褪黑素对PM 2.5暴露大鼠肺部炎症反应和氧化应激的影响

为探讨褪黑素对大气细颗粒物(PM 2.5)暴露大鼠肺部炎症反应和氧化应激的影响及其机制,本实验将48只清洁级SD大鼠随机(随机数字法)分成4组:空白对照组、NS对照组、PM 2.5组及褪黑素(MT)组,通过气管向肺内注入PM 2.5悬液构建大鼠肺组织PM 2.5染毒模型,并通过灌胃MT溶液,采用肺组织HE染色、ELISA法及蛋白印迹等方法分别检测肺组织病理改变、TNF-α、IL-6、IL-1、MPO、SOD及MDA表达以及NF-κBp65蛋白表达。结果显示:(1)与空白对照组及NS对照组比较,PM 2.5组大鼠肺组织出现明显损伤改变,MT组大鼠肺组织损伤较PM 2.5组明显减轻;(2)PM 2.5组大鼠肺组织TNF-α、IL-6、IL-1表达出现明显增加(p0.05),MT组较PM 2.5组TNF-α、IL-6、IL-1表达明显下降(p0.05);(3)PM 2.5组大鼠肺组织SOD表达较空白对照组及NS对照组明显下降(p0.05),而MPO及MDA表达明显增加(p0.05),而与PM 2.5组比较,MT组大鼠肺组织SOD表达出现增加,MPO及MDA表达下降(p0.05);(4)PM 2.5组P65蛋白表达出现明显上调(p0.05),而MT组较PM 2.5组P65蛋白表达出现明显下降(p0.05)。由此得出结论,PM 2.5能通过介导肺组织炎性反应及氧化应激导致肺组织损伤,且与活化NF-κB相关,褪黑素能显著抑制PM 2.5所致NF-κB活化,减轻炎性反应及氧化应激,改善PM 2.5暴露大鼠肺损伤。     

丹皮酚对PM2.5诱导的支气管上皮细胞IL-8表达的影响

目的:观察丹皮酚对PM2.5诱导支气管上皮细胞(BEAS-2B)分泌IL-8的影响。方法:BEAS-2B细胞传代培养,分别加入丹皮酚(15μmol/L、30μmol/L)预处理1 h,ELISA法检测不同浓度的PM2.5悬液(25μg/m L、50μg/m L、100μg/m L)对BEAS-2B细胞分泌IL-8蛋白的影响。结果:随着PM2.5悬液浓度的升高,BEAS-2B细胞上清液中IL-8水平逐渐增高;丹皮酚干预后能够显著降低BEAS-2B细胞上清液中IL-8水平(P0.05),并呈浓度依赖性。结论:丹皮酚具有抑制PM2.5诱导的BEAS-2B细胞分泌IL-8蛋白表达的作用,并呈浓度依赖性。     

肿瘤坏死因子α对大鼠骨髓间充质干细胞生物学特性的影响

目的:探讨不同浓度肿瘤坏死因子α(TNF-α)对大鼠骨髓间充质干细胞(BMSCs)生物学特性的影响。方法:采用全骨髓贴壁法分离培养大鼠BMSCs,倒置显微镜观察细胞形态学变化,流式细胞仪检测BMSCs表面标记物;分别以10、100、1000 ng/mL的TNF-α完全培养液预处理P3代BMSCs,并设置仅含培养基的空白对照组,24 h后采用ELISA试剂盒检测细胞培养上清液中IL-6、IL-10的表达水平;胰酶消化细胞,用Presto Blue法检测10、100、1000 ng/mL TNF-α完全培养液预处理BMSCs后细胞增殖活性。结果:ELISA检测结果显示,与对照组相比,各浓度TNF-α干预组IL-6、IL-10均有不同程度升高,差异有统计学意义(P0.05),且1000 ng/mL TNF-α干预组IL-10表达水平最高,其浓度为170.2±11.9 pg/mL,组间比较差异有统计学意义(P0.05);100 ng/mL TNF-α干预组IL-6表达水平最高,其浓度为144.0±18.6 pg/mL,组间比较差异有统计学意义(P0.05)。Presto Blue检测结果显示,与对照组相比,10、100、1000 ng/mL TNF-α干预组荧光值均增高,差异有统计学意义(P0.05),但组间荧光值比较差异无统计学意义(P0.05)。结论:10~1000 ng/mL TNF-α可促进BMSCs的增殖,且随着TNF-α浓度的升高,BMSCs分泌促炎因子IL-6的能力降低,分泌抑炎因子IL-10的能力升高。     

核转录因子NF-E2相关因子2信号通路在PM_(2.5)致雌性大鼠生殖损伤中的作用

目的研究核转录因子NF-E2相关因子2(NF-E2 related factor 2, Nrf-2)信号通路在PM_(2.5)雌性生殖损伤中的作用。方法 30只雌性SD大鼠随机分为生理盐水对照组、1.5 mg/kg PM_(2.5)低剂量组和37.5 mg/kg PM_(2.5)高剂量组,连续暴露染毒10 d。ELISA试剂盒检测子宫中肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)、白介素-1β(interleukin 1 beta, IL-1β)和白介素-6(interleukin-6, IL-6)含量。荧光定量PCR (qPCR)检测子宫组织Nrf-2和血红素加氧酶-1(heme oxygenase-1, HO-1)mRNA表达水平。Western blot检测子宫组织Nrf-2和HO-1蛋白表达水平。结果低剂量组和高剂量组子宫TNF-α、IL-1β和IL-6含量均明显高于对照组(P0.05);与低剂量组相比,高剂量组子宫TNF-α、IL-1β和IL-6含量明显升高,差异有显著性(P0.05);且子宫组织炎性因子含量与PM_(2.5)暴露量正相关,随着PM_(2.5)暴露浓度的升高,TNF-a、IL-1β和IL-6含量不断升高(r=0.870、0.847和0.855)。荧光定量PCR和western blot检测结果显示,低剂量组和高剂量组子宫组织中Nrf-2和HO-1的mRAN表达水平和蛋白表达水平均明显高于对照组,差异有显著性(P0.05)。结论雌鼠暴露PM_(2.5)后,Nrf-2信号通路被激活,但PM_(2.5)依然能诱发子宫炎症反应,造成子宫组织损伤。     

白术内酯Ⅱ逆转M2型巨噬细胞极化调控PDL1表达抑制A549细胞迁移

探究白术内酯Ⅱ(atractylenolideⅡ,AT-Ⅱ)对M2型巨噬细胞极化与A549细胞迁移能力的影响,并分析其潜在机制。利用PMA将THP-1细胞诱导成M0巨噬细胞,然后加入IL-4和IL-13继续诱导为M2型巨噬细胞。利用Transwell小室将M2型巨噬细胞与A549细胞共培养,分别给予0、2.5、5μmol/L的AT-Ⅱ进行作用。采用MTT实验测定共培养条件下AT-Ⅱ对A549细胞活力的影响;采用Real-time PCR检测M2型巨噬细胞Arg-1的mRNA表达水平;采用ELISA检测共培养体系中TNF-α、IL-1β的含量;采用WB检测A549细胞TLR4、p-p65、NF-κB(p65)、PDL1的蛋白表达水平;采用划痕实验检测A549细胞的迁移能力。结果显示,共培养条件下,与对照组相比,实验组(2.5、5μmol/L)A549细胞活力降低(2.5μmol/L组P>0.05、5μmol/L组P<0.01);M2型巨噬细胞特异性基因Arg-1的mRNA表达水平显著降低(P<0.01);M1型巨噬细胞相关炎性因子TNF-α、IL-1β含量增多但无显著差...     

红景天苷通过调节p38和JNK信号通路抑制BV-2细胞分泌炎性因子

红景天苷是传统中药红景天的主要成分,已有研究显示红景天苷具有一定的抗炎性作用。本研究旨在探讨红景天苷对BV-2细胞炎性反应的调节作用及可能机制。实验分为对照组、脂多糖(lipopolysaccharide,LPS)组、红景天苷组、红景天苷预处理+LPS组,用100μg/L LPS和/或10 mg/L红景天苷处理BV-2细胞,收集细胞培养基上清(条件培养基),采用real-time PCR方法检测细胞IL-6和TNF-αm RNA表达水平,ELSIA方法检测培养基IL-6和TNF-α含量,条件培养基处理PC12细胞24 h后,Hoechst 33258染色检测细胞核形态学改变,cell counting kit 8(CCK-8)试剂盒检测细胞活力,免疫印迹方法检测BV-2细胞p38和JNK的磷酸化水平。结果表明100μg/L LPS处理可显著提高BV-2细胞内IL-6和TNF-α的表达水平(P0.05)。红景天苷可显著下调LPS诱导的BV-2细胞IL-6和TNF-α表达量(P0.05),下调p38和JNK的磷酸化水平(P0.05)。SB202190和SP600125可降低LPS引起的IL-6和TNF-α表达,与红景天苷共处理后可拮抗LPS的诱导效应。与LPS组相比,红景天苷预处理+LPS组的条件培养基处理后,PC12细胞的细胞活力显著升高(P0.05),同时细胞核固缩和聚集情况减少(P0.05)。以上结果提示,红景天苷可在一定程度上抑制小胶质细胞活动,通过调节p38和JNK信号通路减少炎性因子释放,从而降低PC12细胞的损伤。     

补肾活血方中单体成分的体外炎性抑制作用研究

本文采用LC-MS技术进行定性分析,确定补肾活血方水提液中存在芍药苷、阿魏酸、白藜芦醇、蛇床子素及补骨脂素等单体化合物。利用酶联免疫法(ELISA)测定试药对模型细胞释放TNF-α、IL-6及NO的抑制作用。与空白组比较,模型组TNF-α、IL-6、NO含量明显升高(P0.0);与模型组比较,阿魏酸、白藜芦醇、补骨脂素及复方水提部位在100μg/m L,以及蛇床子素在20、100μg/m L均对TNF-α的释放具有显著的抑制(P0.01);阿魏酸及补骨脂素在100μg/m L,白藜芦醇及蛇床子素在20、100μg/m L均对IL-6水平具有显著的抑制(P0.01);芍药苷及复方水提部位在100μg/m L,阿魏酸、白藜芦醇、蛇床子素及补骨脂素在20、100μg/m L均对NO的释放具有显著抑制(P0.01)。结果表明单体对炎性因子的释放抑制作用总体上强于复方水提部位,提示补肾活血方的治疗骨关节炎活性可能是通过抑制炎症介质释放,降低TNF-α、IL-6、NO等含量发挥作用,这对验证复方药效活性,探究效应物质基础具有重要意义。     

PM2.5对人Ⅱ型肺泡上皮细胞A549的作用及机制研究

随着工业化、城市化的飞速发展,空气污染加剧, PM2.5浓度越来越高,对人类的危害也越来越大。由于多数病原体可以直接进入下呼吸道,所以肺的抗炎作用显得尤为重要。大量的资料显示, Ⅱ型肺泡上皮细胞(AECⅡ)是一类具有干细胞潜能、自我更新、参与肺纤维化的多功能细胞。A549是人肺腺癌上皮细胞,其可以合成卵磷脂,并且含有高度不饱和脂肪酸,这对于维持细胞膜磷脂有重要意义。目前, A549细胞被广泛作为Ⅱ型肺泡上皮细胞的体外模型。该文以A549为模型,从PM2.5对A549细胞诱导型一氧化氮合酶合成、各种炎性因子分泌和对细胞自噬和凋亡的影响以及对A549细胞迁移、侵袭能力的增强四个方面展开介绍,就A549在PM2.5作用下的功能机制作一综述。     

补肾活血方中单体成分的体外炎性抑制作用研究北大核心CSCD

本文采用LC-MS技术进行定性分析,确定补肾活血方水提液中存在芍药苷、阿魏酸、白藜芦醇、蛇床子素及补骨脂素等单体化合物。利用酶联免疫法(ELISA)测定试药对模型细胞释放TNF-α、IL-6及NO的抑制作用。与空白组比较,模型组TNF-α、IL-6、NO含量明显升高(P<0.0);与模型组比较,阿魏酸、白藜芦醇、补骨脂素及复方水提部位在100μg/m L,以及蛇床子素在20、100μg/m L均对TNF-α的释放具有显著的抑制(P<0.01);阿魏酸及补骨脂素在100μg/m L,白藜芦醇及蛇床子素在20、100μg/m L均对IL-6水平具有显著的抑制(P<0.01);芍药苷及复方水提部位在100μg/m L,阿魏酸、白藜芦醇、蛇床子素及补骨脂素在20、100μg/m L均对NO的释放具有显著抑制(P<0.01)。结果表明单体对炎性因子的释放抑制作用总体上强于复方水提部位,提示补肾活血方的治疗骨关节炎活性可能是通过抑制炎症介质释放,降低TNF-α、IL-6、NO等含量发挥作用,这对验证复方药效活性,探究效应物质基础具有重要意义。     

EGCG通过STAT3抑制血管内皮细胞炎性因子表达

[目的]研究茶多酚EGCG对脂多糖(LPS)诱导的血管内皮细胞炎性因子表达的抑制作用及其机制。[方法]利用MTT和流式检测LPS和EGCG对血管内皮细胞的毒性作用,实时荧光定量PCR检测炎性因子mRNA的水平,多重液相蛋白定量技术检测炎性因子的蛋白表达,Western Blot检测STAT3及其磷酸化水平。[结果]EGCG最大浓度(100μmol/L)对血管内皮细胞无毒性;LPS处理可显著或极显著诱导炎性因子(TNF-α、IL-1β、IL-6和IL-8)在mRNA和蛋白水平的表达(P<0.05或P<0.01),LPS对炎性因子的促进作用具有剂量效应;25μmol/L或50μmol/L EGCG预处理能极显著抑制LPS诱导的血管内皮细胞炎性因子的表达(P<0.01),同时抑制LPS诱导的STAT3磷酸化;STAT3抑制剂能显著增强EGCG抗炎效果。[结论]EGCG通过STAT3通路抑制LPS诱导的血管内皮细胞炎症因子的表达。     

Contribution of IL-1 beta and TNF-alpha to the initiation of the peripheral lung response to atmospheric particulates (PM10)

Alveolar macrophages (AM) play a key role in clearing atmospheric particulates from the lung surface and stimulating epithelial cells to produce proinflammatory mediators. The present study examines the role of "acute response" cytokines TNF-alpha and IL-1 beta released by AM exposed to ambient particulate matter with a diameter of <10 microm (PM(10)) in amplifying the proinflammatory mediator expression by A549 cells and human bronchial epithelial cells (HBEC). The results showed that supernatants from human AM incubated 24 h with PM(10) (100 microg/ml) contained more TNF-alpha, IL-1 beta, granulocyte-macrophage colony stimulating factor, IL-6, and IL-8 than nonexposed AM supernatants. The 3-h treatment of A549 cells with PM(10)-exposed AM supernatants increased TNF-alpha, IL-1 beta, IL-8, regulated on activation normal T-cells expressed and secreted (RANTES), and leukemia inhibitory factor mRNA compared with the treatment with nonexposed AM supernatants and, compared with untreated A549 cells, additionally increased ICAM-1 and monocyte chemotactic protein-1 mRNA. Preincubating PM(10)-exposed AM supernatants with anti-IL-1 beta antibodies reduced all the above mediators as well as VEGF mRNA expression (P < 0.05), while anti-TNF-alpha antibodies were less effective (P > 0.05), and the combination of the two antibodies most effective. When HBEC were treated similarly, anti-TNF-alpha antibodies had the greatest effect. In A549 cells PM(10)-exposed AM supernatants increased NF-kappa B, activator protein (AP)-1 and specificity protein 1 binding, while anti-TNF-alpha and anti-IL-1 beta antibodies reduced NF-kappa B and AP-1 binding. We conclude that AM-derived TNF-alpha and IL-1 beta provide a major stimulus for the production of proinflammatory mediators by lung epithelial cells and that their relative importance may depend on the type of epithelial cell target.     

Transcriptomic Analyses of the Biological Effects of Airborne PM2.5 Exposure on Human Bronchial Epithelial Cells

Epidemiological studies have associated high levels of airborne particulate matter (PM) with increased respiratory diseases. In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm² PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing.     

右美托咪定对子宫肌瘤切除术患者全麻苏醒期应激反应的影响

目的:探讨盐酸右美托咪定用于全凭静脉麻醉对子宫肌瘤切除术患者应激反应的影响。方法:选择我院收治的择期行子宫肌瘤切除术患者60例,随机分为观察组和对照组,每组30例。两组患者均采用全麻,其中观察组患者在麻醉诱导15 min内静脉输注1 ug/kg盐酸右美托咪定注射液,术中0.3-0.6 ug/(kg×h)维持;而对照组患者采用静脉输注0.9%的Nacl溶液。分别于麻醉前、麻醉后及苏醒期测定并观察两组患者外周静脉血中TNF-α,IL-2和IL-6的浓度变化情况。结果:两组患者麻醉前TNF-α,IL-2和IL-6的浓度无显著性差异(P0.05)。两组患者麻醉后及苏醒期TNF-α,IL-2及IL-6浓度均显著高于麻醉前,差异具有统计学意义(P0.05)。观察组患者麻醉后及苏醒期TNF-α,IL-2及IL-6浓度均显著低于对照组,差异具有统计学意义(P0.05)。结论:右美托咪定用于全凭静脉麻醉对子宫肌瘤切除术患者血清TNF-α、IL-2和IL-6浓度具有调节作用,可缓解或降低手术引起的应激反应。     

无锡惠山三种城市游憩林内细颗粒物(PM2.5)浓度变化特征

在2011年秋、冬季和2012年春、夏季的游憩时段内(5:00-19:00),对无锡惠山香樟林、湿地松林和栓皮栎林3种游憩林内PM_2.5质量浓度进行实时监测,并同步观测气象因子,分析了游憩林内PM_2.5浓度的时间变化规律及其影响因素.结果表明: 惠山3种游憩林内PM_2.5浓度年均值低于道路,湿地松林和香樟林内PM_2.5浓度年均值低于栓皮栎林;3种游憩林和道路的PM_2.5年均浓度低于无锡市背景值.游憩林内PM_2.5浓度的季节变化规律为夏季最低,秋季次之,春季最高;PM_2.5浓度在春、夏、冬季最低的是湿地松林,秋季最低的是香樟林,栓皮栎林在各季节的PM_2.5浓度都较高.PM_2.5浓度在四季的日变化近似于“单峰单谷”型,7:00-9:00和15:00-19:00各出现最大值和最小值.4个季节的湿度和温度与PM_2.5浓度均极显著相关,光照仅在冬季显著影响PM_2.5浓度,较小风速对PM_2.5浓度的影响不大.     

Genotoxicity, inflammation and physico-chemical properties of fine particle samples from an incineration energy plant and urban air

Airborne particulate matter (PM) was sampled by use of an electrostatic sampler in an oven hall and a receiving hall in a waste-incineration energy plant, and from urban air in a heavy-traffic street and from background air in Copenhagen. PM was sampled for 1-2 weeks, four samples at each site. The samples were extracted and examined for mutagenicity in Salmonella typhimurium strains TA98, YG1041 and YG5161, for content of inorganic elements and for the presence of eight polycyclic aromatic hydrocarbons. The induction of IL-6 and IL-8 mRNA expression and the presence of DNA damage - tested by the comet assay - were determined after 24-h incubations with human A549 lung epithelial cells. The PM(2.5) concentration was about twofold greater in the oven hall than in the receiving hall. The particle size distribution in the receiving hall was similar to that in street air (maximum mode at about 25nm), but the distribution was completely different in the oven hall (maximum mode at about 150nm). Also chemically, the samples from the oven hall were highly different from the other samples. PM extracts from the receiving hall, street and background air were more mutagenic than the PM extracts from the oven hall. PM from all four sites caused similar levels of DNA damage in A549 cells; only the oven hall samples gave results that were statistically significantly different from those obtained with street-air samples. The receiving hall and the urban air samples were similarly inflammatory (relative IL-8 mRNA expression), whereas the oven hall did not cause a statistically significant increase in IL-8 mRNA expression. A principal component analysis separated the oven hall and the receiving hall by the first principal component. These two sites were separated from street and background air with the second principal component. Several clusters of constituents were identified. One cluster consisted of all the polycyclic aromatic hydrocarbons (PAH), several groups of metals and one group of the biological endpoints (DNA damage, IL-6 and IL-8 mRNA expression). The PAH and the inorganic content of the air in the receiving hall may be due to vehicle emissions and suspended waste particles. The inorganic content in the street and background air may have been influenced by break wear, road emissions and long-range transport. The results from a partial least-square regression analysis predicted that both PAHs and a group of metals including Fe and Mn contributed to IL-6 and IL-8 induction. Only Mn and Sr were predicted to influence DNA damage statistically significantly. Among the PAHs only chrysene had influence on DNA damage. The PM from the oven hall was markedly different from the PM at other locations in particle size distribution, chemical composition and the resulting biological effects when A549 cells were incubated with the PM. These characteristics and observations in the oven hall indicated that the PM source was oven exhaust, which was well combusted.     

The effects of PM10 particles and oxidative stress on macrophages and lung epithelial cells: modulating effects of calcium-signaling antagonists

We have previously examined the ability of air pollution particles (PM(10)) to promote release of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) from human peripheral blood mononuclear cells and demonstrated a role for calcium as a signaling molecule in this process. We have now studied the ability of oxidative stress induced by a synthetic oxidant tert-butyl hydroperoxide (tBHP) to induce TNF-alpha production via calcium signaling in the mouse macrophage cell line (J774). The oxidant tBHP significantly increased intracellular calcium and the release of TNF-alpha in J774 cells, an effect that was reduced to control levels by inhibition of calcium signaling with verapamil, BAPTA-AM, and W-7. This study also investigated interactions between PM(10)-treated macrophages and epithelial cells by using conditioned medium (CM) from PM(10)-treated mononuclear cells to stimulate the release of the neutrophil chemoattractant chemokine IL-8 from A549 lung epithelial cells. TNF-alpha protein release was demonstrated in human mononuclear cells after PM(10) treatment, an effect that was inhibited by calcium antagonists. Treatment of A549 cells with monocyte/PM(10) CM produced increased IL-8 release that was reduced with CM from monocyte/PM(10)/calcium antagonist treatments. The expression of ICAM-1 was increased after incubation with CM from monocyte/PM(10) treatment, and this increase was prevented by treatment with CM from monocyte/PM(10)/calcium antagonist. These data demonstrate a link between oxidative stress, calcium, and inflammatory mediator production in macrophages and lung epithelial cells.     

Particulate matter 2.5 induced bronchial epithelial cell injury via activation of 5′-adenosine monophosphate-activated protein kinase-mediated autophagy

The impact of particulate matter 2.5 (PM2.5) on the respiratory system is a worldwide concern. However, the mechanisms by which PM2.5 causes disease are still unclear. In this study, we investigated the effect of PM2.5 on autophagy and studied the effect of PM2.5-induced autophagy and 5′-adenosine monophosphate-activated protein kinase (AMPK) on cell proliferation, cell cycle, apoptosis, reactive oxygen species (ROS), and airway inflammation using human bronchial epithelial cells 16HBE140 cells. Results showed that exposure of cells to PM2.5 at a concentration of 100 μg/mL for 24 hours was most effective for inhibiting cell viability. PM2.5 induced cell arrest in the G0/G1 phase and increased mitochondrial membrane potential, ROS, and cell apoptosis with increasing concentration. PM2.5 downregulated cyclin D and matrix metallopeptidase-9 (MMP-9) expression but upregulated tissue inhibitor of metalloproteinases-1 (TIMP-1) expression, significantly promoted interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) production, and enhanced the level and activation of AMPK. The levels of autophagy-related protein 5 (ATG5), Beclin-1, and LC3II/I were significantly increased by PM2.5. The activation of Unc-51-like autophagy activating kinase 1 was significantly inhibited by PM2.5. Moreover, ATG5 knockdown inhibited PM2.5-induced autophagy, ROS, and cell apoptosis significantly. The expression of cyclin D, MMP-9, and TIMP-1 was reversed by ATG5 suppression. PM2.5-induction of IL-6 and TNF-α was significantly inhibited by knockdown of ATG5. Thus, inhibition of autophagy protected the cells from PM2.5-induced injury. PM2.5 induced injury in human bronchial epithelial cells via activation of AMPK-mediated autophagy, suggesting possible therapeutic targets for the treatment of respiratory diseases.     

森林植被与大气颗粒物的关系

近年来,大气颗粒物成为我国城市大气的主要污染物,其中细颗粒物（PM_2.5）粒径小、沉降困难,对环境的危害已成为亟待解决的问题。森林植被可显著消减空气颗粒物,有效改善空气环境质量。本文概述了植被对颗粒物的移除过程和方法,探讨了大气颗粒物与森林植被的相互关系。从单叶、单木及群落3个尺度,结合气象因素讨论了植被对移除大气颗粒物的影响,分析了颗粒物的后续再悬浮过程及对植被的危害。最后,从植被吸附颗粒物的能力测定和评价、本土高吸附PM_2.5能力植被的筛选及综合研究不同植被配置结构的吸附效应等方面提出了植被吸附颗粒污染物,尤其是细颗粒物的研究重点与趋势。     

Adenoviral E1A modulates inflammatory mediator expression by lung epithelial cells exposed to PM10

We examined the hypothesis that ambient particulate matter with a diameter of <10 microm (PM(10))-induced lung inflammation is amplified by latent adenovirus infection. Inflammatory mediator expression in response to PM(10) exposure was compared between adenovirus E1A-transfected A549 alveolar epithelial cells and cells transfected with control plasmid. Messenger RNA was measured by the RNase protection assay and protein by ELISA or immunocytochemistry. Intercellular adhesion molecule-1 and IL-8 mRNA and protein were increased in E1A-positive cells exposed to 500 microg/ml PM(10). Monocyte chemoattractant protein-1 mRNA and protein were unchanged in E1A-positive cells but increased in E1A-negative cells after 100 and 500 microg/ml PM(10) exposure. Electrophoretic mobility shift assays showed increased NF-kappaB and decreased specificity protein 1 nuclear binding in E1A-positive cells exposed to PM(10). These results indicate that E1A modulates cytokine and adhesion molecule expression in epithelial cells in a manner that could amplify PM(10)-induced lung inflammation. We suggest that this amplified inflammatory response may contribute to the pathogenesis of exacerbations of chronic obstructive pulmonary disease associated with exposure to particulate matter air pollution.