南京市某居民区空气 PM2.5和 PM10污染分布特征分析

目的：研究南京市某居民区空气PM2.5和PM10污染的分布特征。方法：于春、夏、秋、冬四季选取同一地点两个不同垂直高度,同步监测PM2.5和PM10两种颗粒物,其中PM10只于春、夏季采集。结果：南京某居民区PM10质量浓度较低,均未超过我国环境空气质量二级标准（GB3095-2012）,秋冬季PM2.5超标,尤其是冬季最为严重。随着高度的增加,春季PM2.5质量浓度逐渐升高,而冬季PM2.5质量浓度则呈现下降的趋势,春冬季节不同高度PM2.5质量浓度差异有统计学意义（P＜0.05）,而且工作日PM2.5质量浓度高于休息日。结论：冬季居民区空气PM2.5污染严重,尤其是在呼吸带高度,同时PM2.5在PM10中占很高的比例,建议南京市要采取相关措施以降低PM2.5污染程度。     

Oxidative Damage to Lung Tissue and Peripheral Blood in Endotracheal PM2.5-treated Rats

Objective To investigate the oxidative damage to lung tissue and peripherial blood in PM2.5-treated rats. Methods PM2.5 samples were collected using an auto-sampling instrument in summer and winter. Treated samples were endotracheally instilled into rats. Activity of reduced glutathione peroxidase （GSH-Px） and concentration of malondialdehyde （MDA） were used as oxidative damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. DNA migration length （μm） and rate of tail were used as DNA damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. Results The activity of GSH-Px and the concentration of MDA in lung tissue significantly decreased after exposure to PM2.5 for 7-14 days. In peripheral blood, the concentration of MDA decreased, but the activity of GSH-Px increased 7 and 14 days after experiments. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. The DNA migration length （μm） and rate of tail in lung tissue and peripheral blood significantly increased 7 and 14 days after exposure to PM2.5. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. Conclusion PM2.5 has a definite oxidative effect on lung tissue and peripheral blood. The activity of GSH-Px and the concentration of MDA are valuable biomarkers of oxidative lung tissue damage induced by PM2.5. The DNA migration length （μm） and rate of tail are simple and valuable biomarkers of PM2 5-induced DNA damage in lung tissues and peripheral blood. The degree of DNA damage in peripheral blood can predict the degree of DNA damage in lung tissue.     

2016~2020年石家庄市大气PM2.5化学成分变化趋势及健康风险评估

目的 分析石家庄市大气细颗粒物(PM_2.5)化学成分的变化趋势和季节分布特征,评估其对人群的潜在健康风险。 方法 以石家庄市环境空气质量监测点2 km范围内两所小学的教学楼楼顶作为采样点,于2016年1月至2020年12月的每月10~16日采集PM_2.5样品共840份,并分别采用离子色谱仪、电感耦合等离子体质谱仪和气相色谱-质谱联用仪检测PM_2.5中水溶性无机离子(WSIIs)、金属及类金属和多环芳烃(PAHs)的含量,并依据《化学物质环境健康风险评估技术指南》(WS/T777-2021)评估其对人群的健康风险。 结果 石家庄市2016~2020年PM_2.5年均浓度呈逐年下降趋势,但仍超过标准限值(35 μg/m³),整体呈现出冬秋季高于夏春季的特点。WSIIs在PM_2.5中含量最高,除硝酸根离子(NO₃^-)外其余WSIIs浓度基本呈现出逐渐下降趋势,并表现出与PM_2.5相似的季节分布特征;金属与类金属元素铝(Al)、铅(Pb)、锰(Mn)在PM_2.5中含量较高,除Al和Mn外,其他元素在5年间基本呈下降趋势,但铬(Cr)浓度仍远高于标准限值,多数元素表现出冬季较高的季节分布特征;16种PAHs总年均浓度呈现出自2016年逐渐上升、2018年后逐渐下降的趋势,多数单体表现出秋冬季浓度较高的季节分布特征。风险评估结果显示,砷(As)、Cr和PAHs在不同年份和季节中均存在一定的致癌风险(CR>1.0×10^-6),同时,PAHs也存在较高的非致癌风险(HQ>1)。 结论 近年来石家庄市空气质量虽然有所好转,但形势依然严峻,PM_2.5中部分成分在目前接触水平下仍存在一定的致癌和非致癌风险,应继续加强监测和风险评估。     

Monitoring of Pollution of Air Fine Particles （PM2.5） and Study on Their Genetic Toxicity

INTRODUCTION The particulate matter is an important air pollutant, and its size, shape and composition are closely related to human health. The different aerodynamic diameters of the particles and the different deposition locations in the respiratory syst…     

Impact of Traffic Emissions on Local Air Quality and the Potential Toxicity of Traffic-related Particulates in Beijing, China

ObjectiveAir-borne particulates from different sources could have different physicochemical properties and inflammatory potentials. This study aims to characterize the chemical compositions and the toxicity of ambient particulate matter (PM) associated with traffic emissions.MethodsThe concentrations of trace elements, organic carbon (OC), elemental carbon (EC) and polycyclic aromatic hydrocarbons (PAHs) in PM_2.5 and PM₁₀ were measured in samples collected at sites in Beijing, China. Their toxic effects on the pulmonary system of rats were investigated. Biochemical parameters (LDH, T-AOC, TP) and inflammatory cytokine(IL-6, IL-1, TNF-a) levels were measured in the lungs of rats exposed to traffic-related PM. Oxidative damage was observed. PM samples were taken from a near road site and an off road site in summer time in 2006.ResultsThe concentrations of the USEPA priority pollutant PAHs in both PM₁₀ and PM_2.5 were higher (299.658 and 348.412) at the near road site than those (237.728 and 268.472) at the off road site. The similar trend was observed for the concentrations of trace elements in PM. Compared to coarse particles (PM₁₀), fine particles (PM_2.5) have a greater adsorption capacity to enrich toxic elements than inhalable particles. Decrease in antioxidant capacity and an increase in the amount of lipid peroxidation products in rat lung tissues was observed.ConclusionThe findings of the present study suggest that the differing inflammatory responses of PM collected from the two road sites might have been mediated by the differing physicochemical characteristics.     

水泥厂粉尘污染与健康

通过水泥厂粉尘污染的监测和实地调查表明:水泥厂粉尘粒径小于2微米的占61.0%,小于5微米占92.9%,可见尘粒小,分散度高,对人群健康危害性大,灰尘自然沉降量夏秋高于冬春,均以立窑点含量(分别为240.4550吨/平方公里·月和227.0514吨/平方公里·月)最高,其次是窑尾点(分别为214.5139吨/平方公里·月和153.4192吨/平方公里·月).大气 TSP(总悬浮微粒)一次最高浓度与日平均最高浓度均越过国家大气环境二级标准.一日时点变化以8时和18时浓度最高,13时最低;空间分布仍以立窑点浓度最高.调查发现,该地区人群中上呼吸道疾病占67.5%,其余为眼疾、慢性鼻炎,慢性咽喉炎、中耳炎、肺功能低下等疾患,表明该厂粉尘已危害人群健康,故发展水泥生产的同时,应千方百计防止环境污染.     

N-乙酰半胱氨酸对PM2.5致大鼠睾丸毒性的保护作用

目的 探讨N-乙酰半胱氨酸(N-acetylcysteine,NAC)改善亚急性暴露于大气细颗粒物(particulate matter,PM)2.5致大鼠睾丸损伤的作用。 方法 30只 Wistar大鼠随机分为3组,分别为生理盐水对照组、PM2.5暴露组、PM2.5+N-乙酰半胱氨酸组。通过气管内滴注的方法进行染毒,每次剂量为5.0 mg/kg,每周染毒一次,共8周;NAC组在PM2.5染毒的基础上,通过灌胃方式连续给予150 mg·kg-1·d-1 NAC;生理盐水对照组通过气管内滴注同体积生理盐水（1 mL/kg）作为对照。造模后HE染色制作睾丸组织病理切片,TUNEL法检测睾丸凋亡情况,分光光度计法检测睾丸组织超氧化物歧化酶（superoxide dismutase,SOD）、谷胱甘肽（glutathione,GSH）、和丙二醛（malondialdehyde,MDA）指标,酶联免疫吸附测定（enzyme-linked immunosorbent assay,ELISA）法测定睾丸白细胞介素10(interleukin-10,IL-10)及睾酮水平。 结果 PM2.5暴露组和PM2.5+NAC组大鼠血清睾酮水平及睾丸组织GSH、SOD、IL-10水平均低于盐水对照组,睾丸组织MDA水平升高,PM2.5+NAC组睾酮水平及睾丸组织GSH、SOD、IL-10水平高于PM2.5组,睾丸组织MDA水平下降(P＜0.05)。在PM2.5暴露组中,曲精小管中多个细胞核表现出明显的深棕色染色,TUNEL阳性细胞的计数明显高于盐水对照组和PM2.5+NAC组(P＜0.05);而PM2.5+NAC组凋亡细胞数明显低于PM2.5组,但高于盐水对照组(P＜0.05)。PM2.5暴露组和PM2.5+NAC组睾丸细胞凋亡指数高于盐水对照组,PM2.5+NAC组低于PM2.5暴露组(P＜0.05)。 结论 PM2.5亚急性暴露可以造成大鼠睾丸组织病理损伤,诱导睾丸细胞凋亡,引起氧化炎症指标改变,而NAC作为一种抗氧化剂,可以明显改善上述损伤作用,对PM2.5致睾丸毒性作用具有拮抗作用。     

The Cellular Toxicity of PM2.5 Emitted from Coal Combustion in Human Umbilical Vein Endothelial Cells

ObjectiveTo explore the relationship between different components offineparticulate matter (PM2.5) emitted from coal combustion and their cytotoxic effect in the vascular endothelial cells. MethodsCoal-fired PM2.5was sampled using a fixed-source dilution channel and flow sampler. The sample components were analyzed by ion chromatography and inductively coupled plasma atomic emission spectroscopy(ICP-AES). The PM2.5suspension was extracted using an ultrasonic water-bath method and thenhuman umbilical vein endothelial cells (EA.hy926) were treated withvarious concentrations of the PM2.5 suspension. Cell proliferation,oxidativeDNA damage, and global DNA methylation levelswere used to measurethe cellulartoxicity of PM2.5emitted fromcoalcombustion. ResultsComparedtoothertypesof coal-fired PM2.5preparations,thePM2.5 suspension from Yinchuan coal had the highest cytotoxicity.PM2.5 suspension from Datong coal hadthe highest toxic effectwhile that fromYinchuan coal had the lowest.Exposure to coal-fired PM2.5 from Jingxi coalresulted inlower 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels. At the same dose, PM2.5 emitted from coal combustion could produce more severeDNAimpairmentcompared to that produced by carbon black.Cell survival rate was negatively correlated with chloride and potassiumionscontent.The5-methylcytosine(5-mC) level waspositively correlated withMnandnegatively correlated withZn levels.The 8-OHdG% level was positively correlated withboth MnandFe. ConclusionPM2.5 emitted from coal combustion can decrease cell viability, increase global DNA methylation, and causeoxidativeDNA damage inEA.hy926 cells. Metalcomponentsmay be important factors that influence cellular toxicity.     

广州市2015年大气PM2.5与呼吸系统疾病日门诊量的关系

目的 定量研究广州市大气细颗粒污染物(PM2.5)对呼吸系统疾病门诊量的影响.方法采用环境流行病学方法,收集2015年1月1日-12月31日大气PM2.5等污染物资料、气象资料以及广州市1家三级甲等综合性医院呼吸系统疾病日门诊量资料,采用广义相加模型研究广州市大气PM2.5与呼吸系统疾病日门诊量的关系(同时控制长期趋势、星期几效应和气象因素等混杂因素的影响).结果 2015年广州市大气PM2s平均浓度为38.6.μg/m3,Spearman相关性分析表明,呼吸系统疾病日门诊量与SO2、NO2、CO、气压均成正相关,均有统计学意义(P＜0.05).GAM模型分析结果显示,PM2.5对呼吸系统疾病日门诊量呈现出0～3 d的明显的滞后效应,均有统计学意义.PM2.5滞后1d效应最大,滞后1d时,模型结果预测ER(％)为2.847(1.310,4.408),PM2.5每增加10 μg/m3,呼吸系统疾病门诊量增加2.847％.结论 广州市大气PM2.5与呼吸系统疾病日门诊量成正相关关系,且存在滞后效应.     

沙尘暴PM2.5对大鼠呼吸系统免疫损伤机制研究

目的探讨沙尘暴细颗粒物(PM2.5)染毒对大鼠呼吸系统的炎症免疫损伤情况及其损伤机制。方法将40只正常成年雄性Wistar大鼠随机分为空白对照组和各染毒组低、中、高剂量4个组,每组10只。采用气管直接注入染毒法,分别给大鼠灌注0、1.5、7.5、37.5mg/kg剂量的颗粒物悬浮液。灌注24h后处死大鼠,并对其肺泡灌洗液(BALF)中白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、肿瘤坏死因子(TNF)、白细胞介素-4(IL-4)、白细胞介素-10(IL-10)、白细胞介素-13(IL-13)水平及免疫球蛋白A(IgA)、免疫球蛋白G(IgG)、免疫球蛋白M(IgM)的含量进行检测。结果高剂量组大鼠BALF中IL-1、IL-6、IL-8、TNF水平高于对照组,差异有统计学意义(P<0.05),IL-4、IL-10及IL-13在各剂量组间表达水平差异无统计学意义;高剂量组大鼠BALF中IgG与IgM的含量与对照组比较显著升高(P<0.01),各组IgA含量的变化差异无统计学意义。结论沙尘暴细颗粒物PM2.5可引起大鼠呼吸系统显著的免疫损伤,其中以高剂量的PM2.5染毒对机体的损伤尤为显著,机体暴露于高剂量沙尘暴细颗粒物PM2.5环境可增加呼吸系统疾病发生的危险。     

Human Serum-derived Extracellular Vesicles Protect A549 from PM2.5-induced Cell Apoptosis

Objective Epidemiological studies reveal that exposure to fine particulate matter(aerodynamic diameter≤2.5μm,PM_2.5)increases the morbidity and mortality of respiratory diseases.Emerging evidence suggests that human circulating extracellular vesicles(EVs)may offer protective effects against injury caused by particulate matter.Currently,however,whether EVs attenuate PM_2.5-induced A549 cell apoptosis is unknown.Methods EVs were isolated from the serum of healthy subjects,quantified via nanoparticle tracking analysis,and qualified by the marker protein CD63.PM_2.5-exposed(50μg/mL)A549 cells were pretreated with 10μg/mL EVs for 24 h.Cell viability,cell apoptosis,and AKT activation were assessed via Cell Counting Kit-8,flow cytometry,and Western blot,respectively.A rescue experiment was also performed using MK2206,an AKT inhibitor.Results PM_2.5exposure caused a 100%in crease in cell apoptosis.EVs treatme nt reduced cell apoptosis by 10%,promoted cell survival,and inhibited the PM_2.5-induced upregulation of Bax/Bcl2 and cleaved caspase 3/caspase 3 in PM_2.5-exposed A549 cells.Moreover,EVs treatment reversed PM_2.5-induced reductions in p-AKT^Thr308and p-AKT^Ser473.A KT inhibition attenuated the anti-apoptotic effect of EVs treatment on PM_2.5-exposed A549 cells.Conclusions EVs treatment promotes cell survival and attenuates PM_2.5-induced cell apoptosis via AKT phosphorylation.Human serum-derived EVs may be an efficacious novel therapeutic strategy in PM_2.5-induced lung injury.     

苏州市大气颗粒物污染状况调查

目的 探讨苏州市主要功能区总悬浮颗粒物(TSP)、可吸入颗粒物(粒径≤10 μm,PM10)、粒径小于5μm的颗粒物(PM5)、细颗粒物(粒径≤2.5μm,PM2.5)等4种大气颗粒物的污染状况、垂直分布特征、24h浓度变化,以及不同类型口罩对大气颗粒物的防护效果.方法 (1)在苏州市选取7个功能区,连续3d监测大气中TSP、PM10、PM5、PM2.5的浓度;(2)选取一栋25层高的居民楼,分别检测第1、5、10、15、20、25层楼大气中TSP、PM10、PM5、PM2.5的浓度;(3)选取一监测点,每2h监测1次大气颗粒物浓度,连续测定3d,观察24h内颗粒物浓度变化;(4)分别使用一次性无纺布医用口罩、时尚型口罩、棉纱口罩、活性炭防尘口罩裹住采样头后监测4种大气颗粒物的浓度,比较不同类型口罩的防护效果.结果 (1)7个功能区PM2.5浓度均超标;(2)不同楼层间大气颗粒物浓度差异无统计学意义(P＞0.05);(3)大气颗粒物浓度在早晨和傍晚各出现1个小高峰,凌晨时大气颗粒物污染最严重(P＜0.05);(4)4种口罩比较,一次性医用口罩防护效果最好.结论 PM2.5是苏州地区主要大气颗粒污染物,4种大气颗粒污染物在凌晨浓度较高,在距地面75 m高的低空范围内差异无统计学意义,建议日常生活中使用一次性无纺布医用口罩来防护大气颗粒物污染.     

北京地区3 236例过敏性疾病患者血清过敏原的季节差异分析

［摘要］ 〖HTH〗目的〖HTSS〗探讨北京地区不同季节过敏原检测患者人群差异及过敏原分布差异。 〖HTH〗方法〖HTSS〗应用免疫印迹法检测3 236例患者血清中19种过敏原特异性IgE抗体,分析不同季节患者数量、性别、年龄及过敏原分布的差异。 〖HTH〗结果〖HTSS〗 3 236例患者中,男性1 273例（春199例/夏250例/秋492例/冬332例）,女性1 963例（春278例/夏372例/秋645例/冬668例）,不同季节过敏原检测患者男女数量构成差异有统计学意义（χ2=24.485,P＜0.05）,秋冬季节患者人数较多,女性多于男性。不同季节患者年龄段数量构成差异有统计学意义（χ2=40.025,P＜0.05）,青年患者人数较多。过敏原阳性率前5位分别为艾蒿（11.12%）、尘螨组合（9.39%）、猫毛（6.61%）、海鱼组合（5.81%）和蟹（4.67%）。春季过敏原阳性率前3位：尘螨组合/海鱼组合/艾蒿（10.06%/6.92%/6.71%）;夏季前3位：尘螨组合/艾蒿/海鱼组合（12.54%/10.29%/5.14%）;秋季前3位：艾蒿/猫毛/尘螨组合（15.83%/8.44%/8.18%）;冬季前3位：尘螨组合/艾蒿/猫毛（8.80%/8.40%/6.64%）;多种过敏原在不同季节分布差异有统计学意义（P＜0.05）。 〖HTH〗结论〖HTSS〗北京地区秋冬季节过敏性疾病人群激增,主要由吸入性过敏原引起,以艾蒿、尘螨和猫毛为主,食物性过敏原以海鱼组合和蟹为主,均呈现明显的季节差异。     

Immunological Effect of PM2.5 on Cytokine Production in Female Wistar Rats1

Objective To investigate the immunological effect of PM2.5 on cytokine production in female Wistar rats.Methods Female Wistzr rats were given 0.3 mg,0.75 mg,2 mg,5 mg of PM2.5 per 0.5mL saline,respectively.Saline was used as the negative control.TNF-α and IL-6 levels in the branchoalveolar lavage were measured by ELISA,and mRNA expression leveIs in lung tissue were detected bv RT-PCR.Alveolar macrophages were collected for testing phogacytic function. Results Exposure to PM2.5 stimulated TNF-α production in a dose-dependent manner(P＜0.05),However,no statistically significant difference was found.No time-dependent change in TNF-α and IL-6 production Was found.TNF-α and IL-6 mRNA expressions were induced by PM2.5-exposure.The phagocytic rate(PR)was significantly decreased by PM2.5 treatment.Conclusion PM2.5 exposure increases inflammation response of the lung in a dose-dependent mauuer.Moreover,tissue injury induced by PM2.5 may be related to altered production of cytokines.PM2.5 may impair the phagocytic activity of alveolar macrophages.     

Immunological effect of PM2.5 on cytokine production in female Wistar rats

Objective To investigate the immunological effect of PM2.5 on cytokine production in female Wistar rats. Methods Female Wistar rats were given 0.3 mg, 0.75 mg, 2 mg, 5 mg of PM2.5 per 0.5 mL saline, respectively. Saline was used as the negative control. TNF-α and IL-6 levels in the branchoalveolar lavage were measured by ELISA, and mRNA expression levels in lung tissue were detected by RT-PCR. Alveolar macrophages were collected for testing phogacytic function. Results Exposure to PM2.5 stimulated TNF-α production in a dose-dependent manner （P〈0.05）, However, no statistically significant difference was found. No time-dependent change in TNF-α and IL-6 production was found. TNF-α and IL-6 mRNA expressions were induced by PM2.5-exposure. The phagocytic rate （PR） was significantly decreased by PM2.5 treatment. Conclusion PM2.5 exposure increases inflammation response of the lung in a dose-dependent manner. Moreover, tissue injury induced by PM2.5 may be related to altered production of cytokines. PM2.5 may impair the phagocytic activity of alveolar macrophages.     

Effects of Lianhua Qingwen on Pulmonary Oxidative Lesions Induced by Fine Particulates (PM2.5) in Rats

Objective To investigate the antagonistic effects of different doses of Lianhua Qingwen on pulmonary injury induced by fine particulates PM2.5 in rats.
Methods Fine particulates suspended in the environment were collected. Forty-eight healthy adult wistar rats were randomly divided into 6 groups with 8 rats in each group. Four groups of rats were exposed to PM2.5 by intratracheally dripping suspensions of fine particulates PM2.5 (7.5 mg/kg)as dust-exposed model rats. Among them 24 rats in three groups received Lianhua Qingwen treatment (crude drug) at a dose of 2 g/kg, 4 g/kg, 8 g/kg per day for 3 daysbefore dust exposure and were defined as low-dose, middle-dose and high-dose Lianhua Qingwen treatment groups respectively. The other dust-exposed model rats without treatment were assigned as PM2.5 control group. The un-exposed rats were set as saline control group (1.5 ml/kg saline) and blank control group. All rats were killed after 24 hours of the exposure. Lung tissue, serum and bronchoalveolar lavage fluid (BALF) were collected. The levels of malonaldehyde (MDA), lactate dehydrogenase (LDH), and glutathione peroxidase (GSH-PX) in blood serum and BALF, and superoxide dismutase (SOD) in blood surum were measured using fluorescent quantitation PCR; Expression of NF-E2-related factor 2(NRF-2), heme oxygenase 1 (HO-1) and quinone oxidoreductase 1 (NQO1) in lung tissues were measured using Western blot. Pathological changes of lung tissues in each group were also examined.
Results Pathology revealed thickened alveolar septum, congestion of capillary, interstitial edema and infiltration of lymphocyte and neutrophil surrounding bronchiole in the PM2.5 control group, which were significantly relieved in the Lianhua Qingwen treatment groups. Compared to the blank and saline control groups, the PM2.5 control group had significantly higher levels of LDH and MDA (p<0.01) and lower level of GSH-PS (p<0.01) in BALF, significantly higher levels of LDH and MDA (p<0.05) and lower level of GSH-PS (p<0.05) in rat serum. The levels of MDA in blood serum and BALF were significantly lower in each treatment group than that in PM2.5 control group (allP<0.05). In both middle-dose and high-dose treatment group the measurements of LDH in serum and BALF as well as GSH-PX in serum were significant difference from those of PM2.5 control group (allP<0.05). Expressions of NRF-2, HO-1 and NQO1 in lung tissues were significantly different among middle-dose and high-dose treatment group compared with those in PM2.5 control group (allP<0.05).
Conclusion Fine particulates PM2.5 in environment may induce pulmonary oxidative lesions in rats. Middle-dose and high-dose Lianhua Qingwen has antagonist effece on the injuries induced by fine particulates.     

PM2.5对THP1巨噬细胞TLR4表达及氧化应激水平的影响

目的探讨大气细颗粒物（particulate matters,PM）2.5对THP1巨噬细胞TLR4表达及氧化应激水平的影响。方法THP1巨噬细胞分别给予来自中国北京、美国巴尔的摩地区的PM2.5刺激24 h,检测巨噬细胞TLR4、Nrf2表达水平,以及细胞内活性氧（ROS）产生水平。结果与对照组比较,低浓度（50 μg/mL）北京地区和巴尔的摩地区PM2.5刺激24 h后,细胞TLR4、Nrf2表达水平与细胞内ROS产生水平均升高（P < 0.05）。与对照组比较,高浓度（200 μg/mL）北京地区和巴尔的摩地区PM2.5刺激24 h后,细胞TLR4表达水平、Nrf2表达水平均降低（P < 0.05）,北京地区组细胞内ROS产生水平降低（P < 0.05）,巴尔的摩地区组细胞内ROS升高（P < 0.05）。结论低浓度PM2.5可促进巨噬细胞TLR4表达,升高氧化应激水平,高浓度PM2.5可降低巨噬细胞TLR4表达,降低氧化应激水平。     

JNK1/2-AP1信号转导通路对PM2.5所致气道黏液高分泌的介导作用

 目的研究直径≤2.5μm空气中可吸入颗粒（PM2.5）所致气道黏液高分泌的信号转导机制。方法PM2.5刺激大鼠建立气道黏液高分泌模型,Wistar大鼠随机分为对照组、PM2.5组、PM2.5+SP600125组。ELISA检测各实验组中粘蛋白（MUC）5AC在蛋白水平的表达量,Realtime-PCR检测MUC5AC在mRNA水平的表达量,Westernblotting检测JNK1、JNK2、p-JNK1/2的蛋白含量,EMSA检测该信号通路下游激活蛋白1（AP-1）与DNA的结合活性。结果PM2.5刺激组与空白对照组相比,前者MUC5AC在mRNA水平和蛋白水平的表达量均显著高于后者（P<0.01）,通过WesternBlotting法测得JNK1、JNK2各自的蛋白总量无明显变化,活化的JNK1/2(p-JNK1/2)的含量则明显高于对照组（P<0.01）,EMSA结果提示：PM2.5组,测得激活蛋白1结合活性明显升高（P<0.01）,给予JNK特异性抑制剂SP600125后,测得激活蛋白1结合活性明显降低（P<0.05）。与PM2.5刺激组比较,PM2.5+SP600125组的MUC5AC在mRNA水平和蛋白水平的表达明显降低（P<0.05）。结论PM2.5可以通过JNK1/2-AP-1信号传导通路调节气道黏液高分泌。     

肺闭宁颗粒止咳、抗炎及促进PM2.5颗粒物排出作用的研究

[目的]考察肺闭宁颗粒在止咳、抗炎以及对促进PM2.5排出方面的药效学作用研究,为其临床用药提供数据支持。[方法]采用二氧化硫引咳小鼠模型、内毒素诱导的肺损伤小鼠模型以及斑马鱼PM2.5排出模型,给予不同浓度的肺闭宁颗粒干预后,观察其止咳、抗炎以及对纳米颗粒从斑马鱼体内排出进入肠道的影响。[结果]肺闭宁颗粒中（3.69 g/kg）、高（7.38 g/kg）剂量组可明显改善二氧化硫引咳模型小鼠咳嗽潜伏期时间及咳嗽次数;可降低内毒素诱导的肺损伤小鼠肺灌流液中白细胞介素-6（IL-6）浓度（P<0.05）;在斑马鱼PM2.5超细颗粒物排出模型中,肺闭宁颗粒125 mg/mL时,纳米活性炭排出发生率为63.3%,与模型对照组（16.7%）比较有统计学差异（P<0.05）。[结论]肺闭宁颗粒具有止咳、抗炎的作用,此外在促进PM2.5超细颗粒物排出、减少PM2.5对机体的损伤方面也有一定的效果,提示其在对抗雾霾天气引起的呼吸道系统疾病治疗中具有一定作用。     

PM2.5对心血管系统的影响及中医药防治

PM2.5(空气动力学等效直径Dp≤2.5μm)是大气颗粒物的主要组成成分和主要毒性成分,大量研究结果发现,PM2.5能直接或间接影响心血管系统,其中氧化应激、炎症是主要的致病机制.本文综述PM2.5通过氧化应激与炎症反应相关途径对内皮细胞的损伤、细胞程序化死亡的研究进展以及中医药防治的相关研究,并提出PM2.5对心血管系统的影响可能与血管内皮细胞焦亡性损伤有关.