云锡等生产性粉尘对大鼠肺泡巨噬细胞吞噬功能的影响

用巨噬细胞吞噬酵母菌的方法检测吞噬粉尘后大鼠肺泡巨噬细胞功能。发现:云锡氧化矿尘、云锡硫化矿尘、香花岭矿尘、二氧化硅尘、宣威煤烟尘等五种粉尘不同程度地抑制巨噬细胞的吞噬功能。SiO_2在染尘后第二周即有改变。其它生产性粉尘均在染尘后3～6周致肺泡巨噬细胞吞噬功能下降,并在第6周仍维持较低水平。结果表明:云锡等生产性粉尘对大鼠肺泡巨噬细胞的吞噬功能有抑制作用,从而使体内非特异免疫受到影响,破坏免疫监视系统,这可能是促使肺癌发生和发展的一个有利因素之一。     

人参,黄芪对染尘大鼠肺泡巨噬细胞功能的影响

采用经喉支气管内注入矽尘制成动物模型,观察染尘大鼠肺泡巨噬细胞功能及人参黄芪的影响。结果表明,人参、黄芪可增加肺泡巨噬细胞存活率及吞噬细菌能力,人参可降低肺泡巨噬细胞分泌肿瘤坏死因子（ ＴＮＦ） ,提示人参、黄芪可改善染尘大鼠肺泡巨噬细胞功能损害     

铁矿尘对肺泡巨噬细胞影响的实验研究

采用大鼠肺泡巨噬细胞（ＡＭ）体外培养的方法,对铁矿积尘进行毒性研究。染尘浓度为０、０．２、０．６和１．２ｍｇ／ｍｌ,染尘１、５、２０小时后,通过对大鼠ＡＭ功能、形态、细胞膜通透性变化以及脂质过氧化、抗氧化等的观察,初步探讨了铁矿尘对ＡＭ的毒作用及其机理。结果表明,染尘后ＡＭ吞噬酵母菌能力降低;随铁矿尘浓度增高和染尘时间延长,细胞培养液中ＬＤＨ活性升高,细胞内ＡＣＰ活性降低,Ｋ＾＋水平降低,说明铁矿     

维生素E对染尘大鼠肺泡巨噬细胞吞噬功能的影响

在SiO_2刺激下,肺的防御和免疫功能获得加强,这是对机体有积极意义的一面。但据文献报告,肺泡巨噬细胞吞噬SiO_2后能导致其溶酶体膜和细胞膜损害以及肺泡巨噬细胞自身的崩解,随之加速纤维化的形成,故肺泡巨噬细胞数目和吞噬SiO_2量的增加,又成为对机体有害的一面。为了探索维生素E对染尘后大鼠肺泡巨噬细胞吞噬功能的影响,借以了解维生素E对抗实验性矽肺形成的机制的某些环节,我们做了以下实验:     

茶多酚联合维生素C、维生素E对染尘大鼠肺泡巨噬细胞DNA损伤的保护实验研究

目的　研究茶多酚联合VC、VE 对染尘大鼠肺泡巨噬细胞DNA损伤的保护作用。方法　采用单细胞凝胶电泳技术 (SCGE)分析大鼠肺泡巨噬细胞DNA损伤情况。结果　染尘后大鼠肺泡巨噬细胞DNA拖尾率增高 ,拖尾长度增大 ,与生理盐水组比差异有显著性 (P <0 0 0 1)。经茶多酚联合VC、VE 处理后 ,肺泡巨噬细胞DNA拖尾率降低 ,拖尾长度缩短 ,与石英粉尘组比差异有显著性 (P <0 0 5 )。结论　茶多酚联合VC、VE 对染尘大鼠肺泡巨噬细胞DNA损伤有一定保护作用。     

内质网应激性凋亡途径在粉尘致大鼠肺纤维化过程中作用研究

目的 研究内质网应激性凋亡途径在粉尘致大鼠肺纤维化过程中的作用.方法 36只健康成年雄性Wistar大鼠随机分为对照组及染尘组.采用非暴露式气管内注入法染尘,染尘组一次性注入含质量浓度为50 g/L粒径＜5μm石英粉尘的生理氯化钠溶液1 ml,对照组注入等体积无菌生理氯化钠溶液,每组分别于染尘结束后14、28、56 d随机处死6只大鼠,进行支气管肺泡灌洗,计算肺系数,羟脯氨酸法检测总胶原蛋白的水平,苏木精-伊红染色法观察肺组织的病理变化;流式细胞术检测肺泡巨噬细胞凋亡率;Western-blot法检测肺泡巨噬细胞Caspase-12的蛋白表达水平.结果 与对照组比较,染尘组大鼠在染尘后第14天细胞凋亡率和Caspase-12的蛋白表达水平均升高(P＜0.05);染毒后第28天肺系数及肺组织总胶原蛋白水平也升高(P＜0.05),细胞凋亡率和Caspase-12的蛋白表达水平持续升高(P＜0.05);染毒后第56天,以上指标仍进一步升高(P＜0.05).结论 内质网应激性凋亡途径可能参与了粉尘致大鼠肺纤维化的发病机制.     

矽肺大鼠肺泡巨噬细胞吞噬功能检测方法研究

目的研究适用于矽肺模型大鼠肺泡巨噬细胞吞噬功能的检测方法.方法气管注入法制备矽肺模型,分别两次通过气道、腹腔给予矽肺大鼠模型及正常对照动物卡介苗（BCG）.第2次免疫后35天气道注入鸡红细胞,评价肺泡巨噬细胞的吞噬功能.结果矽肺动物肺泡巨噬细胞吞噬鸡红细胞百分率、吞噬指数都显著低于正常对照大鼠.结论本实验室应用的大鼠半体内肺泡巨噬细胞吞噬功能测定方法,简单适用,能反映动物肺泡巨噬细胞吞噬功能;矽肺动物肺泡巨噬细胞吞噬功能显著下降.     

云锡矿尘致大鼠气管上皮细胞转化的研究

用大鼠气管上皮细胞体内—体外转化系统检测可能致癌的云南锡业公司（简称云锡）矿场沉积尘的致癌性。云锡矿尘、青石棉尘对Ｗｉｓｔａｒ大鼠气管灌注染尘，ｌ５ｄ后取其气管上皮细胞体外无血清培养，１周后用含血清的选择培养基培养，在接种大鼠气管上皮细胞５～６周后计数转化集落数。结果表明云锡矿尘剂全为３０～１２０ｍｇ／只、青石棉为２２，５ｍｇ／只，有剂量效应关系。提示云锡矿尘可能是云南锡业公司矿工肺癌高发的主要原因。并证明大鼠气管上皮细胞体内—体外转化系统是研究矿尘类物质致癌性的良好模型。     

石棉对大鼠肺泡巨噬细胞毒作用的体外研究

本文研究了新康温石棉,加拿大(UICC)温石棉和石英粉尘,经5,10,15小时体外染尘对大鼠肺泡巨噬细胞的毒作用,结果表明各组细胞的存活率均随培养时间而下降,以石英组下降最快,加拿大组次之,各染尘组与对照组间有明显差异,染尘细胞的形态与功能有明显改变经光镜和电镜检查可见细胞迅速增大,内含多量不同大小的空泡,两石棉组不少细胞成锥形或梭形,肾形核双核和三核细胞明显增加,并有两巨噬细胞共吞长石棉纤维,三种粉尘均无例外地被吞噬,毒性有所差异以石英最大,认为此种差异由粉尘性质和形状不同所致.     

相关从业者必须警惕的尘肺病

<正>尘肺病是一种严重的肺部疾病，从事矿山开采、建筑工程等行业的职业人群长期暴露在生产性粉尘中，罹患尘肺病的风险比较高。长期吸入某些特殊的粉尘，这些细小的粉尘颗粒会沉积在细支气管、肺泡囊等部位。为了保护机体，肺部的巨噬细胞会将粉尘吞噬。在粉尘的毒性作用下，巨噬细胞会释放出炎症因子，引起肺泡炎，最终导致肺纤维化。     

纳米二氧化钛经气管染毒对大鼠肺巨噬细胞免疫功能的影响

[目的]探讨不同粒径的纳米二氧化钛（nanoTiO2）经气管染毒对大鼠肺巨噬细胞（pulmonary alveolar macrophage，PAM）免疫功能的影响。[方法]5、21、50nm粒径的nanoTiO2以50．0mg／kg体重剂量给大鼠经气管一次性滴注染毒，7d后处死并分离PAM，采用中性红吞噬实验方法测定PAM的吞噬功能，4-氨基安替比林比色法检测酸性磷酸酶（ACP），放射免疫方法测定肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）、白介素-6（IL-6）和白介素-8（IL-8），采用硝酸还原酶法测定一氧化氮（NO）。[结果]不同粒径的nanoTiO2的暴露均可增强大鼠PAM的吞噬功能，且50nmTiO2染毒组大鼠PAM的吞噬能力高于5nmTiO2染毒组（P〈0．05）。nanoTiO2对大鼠PAM ACP和IL-8的影响不明显。21nm、50nmTiO2组大鼠PAM的NO合成释放量高于对照组（P〈0．05）。50nm TiO2组大鼠PAM的TNF-α分泌量明显高于5nm、21nm TiO2染毒组（P〈0．05），而5nm、21nmTiO2组PAM的IL-1β分泌量低于对照组（P〈0．05），IL-6分泌量低于50nmTiO2组和对照组（P〈0．05）。nanoTiO2比表面积与大鼠PAM的吞噬功能间有直线相关关系，而与其他效应间未显示有相关性。[结论]nanoTiO2颗粒经气管染毒可以影响大鼠PAM的免疫功能，且影响与TiO2纳米颗粒的粒径大小有密切关系。大粒径TiO2暴露诱导大鼠PAM的免疫功能增强，而粒径小的TiO2纳米颗粒对大鼠PAM的免疫功能诱导作用较弱，其对免疫细胞和免疫功能的影响可能有其特殊性。     

几种矿物粉尘对肺内细胞的毒性作用及其致纤维化作用

测定染尘不同时间大鼠支气管肺泡灌洗液中细胞代谢活性、溶菌酶和总蛋白含量等细胞毒作用与全肺组织干重、全肺胶原蛋白含量及肺组织病理学改变等致纤维化作用。结果表明,多数矿物粉尘对肺内细胞的毒性作用及致肺纤维化作用与粉尘中所含游离SiO_2的量有密切的相关性;复合粉尘或混合性粉尘所致生物学危害作用并不是单一粉尘或组分作用的简单加合。     

蘑菇孢子抗原致敏大鼠肺泡巨噬细胞吞噬功能的变化

在蘑菇的培植过程中,由于吸入担孢子致使蘑菇工人发生肺部疾患,其病因学尚不完全清楚。临床观察表明该病属于呼吸道变态反应性疾病。本文仅对蘑菇孢子抗原致敏大鼠肺泡巨噬细胞(MPH)的吞噬功能进行了观察。结果表明,致敏大鼠经激发后48小时的MPH吞噬率最高。经多次激发后的致敏大鼠的MPH吞噬率亦比正常大鼠高(P<0.05)。蘑菇肺很可能是一种过敏性肺泡炎。     

The effect of lung burden on biopersistence and pulmonary effects in rats exposed to potassium octatitanate whiskers by intratracheal instillation

In our previous inhalation studies on health effects of the asbestos substitute, potassium octatitanate whiskers (POW), we showed that an excess amount of POW deposition in the rat lung increased biopersistence resulting in fibrotic changes. The critical deposition amount which induced the higher biopersistence was estimated to lie between 1.5 mg and 2.4 mg. In order to find the exact amount, the relationship between the lung POW burden and biopersistence was investigated by the intratracheal instillation method. The chemical formula of POW is K2Ti8O17 and the geometric mean fiber diameter (geometric standard deviation, GSD) and geometric mean fiber length (GSD) are 0.35 microm (1.6) and 4.4 microm (2.7), respectively. Rats were intratracheally instilled with 0.5 mg, 1.0 mg, 2.0 mg or 5.0 mg of POW and sacrificed at 1 day and 1, 3, 6 and 12 months after the instillation. The POW amount in each lung was chemically analyzed by ICP-AES after microwave digestion and the biological half time (BHT) of each POW dose was calculated. The BHTs of each group were 10, 15, 20 and 42 months for 0.5, 1.0, 2.0 and 5.0 mg of POW, respectively, and BHT showed a linear dose-dependent increase, but without a threshold within the range of 0.5 mg to 5.0 mg, which was recognized in our earlier inhalation studies. In the histopathological photograph just after the instillation, many macrophages, which had phagocytized many more fibers, existed around the bronchiole compared with the earlier inhalation study at almost the same deposited amount. The relationship between POW amount and biopersistence in this intratracheal instillation study was different from that of our previous inhalation studies, probably due to the unnatural method of the fiber introduction to the lung, which in turn led to a different fiber distribution. It is suggested that an intratracheal instillation study is not an appropriate method for estimating excess deposition amounts of POW and an inhalation study will be needed. However, this intratracheal instillation study clarified that the clearance of POW was delayed as compared with previous inhalation studies at similar deposition amounts and this result has importance for the hazard assessment of dusts in animal experiments.     

Short term effect of silicon carbide whisker to the rat lung

We studied the short-term effect of silicon carbide whisker (SiCW) in vivo by instillation and inhalation to the rat lung. SiCW was instilled low dose (2 mg/0.5 ml saline) or high dose (10 mg/ 0.5 ml) intratracheally into the lungs of 25 rats. SiCW was also inhaled to another 25 rats at the average concentration of 10.4 mg/m3 for 1 month. In instillation study, the lung had focal alveolitis with the destruction of alveolar wall especially at 3 days after the instillation, and the lesion remained as an aggregated foci of SiCW at 6 months. The 'inflammation-score' of the instilled group by point counting method of the specimen correspondingly decreased gradually. In inhalation group, a minimum inflammatory change was observed. Collagen deposition in the aggregated foci of SiCW with accumulated alveolar macrophages and neutrophils was not progressive during the observed period. These findings suggest that SiCW may cause a minor effect to the rat lung in 6 months after exposure.     

大气可吸入颗粒物对大鼠心率变异性的影响

目的研究可吸入颗粒物对大鼠心率变异性的影响。方法24只SD大鼠,均为雄性,体重150~200 g。随机分为两组(实验组、对照组),每组12只。实验组大鼠按25 mg(1 ml)/kg体重经气管内缓慢注入颗粒物生理盐水悬液染毒,每周染毒2次,连续染毒4周;对照组以生理盐水代替颗粒物悬液。大鼠麻醉后经皮下引导电极连续采集心电信号,计算SDNN和r-MSSD。统计学处理采用SPSS统计学软件,组间比较用t检验或方差分析,P0.05为差异有统计学意义。结果2组大鼠首次和末次染毒之后30 min的心率均较染毒之前明显下降;两组大鼠首次染毒之前和末次染毒之前的心率差异无统计学意义;两组大鼠首次染毒之后和末次染毒之后30 min的心率差异无统计学意义。两组大鼠首次染毒之前和首次染毒之后30 min的心率变异性差异无统计学意义;末次染毒之前和末次染毒之后30 min的心率变异性差异无统计学意义;实验组末次染毒之前和末次染毒之后30min的心率变异性分别较首次染毒之前和首次染毒之后30 min时明显下降(P0.05);与对照组比较,实验组末次染毒之前和染毒之后30 min的心率变异性明显下降(P0.05)。结论本研究表明可吸入颗粒物能够导致心率变异性的降低。     

The effect of different mineral dusts on the mechanism of phagocytosis: a scanning electron microscope study.

Alveolar macrophages from normal rats were incubated with crocidolite asbestos fibers and quartz particles in vitro. The early events in phagocytosis were studied sequentially. Differences were found in the way in which macrophages recognized, attached, and phagocytosed the two dusts. Phagocytosis of quartz was extremely rapid: The macrophages typically developed long tenuous filopodia. Crocidolite was phagocytosed more slowly: Many macrophages developed large flattened pseudopodia. These different phagocytic mechanisms may reflect the different biochemical and cytotoxic properties of the dusts.     

Translocation of intratracheally instilled multiwall carbon nanotubes to lung-associated lymph nodes in rats

In order to assess the extrapulmonary effects of multiwall carbon nanotubes (MWCNT), deposition of MWCNT and histopathologic changes in lung-associated lymph nodes (LALN) were examined in MWCNT-administered rats. At the age of 13 wk, male F344 rats were intratracheally instilled with MWCNT at a dose of 0 (vehicle), 40 or 160 μg/rat. The rats were sacrificed on Day 1, 7, 28 or 91 after instillation and light microscopic examinations were performed on LALN tissues. MWCNT was translocated to right and left posterior mediastinal lymph nodes and parathymic lymph nodes. Deposition of MWCNT was greater in the posterior mediastinal lymph node than in the parathymic lymph node, and the amount of MWCNT deposited in these two lymph nodes increased gradually and dose-dependently with time. MWCNT was phagocytosed by nodal macrophages, and some of the MWCNT-laden macrophages were aggregated. Transmission electron microscopic (TEM) observation confirmed the presence of MWCNT fibers with a characteristic multi-walled cylindrical structure.     

Effects of dietary restriction on cellular immunity in rats

Phagocytosis of opsonized sheep red blood cells (SRBC) by alveolar macrophages (AM) was measured in rats fasted for 1 to 9 days or fed on diets restricted 20 to 95% compared to control group for 2 and 8 weeks. In rats fasted for 1 to 6 days, AM showed an increased phagocytosis at 2 days after fasting, but their phagocytic activity remarkably decreased afterwards. Furthermore, phagocytic activity of AM per rat revealed much more decrease at 3 to 6 days after fasting. Then the production of interleukin-1 (IL-1) by AM increased with prolonged fasting, but the production of prostaglandin E2 (PGE2) by AM cultured with lipopolysaccharide (LPS) conversely decreased in rats fasted for 2 days or longer. The proliferation of splenocytes increased with prolonged fasting. On the other hand, 20 to 95% restricted diets induced the increased phagocytosis of AM with prolonged experimental period. However, phagocytic activity of AM per rat showed significant increase only in rats on a 40% restricted diet. The findings suggest that differences in both duration and degree of dietary restriction modulate phagocytic function of AM, and may contribute to explaining, in part, conflicting observations which have been obtained on the immunologic state in malnourished animals.