黄芪多糖在LPS诱导的DF-1细胞炎症反应中的抗炎作用及其调节机制

为探讨黄芪多糖(Astragalus polysaccharide,APS)在LPS(lipopolysaccharide,LPS)诱导的鸡胚成纤维细胞系DF-1(chicken embryonic fibroblast cell line,DF-1)炎症模型中对IL-1β和TNF-α表达的影响,以及细胞因子信号转导抑...     

水资源联合调度模型在额济纳绿洲生态环境建设中的应用

对日趋缺水的额济纳绿洲,进行河水与地下水进行联合运用的目的是:减少水资源浪费,恢复生态水位,保护绿洲。按照国家水利部(1997)496号文件:《现状工程条件下黑河干流水量分配方案》(简称“97甘蒙分水方案),不同保证率下分配给内蒙古的水量。根据狼心山水文断面入境水量丰枯变化的分析结果,建立水资源联合调度模型,对四种不同来水方案进行计算。结果表明,执行“甘蒙分水”,采用内蒙长衬砌渠道输水,当保证率P=50%时,入境狼心山水量为7.527×108m3,到2020年地下水位埋深回升到2.35m,相应绿洲面积将扩大到5005.01km2,绿洲植被总盖度可达到58%。基本满足天然非灌溉林草的需水,逐步回补到生态要求的限定水位,使绿洲逐步得到恢复。     

萘和p,p′-DDE在典型包气带介质上的吸附动力学及吸附-解吸特征

选取3种典型包气带土壤为吸附剂,萘和p,p′-DDE为吸附质,研究了其吸附动力学特征及吸附解吸规律。实验结果显示,初始浓度越大,吸附到达平衡所需时间就越短。数据拟合结果表明,单一级次的动力学方程难以描述两种吸附质的吸附动力学特征,分析认为土壤对有机污染物的吸附过程不是单一反应,而是有机污染物在无机矿物、无定型有机碳和凝聚型有机碳上同时进行吸附反应的复合结果。萘与p,p′-DDE的吸附、解吸过程均表现出非线性,Freundlich方程的吸附指数n在不同程度上偏离1;两种污染物在土样中的吸附过程不完全可逆,Kow、初始浓度以及土壤有机碳含量（fo）c的差异都影响其在土壤不同组分上的吸附百分比,进而影响解吸率。萘更多地吸附在无机矿物表面及无定型有机碳上,随着初始浓度的增大（37.7~780.9μg.L-1）,解吸率可从10%左右增至近85%;而当初始浓度为37.7μg.L-1时,随foc的增大（0.01%~0.65%）,解吸率由12.39%降至3.90%。p,p′-DDE则更多地吸附在凝聚型有机碳上,解吸率随浓度的变化（11.0~275.1μg.L-1）仅在1%~5%内波动,当初始浓度为11.0μg.L-1时,解吸率随foc的增大由4.49%降至1.06%。两者解吸率都和foc呈负相关关系。     

黑麦草（Lolium perenne）根际细菌多样性对Ni污染沉积物修复效果的响应

应用黑麦草（Lolium perenne）对某滨海城市南排污河的重金属污染沉积物——底泥进行植物修复,并结合变性梯度凝胶电泳（DGGE）分析了黑麦草根际土壤的重金属Ni含量和细菌多样性的关系。结果表明,黑麦草对Ni的修复效果较好,种植黑麦草后根际土壤Ni浓度降低了11.8%。根际土壤中Ni有效态含量与根际土壤pH值的变化呈较好的正相关关系,相关系数为0.968 8。对根际土壤细菌多样性进行分析,重金属Ni含量变化能够影响土壤细菌的多样性,根际土壤细菌多样性随黑麦草的生长而不断演变,且与根际土壤中Ni浓度变化有密切联系。对DGGE电泳后回收的部分片段进行测序并建立了进化树,结果表明,测序片段与非培养方法得到的菌种的同源性较高,且其均在土壤或河道底泥的相关研究中被发现。不同时期细菌群体组成和Shannon指数随着修复时间而变化,并与细菌总数有正相关关系。     

菠萝锌指蛋白基因AcRCHY1的克隆与表达分析

 根据植物C3HC4型兼CHY型锌指蛋白的功能保守区设计简并引物, 通过RT2PCR结合RACE 方法从菠萝(Ananas comosus L. Merr) 幼苗中克隆获得了一个新的菠萝锌指蛋白基因cDNA全长, 将其命名为AcRCHY1。该基因cDNA全长1 261 bp, 开放阅读框ORF为918 bp, 推测其编码一个含有306个氨基酸残基的多肽。AcRCHY1蛋白具有保守的C3HC4 (RING finger) 和CHY两个锌指结构域, 与其它植物锌指蛋白的同源性高达81%～91%。半定量RT-PCR分析表明, AcRCHY1 在菠萝中呈组成性表达, 在子房、花瓣和小花中的表达量明显高于根和叶; 低温、高盐、干旱和ABA等非生物胁迫处理后, AcRCHY1在叶片中的表达明显增强。因此, AcRCHY1蛋白可能与花器官生长发育的调控有关, 而且可能作为一个转录调控因子在菠萝响应低温、高盐和渗透胁迫过程中参与了依赖ABA的信号转导途径。     

MicroRNA-142-3p modulates atherosclerosis-associated endothelial cell apoptosis via targeting Rictor

AIM To investigate the role of microRNA-142-3p （miR-142-3p） in endothelial cell apoptosis during atherosclerosis （AS） and the underlying mechanism. METHODS Human aortic endothelial cells （HAECs） were treated with oxidized low-density lipoprotein （ox-LDL）. The expression level of miR-142-3p was detected by RT-qPCR. Apoptosis was determined via flow cytometry （FCM） and caspase-3 activity assay. Prediction of the binding site between miR-142-3p and 3’-UTR of Rictor mRNA was performed by bioinformatics analysis and confirmed by dual-luciferase reporter assay. RESULTS The expression of miR-142-3p was substantially up-regulated during the ox-LDL-elicited apoptosis in HAECs （P<0.05,P<0.01）. Forced expression of miR-142-3p exacerbated apoptosis in HAECs whereas inhibition of miR-142-3p partly alleviated apoptotic cell death mediated by ox-LDL. Further analysis identified Rictor as a direct target gene of miR-142-3p, and Rictor knock-down abolished the anti-apoptotic effect of miR-142-3p inhibitor. Moreover, the Akt/endothelial nitric oxide synthase （eNOS） signaling pathway was found to mediate the beneficial effect of miR-142-3p inhibitor on endothelial cells apoptosis. CONCLUSION Down-regulation of miR-142-3p inhibits endothelial cell apoptosis and atherosclerotic development by up-regulating the expression of Rictor and activating the Akt/eNOS signaling pathway.     

Effect of lncRNA FEZF1-AS1 on viability and apoptosis of LPS-induced vascular endothelial cells by regulating miR-363-3p expression

AIM To investigate the mechanism of long noncoding RNA （lncRNA） FEZF1-AS1 regulating microRNA-363-3p （miR-363-3p） on the viability and apoptosis of lipopolysaocharide （LPS）-induced vascular endothelial cells. METHODS Human umbilical vein endothelial cells （HUVECs） were cultured in vitro. pcDNA-NC, pcDNA-FEZF1-AS1, anti-miR-NC, anti-miR-363-3p, miR-NC and miR-363-3p mimics were transfected into the HUVECs and LPS stimulation was applied for 24 h. RT-qPCR was used to detect the expression of FEZF1-AS1 and miR-363-3p. The cell viability was measured by MTT assay. The apoptotic rate was analyzed by flow cytometry. The dual-luciferase reporter experiment was used to verify the targeted regulation of FEZF1-AS1 and miR-363-3p. Western blot was used to determined the expression of cyclin D1, Ki67 and cleaved caspase-3. RESULTS Compared with control group, the expression level of FEZF1-AS1 in LPS group was significantly reduced （P<0.05）, and the expression level of miR-363-3p was significantly increased （P<0.05）. Compared with pcDNA-NC+LPS group, the cell viability in pcDNA-FEZF1-AS1+LPS group was significantly increased （P<0.05）, the apoptotic rate was significantly reduced （P<0.05）, the protein levels of cyclin D1 and Ki67 were significantly increased （P<0.05）, and the protein level of cleaved caspase-3 was significantly reduced （P<0.05）. Compared with anti-miR-NC+LPS group, the cell viability in anti-miR-363-3p+LPS group was significantly increased （P<0.05）, the apoptotic rate was significantly reduced （P<0.05）, the protein levels of cyclin D1 and Ki67 were significantly increased （P<0.05）, and the protein level of cleaved caspase-3 was significantly reduced （P<0.05）. Dual-luciferase reporter experiment confirmed that FEZF1-AS1 targeted miR-363-3p. Compared with miR-NC+pcDNA-FEZF1-AS1+LPS group, the cell viability in miR-363-3p+pcDNA-FEZF1-AS1+LPS group was significantly reduced （P<0.05）, the apoptotic rate was significantly increased （P<0.05）, the protein levels of cyclin D1 and Ki67 were significantly reduced （P<0.05）, and the protein level of cleaved caspase-3 was significantly increased （P<0.05）. CONCLUSION Over-expression of FEZF1-AS1 promotes the viability and inhibits apoptosis of LPS induced vascular endothelial cells by inhibiting the expression of miR-363-3p.     

miR-140-3p inhibits viability,invasion and migration of non-small-cell lung cancer A549 cells by targeting PD-L1

AIM: To explore the target relationship between microRNA-140-3p (miR-140-3p) and programmed cell death ligand 1 (PD-L1) and their effect on the viability, migration and invasion of non-small-cell lung cancer A549 cells.METHODS: RT-qPCR was used to detect the miR-140-3p expression in HLF-1, A549 and H1299 cells, and then the A549 cells with the most significant difference were selected as the subsequent research object. TargetScan software and dual-luciferase reporter assay were performed to predict and confirm the target relationship between miR-140-3p and PD-L1. RT-qPCR and Western blot were used to determine the effects of miR-140-3p mimic and inhibitor on PD-L1 expression level. MTT assay was used to detect the viability of A549 cells. Transwell assay was performed to detect the migration and invasion abilities of the A549 cells.RESULTS: miR-140-3p was significantly down-regulated in the A549 cells and H1299 cells (P<0.05). Transfection with miR-140-3p mimic decreased the expression of PD-L1 and inhibited the viability, migration and invasion of the A549 cells. Transfection with pcDNA3.0-PD-L1 reversed the inhibitory effect of miR-140-3p on the viability, migration and invasion of the A549 cells.CONCLUSION: miR-140-3p inhibits the viability, migration and invasion of A549 cells by targeting PD-L1.     

Ethanol extract from Cortex Albiziae attenuates mouse acute liver injury induced by carbon tetrachloride via modulation of NF-κB pathway

AIM:To investigate the protective effect of ethanol extract from Cortex Albiziae on acute liver injury, and to explore its possible mechanism. METHODS:Acute liver injury in mice was induced by single intraperitoneal injection of 25% carbon tetrachloride (olive oil solubilization). The effective parts of ethanol extract from Cortex Albizziae against acute liver injury were screened. The pathological changes of the liver tissues were examined by pathological sections with HE staining. The activity of total superoxide dismutase (T-SOD) and the content of malondialdehyde (MDA) of the liver tissues were detected, the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were mea-sured by ELISA, and the protein expression levels of NF-κB p65, Bcl-2 and Bax in the liver cells of the mice in each group were determined by Western blot. RESULTS:Compared with model group, the serum levels of AST and ALT in low-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-L, 4 mg·kg^-1·d^-1) group and high-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-H, 8 mg·kg^-1·d^-1) group were significantly decreased. The necrosis extent and degree of the hepatocytes and infiltration of inflammatory cells were significantly lower than that in model group. Compared with model group, the serum levels of TNF-α and IL-6 in AB-H group and AB-L group were significantly decreased (P<0.05). The protein level of NF-κB p65 in the nuclei of mouse liver cells in AB-H group and AB-L group were also decreased significantly (P<0.05). Compared with model group, the protein expression of Bax was decreased, the protein expression of Bcl-2 was increased, and the Bcl-2/Bax ratio was increased in AB-L group and AB-H group. CONCLUSION:The n-butanol phase of ethanol extract from Cortex Albiziae may protect the liver by reducing the activation of NF-κB p65, inhibiting the excessive release of inflammatory cytokines IL-6 and TNF-α, and decreasing hepatocyte apoptosis via regulating Bcl-2 and Bax expression.