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纤维化

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aim to study the efficaciousness of wuling cap-sules for hepatic fibrosis in rats.methods rat models with hepatic fibrosis were induced by ccl4 compound factors and then treated with wuling capsules.pathology of liver sections,hyaluronic acid and procollagencontents in rat liver and serum were examined respectively.results pathological examinations showed that the liver cells of mod-el rats were injured seriously.collagen fibers proliferated and dissected hepatic lobules in model rats.wuling capsules could protect liver cells and reduce degrees of hepatic fibro-sis.the best effects were achieved at3.0g?

目的 研究五灵胶囊对大鼠肝纤维化的作用。方法采用以四氯化碳为主的复合因素致大鼠肝纤维化,观察五灵胶囊对肝组织病理学、肝组织和血清中羟脯氨酸、ⅰ,ⅲ型前胶原含量的影响。结果病理学检查显示,模型组大鼠肝细胞损伤严重,胶原纤维大量增生,形成假小叶。五灵胶囊组大鼠肝细胞结构破坏不明显,肝纤维化程度轻,在3.0g?kg-1 时治疗效果最好。

ConclusionGR mRNA upregulation in lung tissue could be one of the mechanism of glucocorticoid's effective cure for pulmonary fibrosis,and GR mRNA downregulation in lung tissue in renalyang asthenia syndrome could be one of cause of glucocorticoid's noneffective therapy for pulmonary fibrosis,in addition,the Chinese traditional medicine with warming Yang effect could be effective therapy for pulmonary fibrosis.

结论肺组织GRmRNA表达的上调是糖皮质激素防治肺纤维化之所以有效的机理之一,而肾阳虚状态下肺纤维化肺组织GRmRNA表达下调是临床上许多肺纤维化病人对糖皮质激素不敏感的原因之一,同时,温阳药也极可能具有防治肺纤维化的作用。

Results (1) The degrees of alveolitis and pulmonary fibrosis of the model group was increased remarkably on day 7,14,28 compared with the control group (P.05), The expression of TNF-α, TGF-β1, FN protein of model group on day 7, 14, 28 was remarkably increased compared with the control group (P.05);(2)The degrees of fibrosis and the expression of TNF-α, TGF-β1 , FN protein are decreased significantly in Group B compared with Group A( P.05) but not significantly in Group C.

结果:(1)模型组肺泡炎、肺纤维化程度都明显重于对照组,肺泡炎、肺纤维化第7、14、28d差异显著(P<0.05);TNF-α、TGF-β_1、FN蛋白表达明显上调(P<0.01);(2)治疗组B组第7、14、28d肺泡炎、肺纤维化程度较模型组明显减轻,TNF-α、TGF-β_1、FN蛋白表达明显下调(P<0.05):(3)治疗组C组第28d肺泡炎、肺纤维化程度与模型组相似,TNF-α、TGF-β_1、FN蛋白表达与A组比较无统计学意义(P>0.05)。

Hepatic chymase concentrations in S3 and S4 cases were greater than in S1 and S2,〔53+54=(31.3±24.6)ng/mg vs. S1+S2=(5.7±4.8) ng/mg, P.01〕. Cells immunoreactive for chymase were seen throughout portal areas and intralobular sinusoidal walls, largely colocalizing with fibrosis. Chymase appears to be involved in hepatic fibrosis in chronic hepatitis.

慢性肝炎纤维化分期重的S3和S4患者,其肝组织中Chymase浓度〔S3+S4=(31.3±24.6)ng/mg〕明显高于纤维化轻的S1和S2患者〔S1+S2=(5.7±4.8)ng/mg〕,P.01;免疫组化染色结果,Chymase标记的肥大细胞主要分布于纤维化旺盛的汇管区与类洞壁,其分布与纤维化部位相一致,且肝组织中Chymase浓度高的患者,其肝组织内Chymase标记的肥大细胞分布增多推测肝组织中Chymase浓度可能与慢性肝炎肝纤维化关系密切。

Although the pathogenesis is not very clear, new understandings about development of pulmonary fibrosis has appeared in company with impenetration of cell biology research and molecular biology research. In a word, research of pulmonary fibrosis gradually appears to be integrated and multidisciplinary crossover.

尽管肺纤维化发病机制目前尚不完全清楚,但随着细胞生物学和分子生物学研究不断深入,对肺纤维化的发生、发展机制有了许多新得认识,肺纤维化机制的研究正逐渐走向整体化和多学科交叉方向。

BMP-7 expression was lower markly in Lung-kidney Qi Deficiency 、Liver-kidney yin Deficiency、 Qi-yin asthenia、Speen –kidney Yang Deficiency than normal control. BMP-7 expression decreased with Lung-kidney Qi Deficiency 、Liver-kidney yin Deficiency、 Qi-yin asthenia、Speen –kidney Yang Deficiency.It shows that the level of BMP-7 expression may play a role in Zheng differentiation-classification of TCM of the chronic glomerulonephritis.

中医证型与肾间质纤维化程度显著相关,肺肾气虚、肝肾阴虚型纤维化程度最轻,气阴两虚型其次,脾肾阳虚型纤维化程度最重,提示传统中医辩证分型与纤维化程度有关,在一定程度上可以反映慢性肾小球肾炎组织学损伤程度,肾间质纤维化程度可作为中医临床辨证参考依据。

4The Masson trichrome stain can be used for an important method for the observation of the fibrostic cells, The changes of the mast cell could be considered as an assist marker for the observation of the liver fibrogenesis.In addition the concentration of the hepatic hydroxyproline could be used for diagnosis of the hepatic fibrosis. clinical and experimental study.

Masson三色染色可以作为肝纤维化肝硬化组织细胞观察的一种重要方法:肝纤维化过程中,肥大细胞数量的动态变化,可以作为观察肝纤维化变化的一项辅助指标;肝脏羟脯氨酸的浓度变化可以作为肝纤维化的辅助诊断及应用于相关实验的研究。

Materials and methods: The lung preparation of 6 SARS death patient (died in 9,14,20,29,33,38d) and 6 macaque model (killed in 7,12,14,14, 32, 35d)were objects. Pathological changes, collagen fibers, lattice fibers, elastic fibers, collagen I and III in lungs and fine structure changes were studied by routine H.E dyeing, trigeminy dyeing, trinitrophenol- sirius red staining and polarization microscope, electron microscope and image analysis. Expression of Vimentin、 TGFβ_1、 TNF α、 IL-1β and MMP-2 were detected by immunohistochemistry.Results:1. Pathological changes of SARS death patient.

材料与方法:以6例SARS死亡患者(分别于发病后9、14、20、29、33、38d死亡)和6只猕猴实验模型(分别于染毒后7、12、14、14、32、35d活杀取材)肺标本为对象,应用H.E染色、三联染色、苦味酸-天狼猩红-偏振光法、电镜和图像分析等技术,对比性观察SARS肺组织病理变化和纤维化的病理过程、胶原纤维、网状纤维和弹力纤维的变化特点、Ⅰ型与Ⅲ型胶原纤维的数量和分布规律,旨在探讨SARS肺纤维化的病变经历过程及特点;利用免疫组织化学和形态计量学技术检测SARS死亡患者肺脏的Vimentin、TGFβ_1、TNFα、IL-1β和MMP-2等与炎症反应和纤维化相关活性因子,探讨其发病机制。

These data suggest that gold nanoparticles may bind to TGF-β1 and block its downstream signaling pathway and that Tα1 may reduce inflammatory responses, resulting in reducing the expression of TGF-β1. These activities may have contributed to their anti-fibrotic effects.

因此我们推测金奈米在四氯化碳诱发小鼠肝纤维化的状态下,具有抗纤维化的效果,可能是透过与TGF-β1结合而阻断其下游讯息传递;而Tα1在四氯化碳诱发小鼠肝纤维化的状态下,可能是透过降低发炎反应而减少TGF-β1的表现来达到抗纤维化的效果。

Some cell dropped into the cavity and became free. Thrombosis or part organization could be seen. The internal elastic layer became thin, disappear or broken. In internal and middle layer existed fibroblasts, fibrocytes and collagen. Some of the wall indicated hyaline change, soomth muscle cell decreased greatly. The massive inflammatory cells invaded the middle and external layer. There were many foam cells in the capsule tissue. Cytoplasm was filled with fatty tissue and cholesterol. some cavities were full of thrombosis. Some thrombosis was fibrosis, the bottom was organization. The surface of the thrombosis existed red blood cell and librae.(2)Elatic fibrila staining: the internal elastic menbrane almost completely disappeared, the intact internal elastic menbran could be seen in the new small vessels.

动脉瘤管壁厚薄明显不均,全层或局部区域显著变薄向外膨出,内皮细胞空泡变性或坏死脱落,部分内皮细胞剥离并突入管腔成游离状,可见血栓形成及部分血栓机化;内弹力板变薄、消失或突然中断;在内膜及中膜部位主要为纤维母细胞、纤维细胞和大片胶原;部分动脉瘤壁呈均质状玻璃样变,平滑肌细胞明显减少;中膜和外膜可见大量的炎性细胞浸润;瘤壁组织有纤维母细胞、纤维细胞、大片胶原成分及较多泡沫细胞,胞浆内充满脂类物质及胆固醇结晶;部分动脉瘤腔内充满血栓,有的血拴已经纤维化,血栓基部机化,血栓表面有红细胞和纤维素。

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