大鼠肺纤维化过程中白细胞介素6的观察

采用气管内灌注博莱霉素（ＢＬＭ）复制大鼠肺纤维化模型,动态观察支气管肺泡灌洗液（ＢＡＬＦ）和肺泡巨噬细胞（ＡＭ）培养上清及血清中白细胞介素６（ＩＬ６）的活性变化,从而探讨ＩＬ６和肺纤维化的关系。材料与方法　（１）动物分组：体重１８０～２２０ｇ雄性大鼠８０只,随机分为ＢＬＭ组和对照组,每组４０只,用一次性气管内注入ＢＬＭ法复制肺纤维化模型,分别于灌注ＢＬＭ后的不同时期处死大鼠,收集血清于－２０℃保存,采用支气管肺泡灌洗法获取ＢＡＬＦ,每只大鼠共灌洗１２ｍｌ,平均回收率为（８９±３）％,离心后取…     

肺成纤维细胞在实验肺纤维化中释放生物活性物质和体外研究

目的 阐明在肺纤维化过程中肺成纤维细胞（ＬＦ）产生透明质酸（ＨＡ）,白细胞介素８（ＩＬ－８）和胶原的动态变化及作用。方法 检测博莱霉素（ＢＬＭ）致大鼠肺纤维化不同时期ＬＦ培养上清中ＩＬ－８活性,ＨＡ和羟脯氨酸（ＨＹＰ）水平。结果 ＢＬＭ组ＬＦ的上清中（１）ＨＡ水平于第１天明显升高,第３天达高峰,随后降低,第１４￣２８天降至正常。（２）ＩＬ－８活性于第１天明显增高,每高倍镜视野细胞数为４．０６±０．     

人参对实验性缺血心肌细胞β受体及cAMP含量的影响

目的：观察人参对实验性缺血心肌细胞β受体及ｃ Ａ Ｍ Ｐ含量的影响。方法：对４５ 只健康成年 Ｓ Ｄ 纯种大鼠随机分为假手术对照组、单纯冠状动脉结扎组及冠状动脉结扎加人参治疗组，每组 １５ 只，应用受体放射分析法测定心肌细胞膜 β受体数量和解离常数（ Ｋｄ），放射免疫分析法测定各组心肌细胞内ｃ Ａ Ｍ Ｐ含量，在各组间进行比较。结果：结扎 Ｌ Ａ Ｄ２ 周后心肌细胞β受体的最大结合量（ Ｂｍ ａｘ，０．２７９ ｎｍ ｏｌ）较假手术组（０．０９３ ｎｍ ｏｌ）明显升高（ Ｐ ＜ ０．０５）；心肌细胞 β受体的 Ｋｄ（１２．４３１ ｎｍ ｏｌ）较假手术组（１．３１９ ｎｍ ｏｌ）明显升高（ Ｐ ＜ ０．０５）；心肌细胞内ｃ Ａ Ｍ Ｐ水平〔（１ ２９３．９６±５１９．３６） ｐｍ ｏｌ／ｇ〕亦明显高于假手术组〔（７７４．４４±２１０．５５） ｐｍ ｏｌ／ｇ〕（ Ｐ ＜ ０．０１）；经人参治疗 ２周后缺血心肌内 ｃ Ａ Ｍ Ｐ 水平〔（８０５．０２±３６２．４８） ｐｍ ｏｌ／ｇ〕明显低于单纯冠状动脉结扎组（ Ｐ ＜０．０１），与假手术组相似。结论：人参有降低缺血心肌内ｃ Ａ Ｍ Ｐ水平的作用。     

哮喘气道炎症粘附机制的实验研究

目的评价细胞间粘附分子１（ＩＣＡＭ１）、Ｐ选择素在哮喘气道炎症粘附机制中的作用,进一步阐明哮喘的发病机理。方法用酶联免疫吸附试验、肺组织免疫组化检查和呼吸生理学方法系统观察正常组和哮喘组豚鼠各项指标。结果（１）哮喘组豚鼠肺潮气量、动态肺顺应性（Ｃｄｙｎ）和肺气道阻力与对照组比较差异有显著性（Ｐ＜０．０１及Ｐ＜０．０５）。（２）哮喘组豚鼠血浆和肺泡灌洗液（ＢＡＬＦ）可溶性ＩＣＡＭ１（ｓＩＣＡＭ１）、可溶性Ｐ选择素、血清和ＢＡＬＦ嗜酸粒细胞阳离子蛋白（ＥＣＰ）与对照组比较,差异有显著性（Ｐ＜０．０１）;ＢＡＬＦ中白细胞介素８（ＩＬ８）与对照组比较差异也有显著性（Ｐ＜０．０１）。（３）哮喘组豚鼠肺组织（气道上皮和血管内皮）ＩＣＡＭ１和ＩＬ８表达与对照组比较,差异有显著性（Ｐ＜０．０１）。结论ＩＣＡＭ１、Ｐ选择素、ＩＬ８、ＥＣＰ参与介导了哮喘气道炎症的粘附过程     

间质性肺疾病支气管肺泡灌洗液的酶活性研究

目的探讨支气管肺泡灌洗液（ＢＡＬＦ）多项酶活性与间质性肺疾病（ＩＬＤ）的关系。方法检测３０例ＩＬＤｓ：包括特发性肺纤维化（ＩＰＦ）１８例和结节病（Ｓａｒｃ）１２例与９例正常对照者的ＢＡＬＦ中超氧化歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）、血管紧张素转换酶（ＡＣＥ）和乳酸脱氢酶（ＬＤＨ）活性，并分类计数ＢＡＬＦ细胞成份。结果（１）ＩＰＦ组ＢＡＬＦ中各项酶活性均与对照组间差异有显著性（ＳＯＤ和ＧＳＨ－ＰＸ降低，ＡＣＥ和ＬＤＨ升高）（Ｐ＜０．０５）；而Ｓａｒｃ组仅见ＡＣＥ明显增高（Ｐ＜０．０５）。（２）ＢＡＬＦ－ＡＣＥ与Ｓａｒｃ组淋巴细胞百分比及ＣＤ＋４／ＣＤ＋８比值均有显著线性相关（Ｐ＜０．０５）。结论ＢＡＬＦ中ＳＯＤ、ＧＳＨ－ＰＸ、ＡＣＥ和ＬＤＨ活性测定，有助于进一步探讨ＩＬＤ发病机理和提供辅助诊断依据，ＢＡＬＦ－ＡＣＥ对判断Ｓａｒｃ活动性有重要临床意义。     

肺纤维化大鼠支气管肺泡灌洗液中两种可溶成份的变化

肺纤维化大鼠支气管肺泡灌洗液中两种可溶成份的变化陈佰义姜莉赵洪文吕长俊侯显明以博莱霉素气管内灌注复制大鼠肺纤维化模型，收集支气管肺泡灌洗液（ＢＡＬＦ）［１］，研究其纤维联结蛋附表ＢＡＬＦ中的ＦＭ和ＨＡ及肺ＨＹＰ的动态变化（ｘ±ｓ）项目只数ＦＮ（ｎｇ／...     

搏动性体外循环对肺内白细胞聚集及脂质过氧化的影响

观察体外循环（ＣＰＢ） 心内直视手术期间白细胞总数及分类、血浆丙二醛（ＭＤＡ） 的变化。结果显示搏动性血流（ＰＦ） 灌注组转流结束时左右心房血白细胞总数分别为（８２０±１６７） ×１０９／Ｌ及（ ８７６±１４２） ×１０９／Ｌ; 转流前及转流结束时血浆ＭＤＡ 分别为２８７±０２８ｎｍ ｏｌ／ｍ ｌ及３４０±１４９ｎｍ ｏｌ／ｍ ｌ; 差异均无显著性。而非搏动性血流（ＮＰＦ） 灌注组左心房血白细胞总数明显低于右心房血及血浆ＭＤＡ明显高于转流前, 转流结束时血浆ＭＤＡ明显低于ＮＰＦ组（４３２±０９９ｎｍ ｏｌ／ｍ ｌ）。提示应用搏动性ＣＰＢ可减轻肺内白细胞聚集及脂质过氧化作用, 改善ＣＰＢ肺保护。     

间质性肺疾病支气管肺泡灌洗液中性粒细胞趋化因子和肿瘤坏死因子水平及其临床意义

目的探讨间质性肺疾病（ＩＬＤ）时中性粒细胞趋化因子（ＮＣＦ）和肿瘤坏死因子（ＴＮＦα）与ＩＬＤ活动性的关系。方法用膜滤过和放射免疫法检测１１例结节病、７例特发性肺间质纤维化（ＩＰＦ）患者和８名健康者血清及支气管肺泡灌洗液（ＢＡＬＦ）中ＮＣＦ活性及ＴＮＦα水平。结果７例ＩＰＦ患者ＢＡＬＦ中ＮＣＦ、ＴＮＦα分别为２０３±４４ｃｅｌｓ／１０ＨＰ、１１７±２９ｎｇ／Ｌ，明显高于８名对照组（８３±４５ｃｅｌｓ／１０ＨＰ、６５±１４ｎｇ／Ｌ、Ｐ＜０．０１）；１１例结节病患者ＢＡＬＦ中ＮＣＦ、ＴＮＦα分别为１８６±５０ｃｅｌｓ／１０ＨＰ、１２±３ｎｇ／Ｌ，明显高于８名对照组（Ｐ＜０．０１）。ＩＰＦ组ＢＡＬＦ中ＮＣＦ、ＴＮＦα均与中性粒细胞百分比呈正相关（ＮＣＦ：ｒ＝０．８９，Ｐ＜０．０１，ＴＮＦα：ｒ＝０．８６，Ｐ＜０．０５），结节病组ＢＡＬＦ中ＮＣＦ、ＴＮＦα均与淋巴细胞百分比呈正相关（ＮＣＦ：ｒ＝０．７８，Ｐ＜０．０１；ＴＮＦα：ｒ＝０．７３，Ｐ＜０．０１）。结论ＩＰＦ和结节病患者ＢＡＬＦ中ＮＣＦ、ＴＮＦα水平可做为肺泡炎活动性的标志     

胃十二指肠疾病患者骨矿物质含量的变化意义

目的研究慢性胃炎、胃十二指肠溃疡和胃癌患者骨矿物质含量变化的意义．方法用单光子吸收法，以桡骨长度中下１／３处为测定点，测定慢性胃炎（ｎ＝３１）、消化性溃疡（ｎ＝２６）、胃癌（ｎ＝９）及正常对照组（ｎ＝４３）的骨矿物质含量，并以骨矿含量（ＢＭＣ，ｇ／ｃｍ）及骨面密度（ＢＭＣ／ＢＷ，ｇ／ｃｍ２）表示，并进行比较．结果慢性萎缩性胃炎（ｎ＝１４），ＢＭＣ＝１００８±０２２８ｇ／ｃｍ）和十二指肠球部溃疡（ｎ＝１６），ＢＭＣ＝０９０４ｇ／ｃｍ±０２０５ｇ／ｃｍ，ＢＭＣ／ＢＷ＝０６５２ｇ／ｃｍ２±００８６ｇ／ｃｍ２）骨矿含量显著低于正常对照组（ｎ＝４３，ＢＭＣ＝１１７６ｇ／ｃｍ±０３４１ｇ／ｃｍ，ＢＭＣ／ＢＷ＝０７８２ｇ／ｃｍ２±０１３４ｇ／ｃｍ２，Ｐ＜００５）．结论萎缩性胃炎及十二指肠溃疡患者ＢＭＣ明显下降，需纠正．     

哮喘豚鼠免疫治疗初步观察

目的初步观察抗白细胞介素５（ＩＬ５）单抗对哮喘豚鼠嗜酸性粒细胞（ＥＯＳ）的影响。方法用鸡卵清蛋白（ＯＶＡ）腹腔注射法复制豚鼠哮喘模型，随机分为两组，每组１５只，联合应用雾化吸入和腹腔注射法分别给予生理盐水（ＮＳ）及抗ＩＬ５单克隆抗体（ＭｃＡｂ）治疗，比较基础、治疗前、后外周血（ＰＢ）和支气管肺泡灌洗液（ＢＡＬＦ）中ＥＯＳ的改变。结果ＭｃＡｂ治疗组豚鼠外周血ＥＯＳ计数治疗前［（１７６±０２７）×１０９／Ｌ］与治疗后［（１６３±０２６）×１０９／Ｌ］比较，差异有显著性（Ｐ＜０．０５），而ＮＳ组则无明显改变（Ｐ＞０．０５）；治疗后ＭｃＡｂ组ＢＡＬＦ中ＥＯＳ数［（０４１±００６）×１０９／Ｌ］与ＮＳ组［（０４６±００７）×１０９／Ｌ］比较，差异有显著性（Ｐ＜０．０５）。结论该抗ＩＬ５单抗具有下调外周血和气道ＥＯＳ功能     

红霉素对肺纤维化大鼠核因子κB活性及细胞因子mRNA表达 …

目的 探讨红霉素治疗肺纤维化的机制和疗效。方法 实验用Ｗｉｓｔａｒ大鼠８１只,分成三组;正常一附属博莱霉素模型组和红霉素治疗组。每组２７只。气管内注入单剂量博莱霉素制备大鼠肺纤维化模型,于博莱霉素气管内注入后每日给予口红霉素治疗,各组动物分别于气管内用药后第４,７和２８天处死动物。用凝胶电泳迁移实验测定肺泡巨噬细胞的核因子（ＮＦ）－κＢ活性;     

Implication of CD44 in adhesion-mediated overproduction of TGF-β and IL-1 in monocytes from patients with bone marrow fibrosis

Myelofibrosis (MF) is characterized by bone marrow (BM) fibrosis and excessive deposits of extracellular matrix (ECM) proteins which include fibronectin (FN), collagen type I and hyaluronic acid (HA). We have previously reported that adhesion to polystyrene overactivates MF monocytes. We now confirm their activation by increased CD25 expression and tyrosine phosphorylation. We hypothesize that ECM protein-adhesion molecule interactions induce overproduction of fibrogenic cytokines in MF monocytes leading to BM fibrosis. In this study we found that FN, collagen type I and HA induce 2–3-fold more TGF-β and 6–9-fold more interleukin (IL)-1 in MF monocytes than normal controls (NC). Since CD44 can function as the natural ligand for these proteins, its role was studied. We found that CD44 mediated most of the TGF-β and IL-1 produced. Immunoprecipitation of CD44 revealed three proteins at approximately 110 kD in MF monocytes and one in NC. Our results indicate that adhesion is important in overproduction of TGF-β and IL-1, and that their production is at least partly mediated by adhesion molecule–ECM protein interactions. These results implicate at least one adhesion molecule, CD44, in the pathophysiology of BM fibrosis.     

Ameliorating effect of erythromycin on bleomycin-induced pulmonary fibrosis: Role of alveolar macrophage activation and cytokine release

Abstract The objective of this study was to evaluate the effectiveness of erythromycin (EM) on bleomycin-induced pulmonary fibrosis in rats and its possible mechanisms. Seventy-five rats were divided into three groups. Alveolar macrophages (AM) were harvested through bronchalveolar lavage (BAL) and consecutive changes of tumour necrosis factor-α (TNF-α) and platelet-derived growth factor (PDGF) in AM supernatant and bronchoalveolar lavage fluid (BALF) were assayed with ELISA and bioassay, respectively. The AM-derived TNF-α was elevated on day 3, peaked day 7 and then decreased but remained at higher level until day 28. The AM-derived PDGF was increased on day 3, peaked on day 7 then decreased to non-statistically significant higher level. The TNF-α in BALF was increased significantly on day 3 then decreased to normal level; the peak preceded that of AM-derived TNF-α. The PDGF in BALF was increased on day 3, peaked on day 7, and then decreased to normal, which exhibited a consecutive change similar to that of AM-derived PDGF. The EM significantly suppressed TNF-α and PDGF release by AM, markedly decreased TNF-α and PDGF levels in BALF. The EM also lessened the collagen deposition, the lung hydroxyproline comprised 75.44%, 72.72% and 56.24% that of bleomycin-treated group on day 7, 14 and 28, respectively. In conclusion, EM can ameliorate bleomycin-induced pulmonary fibrosis possibly through suppression of TNF-α and PDGF as well as the inhibition on accumulation of inflammatory cells in the lung.     

老年肺结核患者白细胞介素6分泌水平的研究

目的探讨老年肺结核患者细胞免疫功能。方法采用ＭＴＴ（噻唑蓝）比色法,检测其外周血单个核细胞（ＰＢＭＣ）白细胞介素６（ＩＬ－６）分泌水平。结果①老年肺结核ＩＬ－６水平明显高于正常人（Ｐ＜０．０５）;②肺结核进展期ＩＬ－６水平老年组低于中青年组（Ｐ＜０．０１）,而好转期无此差异（Ｐ＞０．０５）;③老年肺结核进展期与好转期相比ＩＬ－６分泌高峰前移;④ＩＬ－６水平与结核病变范围及排菌情况均有关且差异显著（Ｐ＜０．０１）。结论检测ＩＬ－６水平有助于老年肺结核免疫状况观察及病情监测。     

Increased spontaneous interleukin-10 release from alveolar macrophages in active pulmonary sarcoidosis

The study was designed to determine whether alveolar macrophages (AM) in acute pulmonary sarcoidosis release in vitro the anti-inflammatory cytokine interleukin (IL)-10. To learn more about the coherence between IL-10 and proinflammatory cytokines in active sarcoidosis, the release of interferon (IFN)-gamma, macrophage inhibitory protein (MIP)-1alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF) was studied and additionally compared to normal controls and patients with pneumonia and interstitial lung fibrosis. AM were obtained by bronchoalveolar lavage from 13 patients with active sarcoidosis, 8 patients with interstitial lung fibrosis, 10 patients with bacterial pneumonia, and 14 normal controls. The spontaneous and stimulated (tumor necrosis factor [TNF]-alpha, IL-1beta) cytokine release was measured in the supernatant of cultured AM by enzyme-linked immunosorbent assay (ELISA). Unstimulated AM from sarcoidosis patients released more IL-10, IFN-gamma, MIP-1alpha, and GM-CSF than normal controls and patients with pneumonia and interstitial lung disease. Stimulation with TNF-alpha or IL-1beta increased the MIP-1alpha and GM-CSF release from AM of normal controls and patients with pneumonia and interstitial lung disease: however, no further enhancement of MIP-1alpha and GM-CSF production was observed in AM from sarcoidosis patients. Exogenous IL-10 reduced the spontaneous and stimulated MIP-1alpha and GM-CSF release in sarcoidosis to a lesser extent than in controls and patients with fibrosis and pneumonia. The up-regulated IL-10 in active pulmonary sarcoidosis may be a compensatory response to the enhanced expression of proinflammatory cytokines in order to down-regulate the inflammatory process. The results suggest an involvement of the anti-inflammatory cytokine IL-10 in the immunopathogenesis of sarcoidosis.     

Dynamics of changes of blood inflammatory-oxidative biomarkers in acute coronary syndrome

Some inflammatory cytokines and parameters of low density lipoproteins (LDL) oxidative modification were studied in blood of 250 acute coronary syndrome (ACS) patients--Siberian inhabitants, men and women with myocardial infarction (MI) or unstable angina on first, tenth and thirtieth days of disease. The inflammatory biomarkers in men and women with MI are: increased concentrations of interleukin (IL)-6, IL-8 and C-reactive protein (CRP), especially on the first day of disease. The most significant inflammatory biomarker of ACS is increased CRP level, especially in women. Oxidative biomarkers in men with ACS are increased basal level of LDL lipid peroxidation (LPO) products and decreased LDL resistance to oxidation. Inflammatory-oxidative biomarkers IL-6, IL-8, CRP and basal level of LDL LPO products are correlated and independently associated with MI.     

肺结核患者血清纤维化指标与肺通气功能的相关性研究

目的探讨血清纤维化指标作为肺结核患者肺纤维化诊断及治疗的实验室指标的可行性。方法测定所选病例的肺功能及血清纤维化指标,根据肺功能结果分为肺功能基本正常组[1](A组,20例)、轻度减退组(B组,35例)、显著减退组(C组,46例)、严重减退组(D组,29例)。结果A组血清Ⅲ型前胶原(PⅢP)平均值为16±2 ng/ml,血清透明质酸(HA)、血清层连蛋白(LN)平均水平分别为(88±6)(、98±15)ng/ml,血清Ⅳ型胶原(cⅣ)均值为(120±26)ng/ml;B组PⅢP均值为(19.5±4)ng/ml,HA均值为(92.6±12)ng/ml,LN均值为(102±16)ng/ml,cⅣ均质为(141±31)ng/ml;C组PⅢP均值为(25.4±4)ng/ml,HA均值为(95±21)ng/ml,LN均值为(111.8±30)ng/ml,cⅣ均质为(158±39)ng/ml;D组PⅢP均值为(28.9±5)ng/ml,HA均值为(108±18)ng/ml,LN均值为(132±37)ng/ml,cⅣ均质为(193±46)ng/ml。四组中cⅣ、PⅢP的平均值经方差分析F值分别为17.85、55.9,说明4组cⅣ、PⅢP均值有显著性差异,经F检验各组间有显著性差异;4组中HA、LN的均值经方差分析F值分别为7.388、.69,具有显著性差异,经F检验各组间无显著性差异;cⅣ、PⅢP、HA、LN分别与一秒钟用力呼气容积率(FEV_1.0%)做相关回归分析P值分别为0.015、0.009、0.093、0.12,说明cⅣ、PⅢP与肺功能存在直线关系,而HA、LN则不具有。结论血清纤维化指标与肺结核患者的肺功能状态有相关性,在一定程度上反应了肺纤维化程度,其中cⅣ、PⅢP与肺纤维化程度的相关性最强。     

乌司他丁对放射性肺损伤模型大鼠干预作用及层黏连蛋白和羟脯氨酸的影响

目的 探讨乌司他丁对放射性肺损伤的治疗作用及层黏连蛋白(LN)和羟脯氨酸(Hyp)在放射性肺损伤中的变化.方法 雌性SD大鼠100只随机分为3组:正常对照组(C组)24只,单纯照射组(R组)40只,乌司他丁治疗组(U组)36只.R组及U组动物麻醉后,行直线加速器全胸部照射一次,剂量为25 Gy.U组照射后即按乌司他丁100 000 U/kg,尾静脉注射,而后每天以相同剂量尾静脉注射7 d.C组和R组尾静脉注射等体积生理盐水.于照射后第7、15、30、60、90、150天处死动物,取部分肺组织行HE染色及Masson染色,观察组织学及肺胶原纤维等,使用放射免疫法检测血清中LN水平,碱水解法测定血清中Hyp的含量.结果 U组大鼠生存率(88.9%)明显高于R组大鼠(62.5%).R组大鼠肺部在照射后,早期肺泡明显出现充血和水肿,晚期部分肺泡腔塌陷,可见成纤维细胞构成的成纤维病灶,甚至大面积的肺完全实变;与R组相比,U组中、晚期充血、水肿及肺间隔增宽不明显,少见纤维化病灶及实变.R组血清中LN、Hyp水平随着照射时间逐渐增加,在150 d时达到高峰,分别为(129.70±3.48)ng/ml、(193.70±5.41)ng/ml,这与肺部组织学变化趋势基本一致,U组与R组相比却明显减少(P<0.01).结论 乌司他丁能有效治疗放射性肺损伤,为放射性肺损伤的防治提供了一种新的方法.     

引经药柴胡对胰腺纤维化大鼠细胞外基质合成调控增效的作用

[目的]观察引经药柴胡对大黄丹参调控胰腺纤维化大鼠细胞外基质(ECM)合成增效的作用。[方法]50只雄性SD大鼠随机分为假手术组、模型组、柴胡组、大黄丹参组和柴胡大黄丹参组,每组10只。假手术组开腹后关腹,其他各组通过结扎胰胆管联合腹腔注射雨蛙素3d建立胰腺纤维化模型;柴胡组、大黄丹参组、柴胡大黄丹参组分别于术前、后3d用对应药物灌胃(剂量分别为1.38g.kg-1.d-1、3.04g.kg-1.d-1、4.11g.kg-1.d-1)。术后第4天取材用苏木精-伊红染色观察胰腺病理学变化,免疫组化检测胰腺α-平滑肌肌动蛋白及Ⅰ型胶原表达,ELISA测定血清纤维连接蛋白(FN)、层结合蛋白(LN)含量。[结果]与模型组相比,柴胡组、大黄丹参组和柴胡大黄丹参组均可改善胰腺病理变化,降低α-平滑肌肌动蛋白、Ⅰ型胶原表达,降低血清LN及FN含量,均P0.01;其中柴胡大黄丹参组FN含量降低更显著。[结论]柴胡、大黄丹参、柴胡大黄丹参均可通过抑制ECM合成来发挥抗胰腺纤维化的作用,其中柴胡大黄丹参在降低血清FN含量方面效果最优,提示柴胡在抑制胰腺ECM合成方面对大黄丹参存在一定的增效作用。     

纤维连接蛋白在大鼠肺纤维化中的作用

目的 研究纤维连接蛋白(FN)在肺纤维化中的作用。方法 用免疫组织化学方法观察实验性大鼠肺纤维化纤维连接蛋白（FN）的动态变化;用Northem印迹杂交和免疫细胞化学方法分别观察FN对体外培养的大鼠肺成纤维细胞I、Ⅲ型前胶原mRNA和蛋白表达的影响。结果（1）实验性肺纤维化大鼠肺组织内FN的含量持续增多;（2）体外培养的肺成纤维细胞经FN作有2h,I、Ⅲ型前胶原mRNA的表达即增强,分别在12h、6h达到最大值,平均吸光度（A值）为对照组的1．7、3．2倍;I、Ⅲ型前胶原蛋白的表达亦增强（P＜0．01）。抗FN受体的抗体能部分抑制FN对胶原表达的上调作用（P＜0．05）。结论 FN能够促进大鼠肺成纤维细胞合成I、Ⅲ型胶原、其调控机制之一是在转录水平上增强了前胶原mRNA的表达。