氮掺杂石墨烯量子点(Ti^(3+)-TiO_(2)@NGQDs)纳米复合光催化剂,并通过X射线衍射、透射电镜、X射线光电子能谱和紫外可见漫反射光谱对其进行了详细表征,且研究了其可见光降解双酚A溶液的性能。结果表明,在可见光照射30 min时,Ti^(3+)-TiO_(2)@NGQDs复合光催化剂对双酚A的降解率高达91.9%,其降解双酚A的表观速率常数(k)分别是纯TiO_(2)和Ti^(3+)-TiO_(2)的约33.6倍和6.4倍,这归因于其具有更强的可见光吸收和更快的光诱导电荷传输和分离的协同作用。捕获实验结果表明h+和·OH是Ti^(3+)-TiO_(2)@NGQDs纳米复合光催化剂降解双酚A的过程中的主要活性物质。此外,重复使用性测试结果表明Ti^(3+)-TiO_(2)@NGQDs纳米复合光催化剂具有非常高的稳定性。

Effect and mechanism of reactive oxygen species-mediated NOD-like receptor family pyrin domain-containing 3 inflammasome activation in hepatic alveolar echinococcosis

BACKGROUND The NOD-like receptor family pyrin domain-containing 3(NLRP3)inflammasome is a significant component of the innate immune system that plays a vital role in the development of various parasitic diseases.However,its role in hepatic alveolar echinococcosis(HAE)remains unclear.AIM To investigate the NLRP3 inflammasome and its mechanism of activation in HAE.METHODS We assessed the expression of NLRP3,caspase-1,interleukin(IL)-1β,and IL-18 in the marginal zone and corresponding normal liver of 60 patients with HAE.A rat model of HAE was employed to investigate the role of the NLRP3 inflammasome in the marginal zone of HAE.Transwell experiments were conducted to investigate the effect of Echinococcus multilocularis(E.multilocularis)in stimulating Kupffer cells and hepatocytes.Furthermore,immunohistochemistry,Western blotting,and enzyme-linked immunosorbent assay were used to evaluate NLRP3,caspase-1,IL-1β,and IL-18 expression;flow cytometry was used to detect apoptosis and reactive oxygen species(ROS).RESULTS NLRP3 inflammasome activation was significantly associated with ROS.Inhibition of ROS production decreased NLRP3-caspase-1-IL-1βpathway activation and mitigated hepatocyte damage and inflammation.CONCLUSION E.multilocularis induces hepatocyte damage and inflammation by activating the ROS-mediated NLRP3-caspase-1-IL-1βpathway in Kupffer cells,indicating that ROS may serve as a potential target for the treatment of HAE.

下调PDCD4抑制MAP2K3和p38 MAPK的表达减轻LPS诱导的肾小管上皮细胞炎症和凋亡

目的研究程序性细胞死亡蛋白4(programmed cell death protein 4,PDCD4)在脓毒症诱导的急性肾损伤(acute kidney injury,AKI)中的作用机制,以及调控PDCD4表达通过丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3,MAP2K3)和p38蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)对脓毒症AKI起到潜在治疗作用。方法用脂多糖(lipopolysaccharide,LPS)刺激人肾小管上皮细胞(HK-2)构建脓毒症AKI细胞模型。进一步用腺病毒介导siRNA和过表达载体抑制和上调AKI细胞模型中PDCD4的表达;CCK-8法检测细胞增殖;用DCFH-DA及激光共聚焦显微镜检测细胞中ROS水平,用总SOD活性检测试剂和MDA检测试剂盒检测细胞中SOD和MDA水平;免疫共沉淀验证PDCD4和MAP2K3之间的蛋白相互作用;TUNEL染色法检测细胞凋亡;RT-qPCR和Western blot检测PDCD4及相关基因的mRNA和蛋白表达水平;ELISA法检测患者血清中炎症相关因子水平。结果LPS诱导可以促进HK-2细胞中PDCD4表达,下调PDCD4可抑制LPS诱导的HK-2细胞的炎症、氧化应激及细胞凋亡。数据库预测及免疫共沉淀证实PDCD4可以与MAP2K3相互作用,且在LPS诱导的HK-2细胞中,MAP2K3表达水平显著增强。MAP2K3过表达和p38 MAPK激动剂可以减轻PDCD4下调对LPS诱导的细胞炎症和氧化应激的影响并抑制细胞凋亡。结论下调PDCD4可以通过抑制MAP2K3和p38 MAPK从而抑制LPS诱导的肾小管上皮细胞的炎症和凋亡。

Evolution of the R2R3-MYB gene family in six Rosaceae species and expression in woodland strawberry

R2R3-MYB gene family play important roles in plants development, metabolism, and responses to various biotic and abiotic stresses. In this study, 838 R2 R3-MYB genes were identified from six Rosaceae species, including 105 in woodland strawberry(Fragaria vesca), 173 in European pear(Pyrus communis), 219 in apple(Malus domestica), 121 in peach(Prunus persica), 121 in Chinese rose(Rosa chinensis), and 99 in black raspberry(Rubus occidentalis). All R2 R3-MYB genes in the six Rosaceae species were clustered into 51 species-specific duplicated clades with 109 genes and 50 lineage-specific duplicated clades with 242 genes according to phylogenetic analysis. R2 R3-MYB genes were distributed on all chromosomes in each of the six species, with a small amount of tandem duplication events. The proportion of tandem repeat genes ranged from 0 to 25.1%. The R2 R3-MYB protein was conserved in a clade and likely to share similar functions. The distribution of Ks showed the duplication times of R2 R3-MYB genes in six Rosaceae species. Furthermore, most of the R2 R3-MYB genes had Ka/Ks values less than 1, which indicated they were driven by purifying selection during the evolutionary processes. The GO term enrichment analysis revealed that R2 R3-MYB genes in strawberry and black raspberry were more divergent than in other Rosaceae species. Analysis of transcriptomes of 42 different tissues and development stages of woodland strawberry showed that high expression levels of R2 R3-MYB suggested that the R2 R3-MYB genes in strawberry played a key role in growth and development of both vegetative tissues and fruits. The strawberry R2 R3-MYB genes in sub-group of S1, S2, S11, S20, and S22 had high expression levels both in young leaves(YL) and old leaves(OL) strawberry tissues under drought treatments.

下调XBP1s通过Sirt3/SOD2/mtROS轴减轻缺氧/复氧诱导的肾小管上皮细胞衰老

目的探讨剪接型X-盒结合蛋白1(XBP1s)在缺氧/复氧(H/R)诱导的原代肾小管上皮细胞衰老中的作用及机制。方法将原代肾小管上皮细胞分为空白对照组(NC组)、H/R组、空载腺病毒阴性对照组(Ad-shNC组)、靶向沉默XBP1s腺病毒组(Ad-shXBP1s组)、空载腺病毒+H/R处理组(Ad-shNC+H/R组)、靶向沉默XBP1s腺病毒+H/R处理组(Ad-shXBP1s+H/R组)。检测NC组、H/R组、Ad-shNC组、Ad-shXBP1s组XBP1s的表达情况。检测Ad-shNC组、Ad-shNC+H/R组、Ad-shXBP1s+H/R组β-半乳糖苷酶染色情况,细胞衰老标志物p53、p21、γH2AX表达情况,氧化应激相关指标活性氧(ROS)、丙二醛(MDA)和超氧化物歧化酶(SOD)水平。采用染色质免疫共沉淀验证XBP1s转录调控沉默信息调节因子3(Sirt3),检测下调XBP1s后Sirt3及下游SOD2表达,采用流式细胞术检测线粒体活性氧簇(mt ROS)。结果与NC组比较,H/R组XBP1s表达增多;与Ad-sh NC组比较,Ad-sh XBP1s组XBP1s表达减少(均为P<0.001)。与Adsh NC组比较,Ad-sh NC+H/R组β-半乳糖苷酶染色阳性细胞数增加,p53、p21、γH2AX表达增多,ROS、MDA、mt ROS水平升高,SOD活性下降,Sirt3表达量降低,Ac-SOD2/SOD2比值升高;与Ad-sh NC+H/R组相比,Ad-sh XBP1s+H/R组β-半乳糖苷酶染色阳性细胞数减少,p53、p21、γH2AX表达减少,ROS、MDA、mt ROS水平下降,SOD活性升高,Sirt3表达量升高,Ac-SOD2/SOD2比值下降(均为P<0.05)。结论下调XBP1s可减轻H/R诱导的原代肾小管上皮细胞衰老,可能是通过Sirt3/SOD2/mt ROS信号轴发挥作用。

Electroactive species study in the electrochemical reduction of CO_2 in KHCO_3 solution at elevated temperature

Photoelectrochemical and electrochemical reduction of CO_2 into organic chemicals is promising for directly or indirectly transforming solar energy into chemical energy for further utilization. However,research on the electroactive species in these processes has been rather limited. In this work, we investigated possible electroactive species(CO_2 or HCO_3~– ) involved in the electrochemical reduction of KHCO_3 at elevated temperatures without CO_2 bubbling. The results showed that CO, CH_4, and C_2H_4 were produced after electrochemical reduction of 3.0 mol/L KHCO_3 at elevated temperature on a Cu electrode even without CO_2 bubbling, although their faradaic efficiencies were low(< 6 %). Measurements for CO_2 generation from the decomposition of HCO_3~– showed that elevated temperature and high HCO_3~– concentration strongly promoted this process. These results suggested that the in-situ produced CO_2 from the decomposition of HCO_3~– was probably the electroactive species in the electrochemical reduction of HCO_3~– without CO_2 bubbling. Changes of the Gibbs free energy, rate constant, and activation energy of the decomposition of HCO_3~– into CO_2 were also investigated and calculated from the experimental data.

方铁锰矿型生物源Mn_(2)O_(3)转化阿特拉津的ROS作用分析

生物源锰氧化物具有表面活性高、比表面积大和酸性位点多等特点,常被用于催化分解环境中难降解的有机污染物.阿特拉津作为全球消耗量最大的除草剂之一,经过长期使用和环境积累,已造成全球范围的土壤和水资源污染.目前,关于锰氧化物转化阿特拉津的研究主要集中在化学源锰氧化物,而生物源锰氧化物的转化研究尚处在起步阶段.在本研究中,首先利用Mn(Ⅱ)氧化细菌Providencia manganoxydans LLDRA6制备了生物源锰氧化物,对其进行了X射线粉末衍射(XRD)以判断锰氧化物类型;进一步对其转化阿特拉津过程中的五种活性氧(O_(2)^(·−)、·OH、^(1)O_(2)、H_(2)O_(2)和NO)的含量进行了测定;最后通过自由基淬灭试验和电子顺磁共振(EPR)分析了不同自由基对阿特拉津转化的影响.结果表明,LLDRA6产生的锰氧化物为方铁锰矿型生物源Mn_(2)O_(3)(Bio-Mn_(2)O_(3)),并且具有较强的阿特拉津转化能力.在Bio-Mn_(2)O_(3)转化阿特拉津过程中,经化学法检测到有明显的O2^(·−)、·OH和NO产生,但未检测到^(1)O_(2)和H_(2)O_(2).自由基淬灭和EPR分析发现,O2^(·−)不能有效转化阿特拉津,而^(1)O_(2)和·OH发挥了转化阿特拉津的作用,其中^(1)O_(2)是Bio-Mn_(2)O_(3)转化阿特拉津时起主要作用的自由基.

不同种类秸秆添加对稻田NH_(3)挥发的影响机制

秸秆还田对稻田土壤NH_(3)挥发可产生影响,但相关排放变化规律和调控机制有待系统研究。以南粳46水稻品种为材料,太湖地区典型单季稻田原状土为研究对象,利用连续气流封闭法监测三种秸秆(水稻秸秆:RS;小麦秸秆:WS;玉米秸秆:MS)两种添加量(W秸秆:W_土=0.5%、0.8%)下水稻各生长期NH_(3)挥发通量、土壤理化因子及水稻产量;进而结合分子生物学技术,将环境因子与氮循环相关的功能微生物丰度进行耦合,揭示NH_(3)挥发对不同种类秸秆和不同添加量的响应机制并解析关键因子,从而筛选出稻田生态系统氨减排效果最佳的秸秆还田种类及施用量。试验结果表明,秸秆种类及秸秆种类与其施用量交互作用对稻田土壤NH_(3)挥发均产生显著影响,总体来看,与CK相比,施加秸秆处理NH_(3)挥发变化幅度为-33.2%—27.3%。不同秸秆种类对稻田土壤NH_(3)挥发影响不同,低添加量下,与CK相比,RS与WS施用对NH_(3)挥发量均无显著影响,而MS施用显著增加NH_(3)挥发量21.1%;高添加量下,RS施用显著降低NH_(3)挥发量33.2%。不同秸秆施加量对稻田土壤NH_(3)挥发影响亦不同,RS和MS处理下稻田NH_(3)挥发量随施用量的增加分别降低31.2%和32.8%,而WS处理则呈现相反规律;不同秸秆种类及不同施加量交互作用下RS-0.8处理显著降低稻田土壤NH_(3)挥发33.2%。田面水pH、总氮(TN)浓度、土壤微生物量碳含量(MBC)、土壤氨氧化古菌(AOA)和氨氧化细菌(AOB)群落丰度是导致不同秸秆种类和用量下稻田土壤NH_(3)挥发产生差异的主要影响因素;RS-0.8处理相较于其他处理显著增加土壤AOA、AOB群落丰度并显著降低田面水TN含量,综合效应下显著减少稻田NH_(3)挥发量33.2%,并显著增加水稻产量22.9%。因此,综合稻田NH_(3)挥发总量和水稻产量,秸秆施用水稻种植体系中水稻(RS)秸秆以0.8%施用量模式下减排增产效果最佳。

铜含量对Cu-SAPO-34催化剂NH_(3)选择性催化还原NO_(x)的影响

针对分子筛催化剂低温活性不佳的问题,采用一锅法原位合成了具有不同Cu负载量的Cu-SAPO-34催化剂,研究了催化剂的表面性质、Cu物种分布及种类对Cu-SAPO-34低温活性的影响,探究了NH_(3)选择性催化还原NO_(x)(NH_(3)-SCR)的反应机理。研究结果表明,原位合成有利于SAPO-34骨架稳定,适量的Cu可以使所制备的催化剂具有多级孔道结构并以微孔为主导,有利于SCR反应。丰富的ZCuOH位点和稳定的酸位使0.2 Cu-SAPO-34催化剂具有优异低温SCR活性。经过机理分析发现,SCR反应在0.2 Cu-SAPO-34催化剂上遵循Eley-Rideal和Langmuir-Hinshelwood两种反应机理,并且在低温端时Eley-Rideal机理占主导地位。

NOX2通过干预ROS介导的PI3K/AKT信号通路对多发性骨髓瘤细胞能量代谢重编程的作用

目的探讨烟酰胺腺嘌呤二核苷酸磷酸氧化酶2(NOX2)通过干预活性氧(ROS)介导的磷脂酰肌醇3激酶/蛋白激酶B(PI3K/AKT)信号通路对多发性骨髓瘤(MM)细胞能量代谢重编程的作用。方法收集2019年4月-2022年4月蚌埠医学院第一附属医院收治的50例MM患者骨髓血为MM组,同时收集29例健康正常人骨髓血为对照组,qRT-PCR检测骨髓血NOX2、PI3K相对表达、MM细胞系U266、LP-1的NOX2相对表达水平,分析NOX2与PI3K表达水平、NOX2表达水平与临床病理特征的相关性。WB检测U266、LP-1细胞PI3K/AKT信号通路相关分子表达水平,2′,7′-二氯二氢荧光素二乙酯(DCFH-DA)荧光探针检测细胞ROS水平,2-N(7-硝基苯-2-乙二酸,3-4羟氨基)-2-脱氧葡萄糖(2-NBDG)检测细胞葡萄糖摄取能力,生化实验检测细胞乳酸分泌水平,Seahorse检测细胞代谢情况,通过CCK-8、EdU法、划痕、Transwell实验与体内异种移植实验检测细胞增殖、迁移、侵袭及成瘤能力,免疫组化检测移植瘤NOX2、PI3K/AKT信号通路及糖酵解相关分子表达情况。结果NOX2表达水平在MM患者骨髓血、MM细胞系中均升高。相关性分析结果显示,MM患者骨髓血NOX2与PI3K表达水平呈正相关,ISS分期、β2-微球蛋白、Durie-Salmon分期与NOX2表达水平相关(均P<0.05)。与NC组、sh-NC组相比,NOX2组p-PI3K、p-AKT表达水平升高,sh-NOX2组p-PI3K、p-AKT表达水平降低(均P<0.05)。与NC组相比,NOX2组ROS水平、2-NBDG荧光强度、细胞乳酸分泌水平、细胞外酸化率、糖酵解能力、增殖、迁移、侵袭能力升高,移植瘤体积、质量增大,肿瘤乳酸脱氢酶A(LDHA)、3-磷酸肌醇依赖性蛋白激酶1(PDK1)、p-PI3K、p-AKT表达水平升高(均P<0.05)。结论NOX2在MM患者骨髓血与细胞系中高表达,可能通过促进ROS生成激活PI3K/AKT信号通路,促进MM细胞能量代谢重编程与恶性生物学行为,进而推动MM发展。

Organogermanium (Ge-132) Suppresses Activities of Stress Enzymes Responsible for Active Oxygen Species in Monkey Liver Preparation

Assays of stress enzymes related to active oxygen species were performed by using an in vitro preparation from the liver of a monkey (Japanese Macaque). Ge-132, an organic germanium compound, viz. poly-trans-[(2-carboxyethyl) germasesquioxane] [(GeCH2CH2COOH)2O3]n, suppressed the activities of NADH-dependent oxidase and NADPH-dependent oxidase [NAD(P)H-OD] and xanthine oxidase (XOD) as superoxide-forming enzymes, while promoting the activities of superoxide dismutase (SOD) as a superoxide-scavenging enzyme and catalase (CAT) as an enzyme responsible for degradation of hydrogen peroxide (H2O2). The evidence suggests that the levels of active oxygen species such as and H2O2 would be reduced by Ge-132. The possible connection between Ge-132 and activities of stress enzymes is discussed on the basis of these results.

Study of Reactivity of Oxygen Species on SmMO_3(M=Mn,Fe)by TDS and TPRS

With O_2 and CO as the molecular probes,the reactivity of oxygen species of perovskite-like oxides SmMnO_3 and SmFeO_3 was studied by thermodesorption spectroscopy(TDS)and temperature- programmed reaction spectroscopy(TPRS)in an ultrahigh vacuum system.The results of the experiment implied that the oxidation of CO on SmMO_3 may follow Langmuir-Hinshelwood mechanism.

Ca and Sr co-doping induced oxygen vacancies in 3DOM La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)catalysts for boosting low-temperature oxidative coupling of methane

It is urgent to develop catalysts with application potential for oxidative coupling of methane(OCM)at relatively lower temperature.Herein,three-dimensional ordered macro porous(3 DOM)La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)(A_(2)B_(2)O_(7)-type)catalysts with disordered defective cubic fluorite phased structure were successfully prepared by a colloidal crystal template method.3DOM structure promotes the accessibility of the gaseous reactants(O2and CH4)to the active sites.The co-doping of Ca and Sr ions in La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)catalysts improved the formation of oxygen vacancies,thereby leading to increased density of surface-active oxygen species(O_(2)^(-))for the activation of CH4and the formation of C2products(C2H6and C2H4).3DOM La_(2-x)Sr_(x)Ce_(2-y)CayO_(7-δ)catalysts exhibit high catalytic activity for OCM at low temperature.3DOM La1.7Sr0.3Ce1.7Ca0.3O7-δcatalyst with the highest density of O_(2)^(-)species exhibited the highest catalytic activity for low-temperature OCM,i.e.,its CH4conversion,selectivity and yield of C2products at 650℃are 32.2%,66.1%and 21.3%,respectively.The mechanism was proposed that the increase in surface oxygen vacancies induced by the co-doping of Ca and Sr ions boosts the key step of C-H bond breaking and C-C bond coupling in catalyzing low-temperature OCM.It is meaningful for the development of the low-temperature and high-efficient catalysts for OCM reaction in practical application.

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.

ISOLATION AND PURIFICATION OF METHANE IVf ONOOXYGENASE FROM METHYLOMONAS SPECIES GYJ3

A three—component enzyme system that catalyzes in vivo the oxidation of CH_4 to CH_3OH has been purified with high specific activity from an unusual type I methanotroph through the use of stabilizing reagents.

缬沙坦调节ROS/NLRP3/caspase-1信号通路对缺氧复氧诱导心肌细胞焦亡的影响

目的探究缬沙坦(VAL)调节活性氧(ROS)/核苷酸结合寡聚结构域样受体蛋白3(NLRP3)/胱天蛋白酶1(caspase-1)信号通路对缺氧复氧(H/R)诱导心肌细胞焦亡的影响。方法用浓度为0.1~3.2μmol/L的缬沙坦处理后,H/R处理H9C2细胞,MTT法测细胞活性,筛选缬沙坦最佳浓度;将H9C2细胞分为Control组,H/R组,缬沙坦低、中、高浓度组(VAL-L组、VAL-M组、VAL-H组),缬沙坦高浓度+ROS激活剂组(VAL-H+TMAO组);用JC-1染色法检测细胞线粒体膜电位(MMP)水平;用ELISA法检测H9C2细胞丙二醛(MDA)含量、超氧化物歧化酶(SOD)、乳酸脱氢酶(LDH)、活性氧(ROS)含量;Western blot检测IL-1β、IL-18、NLRP3、caspase-1蛋白表达。结果浓度为0.1~3.2μmol/L的缬沙坦可促进H/R诱导的H9C2细胞增殖,选择缬沙坦浓度为0.4μmol/L、0.8μmol/L、1.6μmol/L进行实验。与Control组相比,H/R组ROS、LDH、MDA、PI阳性率、IL-1β、IL-18、ROS、NLRP3、caspase-1表达水平明显升高,MMP、SOD水平降低(P<0.001);与H/R组比较,VAL-L、VAL-M、VAL-H组H9C2细胞ROS、LDH、MDA、PI阳性率、IL-1β、IL-18、ROS、NLRP3、caspase-1表达水平降低,MMP、SOD水平上升(P<0.001);与VAL-H组比较,VAL-H+TMAO组H9C2细胞ROS、LDH、MDA、PI阳性率、IL-1β、IL-18、ROS、NLRP3、caspase-1表达水平明显上升,MMP、SOD水平下降(P<0.001)。结论缬沙坦可能抑制ROS/NLRP3/caspase-1信号通路抑制H/R诱导心肌细胞焦亡。

长链非编码RNA-MEG3在人心脏微血管内皮细胞缺氧损伤中的作用

目的研究长链非编码RNA-MEG3在人心脏微血管内皮细胞(HCMEC)缺氧损伤中的作用。方法将HCMEC分为对照组、缺氧/复氧(H/R)组及缺氧/复氧联合MEG3敲减(H/R+siMEG3)组。荧光定量PCR检测MEG3及炎性因子的表达情况[白介素1β(IL-β)、IL-6、IL-8、IL-10、肿瘤坏死因子(TNF-α)];CCK-8检测HCMEC细胞的增殖活性;流式细胞术分析细胞凋亡情况;Western blotting检测PI3K/AKT/eNOS信号通路表达变化,ELISA检测一氧化氮(NO)、超氧化物歧化酶(SOD)、血管内皮生长因子(VEGF)和活性氧(ROS)表达水平。结果利用qPCR检测对照组及H/R组细胞MEG3表达,结果发现:H/R组MEG3相对表达倍数[(6.87±0.239)倍]较对照组MEG3表达倍数(1.00±0.026)倍显著升高(n=3,t=42.32,P<0.0001),提示MEG3可能在心脏微血管内皮细胞IRI中起到重要作用。H/R组细胞与对照组比较,细胞增殖活性显著减弱(P<0.01);而H/R+siMEG3组与H/R组比较,细胞增殖活性进步受到抑制(P<0.01)。H/R组较对照组PI3K、AKT及eNOS磷酸化水平显著减低,而H/R+siMEG3组细胞较H/R组磷酸化水平更低(P<0.05)。H/R组与对照组比较,NO、SOD及VEGF显著减低,而ROS水平升高(P<0.05);而H/R+siMEG3组与H/R组比较,NO、SOD及VEGF水平进步下降,ROS升高显著。利用qPCR检测各处理组细胞相关炎症基因表达,结果发现:H/R组较对照组基因表达显著升高(P<0.05);H/R+SiMEG3组较H/R组基因表达进一步升高(P<0.01)。结论长链非编码RNA-MEG3在心脏微血管内皮细胞H/R损伤过程中起到重要保护作用,靶向提升MEG3水平有望成为减缓心脏微血管IRI的潜在治疗靶点。

Ti^(3+)自掺杂的TiO_2(A)/TiO_2(R)/In_2O_3纳米异质结的制备与可见光催化性能

以TiCl_3和InCl_3为Ti源和In源,在不使用还原剂的条件下,首先通过液相沉淀反应制备前驱体沉淀,然后采用后续水热处理制备Ti^(3+)自掺杂的TiO_2(A)/TiO_2(R)/In_2O_3纳米异质结,考察了水热处理温度对材料结构和性能的影响。利用X射线衍射、透射电子显微镜、X射线光电子能谱和紫外-可见漫反射光谱对样品进行表征。分别以罗丹明B和苯酚溶液为模拟废水评价了样品的可见光催化降解性能。结果表明,与纯的TiO_2、In2O_3以及Ti^(3+)自掺杂的TiO_2相比,Ti^(3+)自掺杂的TiO_2(A)/TiO_2(R)/In_2O_3纳米异质结在可见光区有明显的吸收,并具有良好的可见光催化降解性能,200℃下水热处理24h所得样品光催化降解罗丹明B的反应速率常数(0.0444min-1)分别是纯TiO_2和In_2O_3的17.76倍和8.71倍。瞬态光电流时间响应结果表明样品的光催化性能主要来源于TiO_2(A)/TiO_2(R)/In_2O_3纳米异质结导致的提高的光生电子和空穴分离效率。