Lung oxidative response after acute coal dust exposure

Coal dust exposure can induce an acute alveolar and interstitial inflammation that can lead to chronic pulmonary diseases. The objective of this study was to describe the acute and later effects of acute coal dust exposure in lung parenchyma and the involvement of reactive oxygen species in coal dust effects. Forty-eight male Wistar rats (200-250 mg) were separated into four groups: 48 h, 7 days, 30 days, and 60 days after coal dust instillation. Gross mineral coal dust (3 mg/0.5 mL saline) was administered directly in the lungs of the treatment group by intratracheal instillation. Control animals received only saline solution (0.5 mL). Lipid peroxidation was determined by the quantity of thiobarbituric acid-reactive species (TBARS), oxidative damage to protein was obtained by the determination of carbonyl groups, the total radical-trapping antioxidant parameter (TRAP) was estimated by luminol chemoluminescence emission, catalase activity was measured by the rate of decrease in hydrogen peroxide, and superoxide dismutase activity was assayed by the inhibition of adrenaline autooxidation. Histological evaluation of coal dust-treated rats demonstrated an inflammatory infiltration after 48 h of the exposure. Initially, this was a cellular infiltration suggestive of lymphocyte infiltration with lymphoid hyperplasia that remained until 7 days after induction. This initial response was followed by a chronic inflammatory infiltration characterized by aggregates of macrophages 30 days after induction. This inflammatory response tended to resolve 60 days after induction, being similar to that of control animals. During both the acute and chronic phases of lung inflammation we observed a decrease in the TRAP in the lung of coal dust-exposed animals compared to that in control animals. We also observed an activation of superoxide dismutase 60 days after coal dust exposition. TBARS were increased 60 days after coal dust exposure and protein carbonyl groups increased at all times after coal dust exposure (48 h, 7 days, 30 days, and 60 days). These data suggested a biphasic inflammatory response and the involvement of oxidative damage in coal dust-induced lung damage.     

Melatonin reduces oxidative stress induced by chronic exposure of microwave radiation from mobile phones in rat brain

PURPOSE: The aim of the study was to evaluate the intensity of oxidative stress in the brain of animals chronically exposed to mobile phones and potential protective effects of melatonin in reducing oxidative stress and brain injury. MATERIALS AND METHODS: Experiments were performed on Wistar rats exposed to microwave radiation during 20, 40 and 60 days. Four groups were formed: I group (control)- animals treated by saline, intraperitoneally (i.p.) applied daily during follow up, II group (Mel)- rats treated daily with melatonin (2 mg kg(-1) body weight i.p.), III group (MWs)- microwave exposed rats, IV group (MWs + Mel)- MWs exposed rats treated with melatonin (2 mg kg(-1) body weight i.p.). The microwave radiation was produced by a mobile test phone (SAR = 0.043-0.135 W/kg). RESULTS: A significant increase in the brain tissue malondialdehyde (MDA) and carbonyl group concentration was registered during exposure. Decreased activity of catalase (CAT) and increased activity of xanthine oxidase (XO) remained after 40 and 60 days of exposure to mobile phones. Melatonin treatment significantly prevented the increase in the MDA content and XO activity in the brain tissue after 40 days of exposure while it was unable to prevent the decrease of CAT activity and increase of carbonyl group contents. CONCLUSION: We demonstrated two important findings; that mobile phones caused oxidative damage biochemically by increasing the levels of MDA, carbonyl groups, XO activity and decreasing CAT activity; and that treatment with the melatonin significantly prevented oxidative damage in the brain.     

Pistacia lentiscus resin regulates intestinal damage and inflammation in trinitrobenzene sulfonic acid-induced colitis

Mastic (Pistacia lentiscus) of the Anacardiaceae family has exhibited anti-inflammatory and antioxidant properties in patients with Crohn's disease. This study was based on the hypothesis that mastic inhibits intestinal damage in inflammatory bowel disease, regulating inflammation and oxidative stress in intestinal epithelium. Four different dosages of P. lentiscus powder in the form of powder were administered orally to trinitrobenzene sulfonic acid-induced colitic rats. Eighty-four male Wistar rats were randomly assigned to seven groups: A, control; B, colitic; C-F, colitic rats daily supplemented with P. lentiscus powder at (C) 50 mg/kg, (D) 100 mg/kg, (E) 200 mg/kg, and (F) 300 mg/kg of body weight; and G, colitic rats treated daily with cortisone (25 μg/kg of body weight). Colonic damage was assessed microscopically. The cytokines tumor necrosis factor-α, intercellular adhesion molecule-1 (ICAM-1), interleukin (IL)-6, IL-8, and IL-10 and malonaldehyde were measured in colonic specimens. Results were expressed as mean ± SE values. Histological amelioration of colitis (P≤.001) and significant differences in colonic indices occurred after 3 days of treatment. Daily administration of 100 mg of P. lentiscus powder/kg of body weight decreased all inflammatory cytokines (P≤.05), whereas 50 mg of P. lentiscus powder/kg of body weight and cortisone treatment reduced only ICAM-1 (P≤.05 and P≤.01, respectively). Malonaldehyde was significantly suppressed in all treated groups (P≤.01). IL-10 remained unchanged. Cytokines and malonaldehyde remained unaltered after 6 days of treatment. Thus P. lentiscus powder could possibly have a therapeutic role in Crohn's disease, regulating oxidant/antioxidant balance and modulating inflammation.     

沙尘暴PM_(2.5)对大鼠肺、心、肝组织的氧化损伤效应

目的探讨沙尘暴细颗粒物(PM2.5)对大鼠肺、心、肝组织的氧化损伤作用。方法采用气管直接注入染毒法,灌注24h后处死大鼠,测定肺、心、肝组织超氧化物歧化酶(SOD)活性、谷胱甘肽(GSH)含量及脂质过氧化作用(LPO)水平。结果(1)沙尘暴和正常天气PM2.5均可引起肺、肝脏SOD酶活性的降低,而心脏SOD酶活性无显著性变化。(2)沙尘暴和正常天气PM2.5均可引起肺脏GSH含量降低,使肝脏中GSH含量呈现先升高后降低的非线性变化特征,而心脏GSH含量无显著性变化。(3)沙尘暴和正常天气PM2.5均可引起肺、心、肝脏的LPO水平升高。(4)正常天气PM2.5比沙尘暴PM2.5对各测量指标的影响较大,但统计学上均无显著性差异,但由于沙尘暴PM2.5浓度远高于正常天气PM2.5,所以沙尘暴PM2.5产生的效应较大。结论沙尘暴和正常天气PM2.5对大鼠肺、心、肝组织均有不同程度的氧化损伤作用,沙尘暴PM2.5的急剧增高使其毒性作用更为严重。     

搪瓷喷花粉尘致肺纤维化的实验研究

目的：研究搪瓷喷花粉尘的致肺纤维化作用。方法：３组ＳＤ大鼠气管内分别注入搪瓷喷花（白下底料）粉尘、石英石粉尘和生理盐水,染尘后６０ｄ和１８０ｄ宰杀,称取肺鲜重,测定肺胶原含量,肺组织病理学改变。结果：熟料粉尘组大鼠的肺鲜重和肺胶原含量高于生理盐水组,但明显低于石英尘组。病理观察结果显示,熟料粉尘能在肺内形成异物结节及周围轻度纤维增生。结论：一定量的搪瓷喷花粉尘进入肺内不至引起进行性肺纤维化,而是引     

Anti-Inflammatory and Antioxidant Effects of Carvacrol on N-Methyl-N′-Nitro-N-Nitrosoguanidine (MNNG) Induced Gastric Carcinogenesis in Wistar Rats

Carvacrol is a dietary polyphenol from Lamiaceae plants that has been shown to possess a wide range of biological activities including antioxidant and antitumor effects. This study aimed to investigate its anti-inflammatory and antioxidant effects on N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) induced gastric carcinogenesis in Wistar rats. Forty-nine rats were randomly assigned to four treatment and three control groups. Over 60 days, MNNG (200 mg/kg BW) was orally applied to animals of groups 1–5 while the rats in groups 2–5 also received different doses of carvacrol (10, 25, 50, and 100 mg/kg BW, respectively) until the end of the experiment. Group 6 rats were treated with 100 mg/kg BW carvacrol and no MNNG whereas group 7 was the control group without any treatment. After the euthanasia of all rats, the inflammatory cytokines and oxidative stress parameters were assessed in the blood and tissues. The expression of caspase 9, Bax, and Bcl-2 proteins in the stomach tissues were investigated through histopathological examinations. Statistically significant differences were observed in the body weight, oxidative stress, and inflammation parameters of groups 1 to 6 compared to group 7 (p ≤ 0.001). Animals in MNNG groups 2 and 3 treated with the low dose carvacrol (10 and 25 mg/kg BW) showed significantly reduced oxidative stress, inflammation, and apoptotic effect compared to animals of the MNNG groups receiving increased doses of carvacrol (50 and 100 mg/kg BW) or no carvacrol. Rats exposed to MNNG exhibited gastric cancer cells in several areas. In the MNNG group receiving 100 mg/kg BW carvacrol, the inflammatory cell infiltration was observed in gastric mucosal and submucosal areas whereas MNNG rats supplemented with 10 and 25 mg/kg BW carvacrol showed no pathological alterations of the gastric cells. The results of this study indicate that significant antioxidant and anti-inflammatory effects induced by carvacrol at doses of 10 and 25 mg/kg BW interfered with gastric carcinogenesis induced by MNNG in Wistar rats as well as provide hepatoprotection. However, high doses of carvacrol (50 and 100 mg/kg BW) increased oxidative stress, inflammation, and apoptosis.     

褐煤尘细胞毒性和致纤维化作用

为了评价褐煤尘的细胞毒性及致纤维化作用，对２个褐煤矿的煤尘成分、体外细胞毒性、体内致肺损伤作用进行了研究。甲矿煤尘游离ＳｉＯ２含量为３．４％，乙矿煤尘为１．５％。培养液中加入褐煤尘后肺巨噬细胞存活率明显降低，乳酸脱氢酶（ＬＤＨ）和酸性磷酸酶（ＡＣＰ）活力明显增高。乙矿煤尘组细胞存活率明显低于甲矿煤尘组，ＬＤＨ明显高于甲矿煤尘组。染褐煤尘大鼠肺体积、湿重、干重和胶原蛋白含量增加，病理检查可见到煤尘灶、肺气肿、网状纤维和胶原纤维轻度增生。结果表明：褐煤尘具有细胞毒性和轻度致纤维化作用，乙矿煤尘细胞毒性和致纤维化作用均高于甲矿煤尘，用煤尘中元素含量解释煤尘毒性与以往的研究结果不尽相同。     

NAC对染尘大鼠模型血清及肺组织中丙二醛的影响

目的探讨N-乙酰半胱氨酸(NAC)对二氧化硅所致大鼠肺纤维化血清及肺组织中丙二醛(MDA)的影响。方法取健康、雄性Wistar大鼠90只,随机分为3组:染尘组:采用经非暴露气管注入法,气管内注入无菌SiO2粉尘悬液(50 mg/ml)1 ml建立矽肺模型;4周后再次予以染尘1次。NAC预防治疗组:模型制备同染尘组,于染尘前1周及此后每日予以NAC[500 mg/(kg.d)]灌胃;对照组:同样条件下向气管内注入等量生理盐水。3组动物于实验第8周处死,取肺组织标本行病理学观察、测定肺组织及血清中MDA水平。结果染尘组及预防治疗组MDA含量明显高于对照组;预防治疗组MDA的含量明显低于染尘组,差异有统计学意义(P0.01)。结论 NAC可降低SiO2所致肺纤维化大鼠MDA的产生,抑制肺纤维化的发展,减轻对肺组织的损伤。     

Expression of clara cell secretory protein in the lungs of rats exposed to crystalline silica in vivo

It has been theorized that Clara cell secretion protein (CCSP) plays a critical role in regulating the acute inflammatory response in the lung. We hypothesized that CCSP is also related to lung injury induced by occupational dust. The present study was conducted to investigate the time course of the expression of CCSP in lungs exposed to crystalline silica in vivo. Male Wistar rats were administered 1 mg or 2 mg of silica suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 month, 3 months and 6 months of recovery time. The expression of CCSP was observed by RT-PCR and western blot analysis. Exposure to 2 mg of silica decreased in levels of CCSP mRNA at 3 d, 1 wk, 1 month and 6 months following intratracheal instillation. The protein level of CCSP in silica-exposed rats was decreased at 3 d, 7 d and 1 month after a single instillation of 2 mg. The decreases in CCSP at the acute phase in this experiment suggest that CCSP may regulate the acute injury of the lung exposed to silica.     

汽油尾气对大鼠睾丸组织的氧化损伤和遗传毒性作用

目的探讨汽油尾气对大鼠睾丸的遗传毒性及氧化损伤作用。方法将汽油尾气的颗粒物、冷凝物和半挥发性有机物的二氯甲烷提取物以0、5.6、16.7和50.0L/kg的剂量经气管滴注染毒SD大鼠,每周一次,共4次。末次染毒24h后处死动物,测定睾丸脏器系数、睾丸组织内丙二醛(MDA)和羰基蛋白(CP)含量以及超氧化物岐化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性;并用彗星实验检测睾丸组织细胞中DNA的单链断裂水平。结果各剂量组体重增重和睾丸脏脏器系数与对照组相比差异无显著性(P>0.05);中、高剂量染毒组睾丸组织中MDA和CP含量显著升高;各剂量组SOD酶活力明显降低(P<0.05),而GSH-Px活性的下降仅在高剂量组具有显著性。在16.7L/kg和50.0L/kg组,睾丸组织细胞的拖尾率较对照组明显增加(P<0.05),但尾长的增加仅在50.0L/kg组具有统计学意义。结论汽油尾气可诱导大鼠睾丸组织生物大分子的氧化损伤和DNA单链断裂。     

Acute silica toxicity: attenuation by amiodarone-induced pulmonary phospholipidosis.

Exposure to the toxic mineral dust silica has been shown to produce an acute inflammatory response in the lungs of both humans and laboratory animals. Coating silica with phospholipids reduces its toxicity when studied with in vitro systems. The drug amiodarone increases phospholipid within the cells, airways, and alveoli of the lungs. This increase in phospholipid is due to amiodarone's ability to inhibit phospholipase activity within alveolar macrophages (AMs) and whole lung. The purpose of this study was to determine whether the amiodarone-induced increase in pulmonary phospholipid would protect the lungs from acute damage caused by the intratracheal instillation of silica. Treatment of male Fischer 344 rats with amiodarone for 14 days caused an increase in phospholipid content in bronchoalveolar lavage fluid and AMs compared to vehicle-treated controls. The rats were then instilled with silica or saline vehicle. At both 1 and 14 days after silica exposure, pulmonary phospholipidosis was associated with a marked reduction in acute silica-induced pulmonary damage as assessed by biochemical parameters in bronchoalveolar lavage fluid, however, the influx of neutrophils into the airspaces was not reduced. Four times more phospholipid was bound to the silica recovered from amiodarone-treated rats compared to controls. The results of these in vivo experiments indicate that pulmonary phospholipidosis attenuates the acute damage associated with the intratracheal instillation of silica in rats. By using an in vitro cell culture system, we demonstrated that, in contrast to control AMs, phospholipidotic AMs were significantly more resistant to the cytotoxicity of surfactant-coated silica.(ABSTRACT TRUNCATED AT 250 WORDS)     

二氧化硅对大鼠血浆中微量元素含量的影响

给大鼠经气管分别注入４、１６、６４ｍｇ石英粉尘生理盐水混悬液。在染尘后第７，１５和３０天解剖动物，测定血浆中Ｃｕ、Ｚｎ，Ｍｎ、Ｍｏ、Ｓｉ、Ｒｂ和Ｓｒ等７种微量元素的含量。实验结果表明，随着染尘剂量的增加，血浆中铜的含量明显增高，呈正相关，相关系数为０．９９９。而血浆锌的含量随着染尘剂量的增加而明显的降低，呈负相关，相关系数为－０．９９８。血浆中Ｍｏ、Ｍｎ、Ｓｉ、Ｒｂ和Ｓｒ含量与对照组比无明显差异。     

高浓度矽尘接触对大鼠氧化应激的作用研究

目的探讨大鼠高浓度矽尘接触过程中是否存在氧化应激反应。方法选40只SPF级Wistar雄性大鼠随机分为4组,即高剂量染尘组（1 000mg/m^3）、中剂量染尘组（500mg/m^3）、低剂量染尘组（100mg/m^3）和对照组,选用自然动式染尘装置每天染尘2h。染尘49d后处死大鼠,测定肺组织匀浆超氧化物歧化酶（SOD）、总抗氧化能力（T-AOC）活性及丙二醛（MDA）、还原性谷胱甘肽（GSH）含量。结果长时间、高浓度矽尘接触降低大鼠肺组织的SOD（30.25±0.49）U/ml、T-AOC活性（7.93±0.74）kU/L和GSH（2.34±0.96）g/L含量,同时MDA（5.65±0.13）nmol/ml水平升高,与对照组比较,差异有统计学意义（P〈0.01）。结论大鼠高浓度矽尘接触过程早期炎症反应发生可能与机体氧化应急有关。     

车间空气中玻璃钢粉尘卫生标准研制

目的　制订车间空气中玻璃钢粉尘卫生标准。方法　采用现场劳动卫生流行病学调查方法及用玻璃钢粉尘对大鼠肺脏进行致纤维化实验研究 ,观察大鼠全肺干质量和全肺胶原蛋白含量。结果　该粉尘可引起大鼠全肺干质量和全肺胶原蛋白含量增加 (P <0 0 1或P <0 0 5 ) ,且有剂量 反应关系 ,作业工人有“尘肺”样改变。结论　根据动物实验研究和现场劳动卫生学调查结果 ,提出车间空气中玻璃钢粉尘最高容许浓度为 6mg/m3,时间加权平均容许浓度为 3mg/m3。     

Remedial effect of lupeol and its ester derivative on hypercholesterolemia-induced oxidative and inflammatory stresses

In the hypercholesterolemic condition, the net result of combined lipemic-oxidative and inflammatory aberrations is manifested as an increase in adhesion molecule expression, increased vascular permeability, and the progress of atherogenesis. The aim of the present work is to evaluate the role of lupeol and its ester derivative on oxidative and inflammatory abnormalities in hypercholesterolemic condition. Hypercholesterolemia was induced in male albino rats of Wistar strain by feeding them a high-cholesterol diet (HCD) containing normal rat chow supplemented with 4% cholesterol and 1% cholic acid for 30 days. The pentacyclic triterpene, lupeol, and the ester derivative of lupeol, lupeol linoleate, were supplemented (50 mg/kg body weight per day, PO) during the last 15 days. Oxidative stress in HCD-fed animals was characterized by a significant increase in reactive oxygen species with concomitant decrease in the thiol levels in heart. Cardiac nuclear factor-κB nuclear translocation was confirmed by immunohistochemisty in HCD-fed rats. The tumor necrosis factor- levels showed an increase in hypercholesterolemic condition, whereas a departure toward control values and decreased nuclear translocation of nuclear factor-κB and oxidative stress were notable in supplementation with triterpenes. The nitric oxide levels and mRNA expression for inducible nitric oxide synthase was also significantly increased in HCD-fed animals. Treatment with lupeol and lupeol linoleate reversed the nitrosative stress to near normalcy. These observations highlight the beneficial effects of the triterpene, lupeol, and linoleate ester in ameliorating the oxidative and inflammatory abnormalities in the hypercholesterolemic conditions.     

Lung dust content and response in guinea pigs inhaling three forms of silica

Guinea pigs were exposed by inhalation to atmospheric suspensions of crystalline free silica (cristobalite), amorphous free silica (diatomaceous earth), and amorphous silicate (volcanic glass). Randomly selected animals were killed at 2-month intervals and their lungs were examined. Tissue samples were collected and analyzed for total silica content and total ash. Total silica content per lung increased linearly throughout at least 21 months in each experiment and total ash weight increased more rapidly than dust was accumulating. Crystalline silica produced a greater increment in ash weight that did the amorphous free silica and the silicate produced the least increase. Furthermore, although atmospheric dust concentrations were roughly comparable for the three preparations, the total amount of silica accumulated varied inversely with the degree of tissue damage occurring. Thus, the maximum total content of the crystalline silica reached only 68 mg per lung, while that of the amorphous silica and silicate was 120 mg and 465 mg, respectively. This suggests that a silicious dust that produces cell damage may be cleared more effectively from the lung than is an innocuous dust.     

Maganese retention in rat brain

Manganese retention was observed in brains and in several other tissues of female Wistar rats after the intratracheal instillation of an inorganic manganese compound: manganese dioxide. Two categories of rats, younger (180 to 200g) and older (330 to 350g), were divided into a control group, in which animals received vehicle only (0.5 mL physiological saline), and an experimental group, in which rats received a dose of 0.48 mg of Mn/kg body weight (in 0.5 mL saline), twice a week for 3 months, for a total dosage of 11.80 mg of Mn/kg body weight. At the end of the exposure period, manganese retention in selected rat organs, brain, liver, kidney, and lung, was analyzed using atomic absorption spectrophotometry. At the end of the 6-wk or 12-wk manganese dioxide exposure period, analysis of variance of the manganese retention results revealed significant differences between Mn-exposed and unexposed rats in brain, kidney, and lung tissues (p<0.01) for both experimental age categories. Moreover, at the end of the 12-wk exposure period, significant results (p<0.05) between younger and older rats were obtained for both brain and kidneys. In both types of tissue, the manganese retention in the younger group was higher than that in older animals.     

Pulmonary response to exposure to ozone of emphysematous rats

Rats were treated with a single intratracheal instillation of 6.5 units elastase or normal saline. Seven weeks after treatment, the animals were exposed for 24 hr to filtered air or 1 ppm O3, and their lung functions were measured. The exposure to O3 resulted in functional changes depending mainly on peripheral airway obstruction, and the direction and degree of those functional changes were in general similar between the saline- and elastase-treated animals. Another group of saline- or elastase-treated rats were exposed to 3 ppm O3 for 3 hr and the edematous response of their lungs was again similar. These results indicate that elastase-treated lungs responded to the exposure to O3 in a fashion similar to normal lungs in rats, but lung damage caused by the exposure to O3 superimposed over preexisting emphysematous damage, resulted in an additional lessening of the margin of pulmonary reserve capacity.     

Purple grape juices prevent pentylenetetrazol-induced oxidative damage in the liver and serum of Wistar rats

Oxidative damages in hepatocytes may be caused by epilepsy and/or anticonvulsant drugs. Epilepsy is one of the most common neurological disorders, characterized by recurrent seizures, which may increase the content of reactive oxygen species. Organic and conventional grape juices are rich in polyphenols, compounds with important antioxidant activity. It is hypothesized that organic and conventional purple grape juices may have protective effect against oxidative damage induced by pentylenetetrazole (PTZ) (a standard convulsant drug) in the liver and serum of Wistar rats. Animals (n = 16 in each group) received, by gavage, saline, organic grape juice or conventional grape juice (10 μL/g of body weight) for 17 days. Subsequently, half of the rats in each group received PTZ (60 mg/kg). After 30 minutes, the animals were euthanized by decapitation. Liver and blood samples were isolated to evaluate oxidative parameters (lipid and protein oxidation, nitric oxide metabolite content, antioxidant defenses, and protein sulfhydryl content). The results of this study showed that although organic juice contains higher polyphenol content than conventional juice, both juices conferred protection against lipid and protein oxidative damage and limited the increase in PTZ-induced nitric oxide metabolite content in the liver and serum. In addition, both juices inhibited the PTZ-induced reduction in enzymatic antioxidant defenses (superoxide dismutase and catalase activities) and sulfhydryl protein content in the liver and serum. In summary, both organic and conventional grape juices were able to reduce oxidative damage induced by PTZ in the liver and serum of Wistar rats.     

吡非尼酮对大鼠矽肺纤维化的抑制作用

目的 探讨吡非尼酮(PFD)对大鼠矽肺纤维化的抑制作用.方法 75只SD雄性大鼠,随机分成未处理对照组、生理盐水组、生理盐水+PFD组、SiO2组、SiO2+PFD组,每组15只,采用非暴露式气管内染尘法,SiO2组和SiO2+PFD组注入SiO2粉尘悬液(25 mg/ml),生理盐水组和生理盐水+PFD组注入等量生理盐水,染尘后第2天灌胃给予PFD(50 mg/kg),分别观察7、21、42 d后处死.HE、VG和Foot染色观察肺组织的病理形态学改变并进行病理分级,测定肺组织中羟脯氨酸(HYP)的含量.结果 大鼠肺组织病理观察显示,SiO2+PFD组肺组织纤维化程度比同期SiO2组明显减轻,胶原纤维形成缓慢,矽结节分级评分降低.第42天时,SiO2+PFD组大鼠肺组织HYP含量[(0.75±0.12)mg/g肺组织]比SiO2组[(1.19±0.17)mg/g肺组织]明显降低,差异有统计学意义(P＜0.05).结论 PFD能降低大鼠矽肺纤维化程度并减少肺组织中HYP的含量,对实验性大鼠矽肺纤维化具有抑制作用.