Detection of Ⅴ,Ⅲ and Ⅰ Type Collagens of Dermal Tissues in Skin Lesions of Patients with Systemic Sclerosis and Its Implication

This study investigated the contents and distribution of collagen Ⅴ (Col Ⅴ) in skin lesions of the patients with systemic sclerosis (SSc) and its roles in the pathogenesis. The contents and distribution for α1 chain of collagen type Ⅰ, Ⅲ and V [α1 (Ⅰ), α1 (Ⅲ) and α1 (Ⅴ)] in skin lesions of 36 patients with SSc (9 cases of mild fibrosis, 14 moderate, and 13 severe) were detected by using im- munohistochemical SP method. Six cases of normal skin tissues served as controls. The results showed that there was diffuse distribution for three kinds of collagens in dermis. The deep staining α1 (Ⅰ) and α1 (Ⅲ) masses or bands were seen in reticular layer, while α1 (Ⅴ) was distributed more ho- mogeneously. From control to weak, moderate and severe fibrosis stages, α1 (Ⅰ), α1 (Ⅲ) and α1 (V) showed a gradually increased trend in skin lesions (P<0.05). α1 (Ⅴ) was obviously elevated in skin lesions at early stage and persisted in whole fibrotic process and risen in greater contents, while α1 (Ⅰ) and α1 (Ⅲ) were to go higher late and were apparently elevated at moderate and late stages. Com- pared with α1 (Ⅰ), α1 (Ⅴ) took leading increase at early stage in skin lesions (P<0.01), and had more elevated contents than α1 (Ⅲ) at moderate and late stages. The fibrotic changes in dermal reticular layer occurred earlier than those in papillary layer, and the abnormalities of α1 (Ⅴ)/α1 (I) ratio ap- peared before α1 (Ⅲ)/α1 (Ⅰ) ratio. It was concluded that a lot of α1 (Ⅴ) began to deposit in greater contents prior to α1 (Ⅰ) and α1 (Ⅲ) at early stage in SSc and persisted in whole fibrotic process. The changes of α1 (Ⅴ) contents in reticular layer occurred earlier than those in papillary layer, and it sug- gested that the fibrosis in reticular layer appeared earlier.     

A Survey of TCM Studies on Systemic Scleroderma

Systemic scleroderma （SSc） is a progressive dermatosis with symmetric skin sclerosis and ischemia of the fingers or toes, accompanied with lesions of the joints, muscles and many internal organs, and it may clinically result in functional disablement due to sclerosis, rigidity and atrophy of the skin. The following is a survey of the basic and clinical studies of TCM on SSc.     

Estimation of Acute Toxicity of Ammonium Sulphate to the Fresh—Water Catfish,Heteropneustes fossilis——Ⅱ.A Histopathological Analysis of the Epidermis

The toxicity of 4000 ppm(96h LC50 value)of the inorganic fertilizaer ammonium sulphate on the epidermis of Heteropneustes fossilis(H.fossilis)at different intervals of time has been studied.The destruction induced by the ammonium salt is massive.Secretion of a copious amount of slime from the goblet mucous cells leading to their exhaustion and/or shedding and subsequent disappearance is perhaps the first reaction to the toxicity of the irritant.Later,the polygonal epithelial cells of the outermost layer show cyclic stages of necrosis and sloughing followed by their regeneration and repair.The contents of the club cells show enormous shrinkage and condensation with subsequent replacement of their areas with a hazy substance.In the earlier stages of exposure,regeneration takes place quickly,side by side with the degenerative changes at different stages of experimentation.Later after 8 50 10d,the degenerative changes slow down and the epideris appears identical to that of the normal skin.Goblet mucous cells also showed several cyclic increases followed by decreases in number and activity.     

Expression of MMP-9 and TIMP-1 in Lesions of Systemic Sclerosis and Its Implications

In order to investigate the role of MMP-9 and TIMP-1 in the pathogenesis of systemic sclerosis, the expression of MMP-9 and TIMP-1 was immunohistochemically detected in skin lesions of the patients with diffuse cutaneous systemic sclerosis, skin lesions of the patients with limited cutaneous systemic sclerosis, and skin tissues of normal subjects. The results showed that the expression of MMP-9 in lesions of diffuse cutaneous systemic sclerosis was significantly lower than that of normal skins （P〈0.05）. However, no significant difference in the level of MMP-9 in the limited cutaneous systemic sclerosis and normal skin was found. Meanwhile, the expression of TIMP-1 in lesions of diffuse cutaneous systemic sclerosis and limited cutaneous systemic sclerosis were significantly higher than that of normal skins （both P〈0.05）. It was suggested that the expression of MMP-9 and TIMP-1 might play an important role in the development of systemic sclerosis.     

Fasudil hydrochloride hydrate, a Rho-kinase inhibitor, ameliorates hepatic fibrosis in rats with type 2 diabetes

Background Hyperglycemia may accelerate liver fibrosis.Currently,there is no effective treatment for liver fibrosis induced by type 2 diabetes.The study aim was to investigate whether RhoA/Rho kinase （ROCK） pathway is involved in liver fibrosis in the rats with type 2 diabetes and define the protective effects of fasudil on livers.Methods A rat model of type 2 diabetes was established by high fat diet combined with streptozotocin （30 mg/kg,intraperitoneal injection）.Animals were randomly assigned to 3 groups：control rats,untreated diabetic rats that received vehicle and fasudil-treated diabetic rats that received ROCK inhibitor fasudil hydrochloride hydrate （10 mg/kg per day,intraperitoneal injection,for 14 weeks）.The morphological features of liver were observed by HE staining.Accumulation of collagen in livers was determined by Masson staining and the measurement of hydroxyproline.The mRNA expression of transforming growth factor-β1 （TGFβ1）,connective tissue growth factor （CTGF）,type-Ⅰ,and type-Ⅲ procollagen was assessed with real-time polymerase chain reaction.The phosphorylation of myosin phosphatase target subunit-1 （MYPT1）and the protein levels of TGFβ1 and α-smooth muscle actin （α-SMA） were evaluated by Western blotting.Results Compared with control rats,untreated diabetic rats showed higher values of collagen and hydroxyproline in livers （P ＜0.01）,the phosphorylation of MYPT1 and the protein levels of TGFβ1 and α-SMA were increased （P ＜0.01）,and the mRNA expression of TGFβ1,CTGF,type-Ⅰ,and type-Ⅲ procollagen was upregulated （P ＜0.01）; compared with untreated diabetic rats,treatment with fasudil signifcantly reduced values of collagen and hydroxyproline （P ＜0.01）,and decreased the phosphorylation of MYPT1 and the levels of TGFβ1 and α-SMA （P ＜0.01）,concomitant with the downregulation of TGFβ1/CTGF,type-Ⅰ,and type-Ⅲ procollagen mRNA expression （P ＜0.01）.Conclusions Fasudil ameliorates liver fibrosis in rats with type 2 diabetes at least partly by inhibiting TGFβ1/CTGF pathway and α-SMA expression.Inhibition of RhoA/ROCK may be a novel therapeutic target for liver fibrosis in diabetic non-alcoholic steatohepatitis.     

Correlation of Thl7 cells and CD4＋CD25＋ regulatory T cells with clinical parameters in patients with systemic sclerosis

Background Systemic sclerosis （SSc） is an autoimmune disease that has three major components： inflammation, fibrosis, and vasculopathy. T-helper 17 cell （Th17） and regulatory T cell （Treg） are considered to be critical for autoimmune disease pathogenesis. The role of Th17 and Treg in SSc is still unclear. The aim of this study was to detect the presence of Th17s and CD4＊CD25~ Tregs in peripheral blood samples from SSc patients and to investigate the possible roles of these two T cell subsets in SSc pathogenesis. Methods Th17s （CD4 and IL-17 positive） and CD4＊CD25~ Tregs （CD4, CD25 and Foxp3 positive） in the peripheral blood mononuclear cells of 53 SSc patients and 27 healthy controls were counted by flow cytometry. The differences between SSc and control patients were analyzed. Clinical parameters, including disease duration, duration of the second symptoms, Modified Rodnan Skin Score （MRSS）, anti-topoisomerase I antibody, anti-U1 ribonucleoprotein （RNP） antibody, systemic involvements, pulmonary function test （PFT） and high resolution computed tomography （HRCT） score were prospectively collected following EUSTAR （EULAR scleroderma trial and research group） protocols. The correlations between the experimental and clinical data were investigated. Results The ratio of Th17 in SSc patients was significantly elevated compared to healthy controls （8.74% vs. 4.41%, P 〈0.001）. The amount of Th17 was positively correlated with disease duration （R=-0.531, P=-0.013） and duration of the second symptoms （R=-0.505, P=0.023）. The ratio of CD4＊CD25＊ Treg in SSc patients also significantly differed from the healthy controls （3.04% vs. 2.24%, P=0.018）. Elevated Tregs were more frequently observed in patients with a high interstitial lung disease （ILD） score on computed tomography （24/36） compared with patients with normal ILD scores （4/12, ,P=-0.043）. Elevated Tregs were also more often observed in patients with low carbon monoxide diffusing capacity     

Simvastatin attenuates bleomycin-induced pulmonary fibrosis in mice

Background Bleomycin-induced fibrosis is extensively used to model aspects of the pathogenesis of interstitial pulmonary fibrosis. This study aimed to determine the benefic effects and mechanisms of simvastatin on bleomycininduced pulmonary fibrosis in mice. Methods Bleomycin-induced pulmonary fibrosis mice were administered with simvastatin in different doses for 28 days. We measured inflammatory response, fibrogenic cytokines and profibrogenic markers in both bleomycin-stimulated and control lungs, and correlated these parameters with pulmonary fibrosis. Results Simvastatin attenuated the histopathological change of bleomycin-induced pulmonary fibrosis and prevented the increase of lung hydroxyproline content and collagen （Ⅰ and Ⅲ） mRNA expression induced by bleomycin. Moreover, simvastatin down-regulated the increased expression of transforming growth factor-β1 （TGF-β1） and connective tissue growth factor （CTGF） induced by bleomycin at both gene and protein levels. Simultaneously, the accumulation of neutrophils and lymphocytes and the increased production of tumor necrosis factor-a （TNF-α） in bronchial alveolar lavage fluid were inhibited by simvastatin in early inflammatory phase after bleomycin infusion. The higher dose of simvastatin was associated with a more significant reduction in these inflammatory and fibrotic parameters. Furthermore, the inactivation of p38, RhoA and Smad2/3 signaling pathways was observed during simvastatin administration. Conclusions Simvastatin attenuated bleomycin-induced pulmonary fibrosis, as indicated by decreases in Ashcroft score and lung collagen accumulation. The inhibitory effect of simvastatin on the progression of pulmonary fibrosis may be demonstrated by reducing inflammatory response and production of TGF-β1 and CTGR These findings indicate that simvastatin may be used in the treatment of pulmonary fibrosis.     

The Expression of Interleukin-22 and S100A7, A8, A9 mRNA in Patients with Psoriasis Vulgaris

In order to study the expression of interleukin-22 （IL-22） and S 100A7, A8, A9 mRNA in the skin lesions of patients with psoriasis vulgaris and their relationship, the biopsies were taken from skin lesions in 35 patients with psoriasis vulgaris and the skin of 16 normal controls, and the expression levels of 1L-22 and S 100A7, A8 and A9 mRNA were detected by semi-quantitative RT-PCR. The results showed that （1） IL-22 and S 100A8, A9 mRNA were positively expressed in the psoriatic skin lesions but negatively expressed in the normal controls; The expression level of S 100A7 was （1.133±0.040） in the psoriatic skin lesions, significantly higher than that in the normal controls （0.744±0.037, P〈0.01）. （2） There were significantly positive correlations between the expression of IL-22/S100A7 mRNA, IL-22/S100A8 mRNA, IL-22/S100A9 mRNA in the psoriasis vulgaris （r1=-0.543, r2=0.774, r3=0.621, P〈0.01）. It was concluded that IL-22 and S 100A7, A8, A9 might play important roles in the occurrence and progression of psoriasis.     

Correlational Research of Platelet-derived Growth Factor（PDGF）-BB and Chronic Hepatitis B

Objective To explore the relevance of CHB patients＇ serum levels of PDGF-BB with their ages, sexes, medical histories, serum HBVDNA levels, liver function and Liver Fibrosis markers （HA, CⅣ, PCⅢ, LN）, and relevance between serum levels of PDGF-BB and CHB patients＇ liver fibrosis degrees. Methods （1） 74 CHB patients with serum levels of PDGF-BB and their ages, sexes, medical histories, serum HBVDNA levels, liver functions and serum hepatic fibrosis markers （HA, CⅣ, PCⅢ, LN） to conduct an analysis of their relations; （2） 74 CHB patients were divided into three groups： mild, moderate and severe, and analyzed the relevance of PDGF-BB levels and serum HBVDNA levels, hepatic fibrosis and liver functions. Results （1） serum levels of PDGF-BB have no significant correlation with CHB patients＇ ages, sexes, medical histories and HBVDNA （P〉0.05）; but liver function parameters and serum HA, PCIH, CIV, LN were significantly correlated （P〈0.01）; （2） PDGF-BB levels in serum and liver fibrosis markers： HA, PCⅢ, CⅣ, LN level and liver function were positively correlated （P〈0.01）; （3） PDGF-BB levels in serum and hepatic fibrosis markers： HA, PCⅢ, CⅣ, LN level were positively correlated （P 〈0.01）. Conclusions （1） The extent of the development of liver fibrosis in CHB patients is not determined by their ages, sexes, the length of a histories or the levels of HBVDNA. Liver inflammation activity is the beginning promote in the development of liver fibrosis, which decide the extent of fibrosis; the levels of serum PDGF-BB not only can reflect the CHB patients with liver damage but also can reflect the degree of liver fibrosis; （2） It can be used in CHB patients＇ liver function and fibrosis assessment.     

结缔组织生长因子在硬皮病患者皮损中的表达及其作用探讨

目的 探讨结缔组织生长因子(CTGF)在硬皮病(SD)发病机制中的作用及其与SD分型、分期的关系.方法 分别采用原位RT-PCR和免疫组化SABC法检测36例SDC其中系统性硬化疗(SSc)29例,局限性SD 7例;水肿硬化期28例,萎缩期8例]皮损中CTGF mRNA与蛋白的表达,并以20例正常皮肤组织作为对照.结果 SD组CTGF mRNA(阳性表达率:80.6%vs 40.0%,P=0.002;范围强度积分:2.67±1.33 vs 1.30±1.03,P<0.01与蛋白(阳性表达率,88.9 % vs 45.O%,P<0.001;范围强度积分:2.83 1.06 vs 1.40 1.10.P=0.001)表达阳性率和范围强度均高于正常对照组.SSc组发CTGFmRNA与蛋白表达阳性率和范围强度与局限性SD组间差异均无统计学意义.SD水肿硬化期皮损中CTGF mRNA(阳性表达率:89.3%vs 50.0%,P=0.030;范围强度积分:2.89±0.99 Vs 2.00±1.20,P=0.039)与蛋白(阳性表达率:96.4%vs 62.5%,P=0.028;范围强度积分:3.07士O.86 vs 2.00±1.31,P=0.009)表达阳性率和范围强度均高于萎缩期皮损.结论 CTGF在SD发病机制中起重要作用,与皮肤纤维化的发展密切相关,局限性SD和SSc发病机制可能相似.     

系统性硬化症合并强直性脊柱炎1例及文献复习

系统性硬化症是一种以皮肤增厚和纤维化为特征的自身免疫性疾病，强直性脊柱炎是一种以中轴关节受 累为主的关节炎，强直性脊柱炎极少与弥漫性结缔组织病合并存在。既往文献报道了5例强直性脊柱炎合并系统性硬 化症的病例，其中仅1例患者诉有肌无力，且5例患者的血清肌酸激酶水平均无明显异常。本文报道1例青年男性患者 符合系统性硬化症与强直性脊柱炎的诊断标准，同时出现肌无力、肌酸激酶水平明显增高。人类白细胞抗原(human leukocyte antigen，HLA)分型检测发现该患者携带这两种疾病的HLA易感基因。对该患者予以强的松30 mg/d及环磷 酰胺治疗，2个月后皮肤增厚好转，肌酸激酶降至正常。     

进行性系统性硬化症皮损中前胶原基因和SMAD mRNA的表达

目的探讨进行性系统性硬化症（PSS）硬化皮肤组织中Ⅰ型和Ⅲ型前胶原基因以及细胞内信号转导分子SMAD mRNA的表达情况,分析它们在发病机制中的作用。方法用荧光实时定量聚合酶链反应法分别检测11例PSS患者硬化皮损及11例正常对照皮肤组织中Ⅰ型和Ⅲ型前胶原基因以及不同类型SMAD（SMAD2、SMAD3、SMAD4、SMAD7）mRNA的表达水平。结果Ⅰ型前胶原基因α1、Ⅲ型前胶原基因α1、SMAD4及SMAD7的mRNA在硬化皮损中的表达明显高于在正常皮肤组织的表达,差异有统计学意义（均P〈0．05）。SMAD4 mRNA的表达与Ⅰ型、Ⅲ型前胶原基因α1 mRNA的表达成正相关（r值分别为0．728和0．678,均P〈0．05）。SMAD3 mRNA的表达与Ⅰ型前胶原基因α1 mRNA的表达成正相关（r=0．859,P〈0．01）。结论PSS硬化皮肤组织中存在有SMAD4 mRNA的高表达,可能是导致Ⅰ型、Ⅲ型胶原在硬化组织中过度堆积的原因之一。     

干扰素α对肝纤维化鼠星状细胞I和Ⅲ型前胶原mRNA表达及胶原？…

目的 观察干扰素α对大鼠纤维化时星状细胞增殖,Ｉ,Ⅲ型前胶原ｍＲＮＡ表达和肝脏胶原沉积的影响。方法 以ＣＣｌ４制造肝纤维化模型,培养肝星状细胞,抽提ＲＮＡ,用地高辛标记Ｉ,Ⅲ型前胶原和胶原酶ｃＤｎＡ探针,Ｎｏｒｔｈｅｒｎ杂交分析Ｉ,Ⅲ型前胶原和胶原酶ｍＲＮＡ表达,Ｄｏｔｂｌｏｔ测定大鼠肝Ｉ,Ⅲ型胶原沉积,分别用＾３Ｈ－ＴｄＲ和＾３Ｈ－脯氨酸掺入观察干扰素α对星状细胞增殖和胶原合成的影响。结果 干扰     

Th17细胞及相关细胞因子在系统性硬化病小鼠模型中的表达及意义

目的:研究T辅助细胞17(Th17)及相关细胞因子在系统性硬化病(systemic sclerosis,SSc)小鼠模型外周血、皮肤、肺部的表达及意义。方法:20只雌性BALB/c小鼠随机分为对照组和博莱霉素注射4周组(SSc组),观察小鼠皮肤/肺部炎症和纤维化(pulmonary fibrosis,PF)的病理切片,流式细胞计数检测外周血、皮肤/肺组织CD4+IL-17+Th17细胞,荧光定量PCR检测小鼠皮肤/肺部维甲酸相关孤独受体(RORγt)、IL-17A和IL-6 mRNA的表达,酶联免疫吸附试验检测血清IL-17、IL-6水平,并分析这些指标的相关性。结果:SSc组比对照组皮肤炎症和肺纤维化评分(Ashcroft评分)明显增加(2.6±0.84 vs.0.4±0.52,2.80±1.81 vs.0.60±0.70),皮肤/肺羟脯氨酸(hydroxyproline,HYP)的含量明显增多[(3.17±1.74)mg/g vs.(1.45±0.40)mg/g,(0.53±0.14)mg/g vs.(0.38±0.16)mg/g],均P<0.05。SSc组外周血、皮肤和肺组织Th17细胞比例较对照组明显增加[(2.07±0.89)%vs.(1.02±0.32)%,(5.80±2.02)%vs.(1.64±0.58)%,(5.24±2.43)%vs.(1.92±0.98)%,P<0.01];与对照组相比,SSc组皮肤/肺组织IL-17A、IL-6 mRNA的表达量,皮肤RORγt mRNA的表达量增高,均P<0.05。SSc组外周血IL-17、IL-6含量明显增高(P<0.01)。外周血Th17细胞、IL-17和IL-6的含量与皮肤/肺部炎症、PF评分、皮肤HYP含量呈密切正相关,皮肤/肺组织Th17细胞分别与皮肤/肺部炎症、皮肤/肺HYP含量密切正相关。结论:Th17细胞在SSc小鼠模型外周血、皮肤及肺组织表达增高,与皮肤/肺部炎症、纤维化病变密切正相关,并通过IL-17、IL-6等细胞因子参与SSc的发病。     

增损甘露消毒丹对肝纤维化大鼠血清PCIII、IV-C影响的实验研究

目的探讨增损甘露消毒丹抗肝纤维化的疗效及作用机理。方法采用四氯化碳皮下注射和酒精灌胃等复合因素建立大鼠肝纤维化模型,设6组,各组用药8周。治疗结束后采用放射免疫法检测大鼠血清III型前胶原（PCIII）、IV型胶原（IV-C）的含量。采用胶原纤维（Van-Gieson）染色法和网状纤维（Gomori）染色法光镜下观察并进行肝纤维化病理分级;网状纤维增生程度采用计算机图像分析系统进行分析。结果病理模型组大鼠血清PCIII、IV-C含量均较正常组明显升高（P＆lt;0.05）;经用药治疗后,增损甘露消毒丹大剂量组、中剂量组、复方鳖甲软肝片组血清PCIII、IV-C含量与病理模型组比较明显降低（P＆lt;0.05）;增损甘露消毒丹大剂量组、中剂量组血清PCIII、IV-C含量与增损甘露消毒丹小剂量组比较有明显差异（P＆lt;0.05）。结论增损甘露消毒丹可以抑制细胞外间质中胶原的生成,降低肝纤维化大鼠血清PCIII、IV-C的含量并能明显减轻大鼠的肝纤维化程度、减少胶原纤维与网状纤维,对四氯化碳诱导的大鼠肝纤维化有良好的治疗作用。     

原发性高血压病细动脉改变及主要脏器的病理形态变化—45？…

对４５例原发性高血压病尸检资料进行回顾性研究，重点观察了全身细脉的改变，将直径〈１００μｍ者称远端细动脉，而１００～３００μｍ者称为近端细动脉，结果：所观察到的病变可分为：管壁血浆蛋白浸润及透明变性两类，后者又视其严重程度分布，Ｉ，ＩＩ，Ⅲ级，并有如下发现；（１）身体不同区域的细动脉处于不同改变程期；（２）远端细动脉改变在先，近端细动脉类后，而脑近端细动脉先发生扩张，相继才发生透明变性；（３）腹腔     

干扰素α治疗慢性乙型肝炎患者肝纤维化的实验研究

目的 观察干扰素α对慢性乙型肝炎（乙肝）患者肝组织纤维化程度的影响。方法选取病理诊断为S3-S4期的16例乙肝患者,干扰素治疗期前后3次进行肝组织炎症程度及纤维化程度病理分析，免疫组化检测肝组织TGF-β1蛋白、Fas及HBcAg抗原,TUNEL方法观察肝细胞凋亡情况。同期检测血清肝纤维化指标及肝功能。结果在S3-S4期，患者Fas、TGF-β1显著表达，肝细胞的DNA损伤严重。干扰素α治疗3个月后Fas抗原、TGF-β1表达程度显著下降（P〈0．05）；细胞凋亡程度减轻（P〈0．05）；肝组织HBcAg表达程度无显著改变；连续6～9个月治疗后，肝组织炎症及纤维化程度逐渐改善（P〈0．05），血清肝纤维化指标及肝功能水平与治疗前差异显著。结论干扰素仪能显著改善S3-S4期患者肝细胞凋亡和肝组织纤维化程度，但需持续治疗。     

垂体肿瘤转化基因1在系统性硬化症中的表达及作用

目的 研究垂体肿瘤转化基因（PTTG1）在系统性硬化症（SSc）中的表达及其对成纤维细胞的作用。方法 收集皮肤活检组织,其中SSc患者组21例,正常组22例。分别应用实时荧光定量聚合酶链式反应法（Real-time PCR）检测皮肤组织中PTTG1基因表达水平;应用免疫组化方法检测皮肤组织中PTTG1蛋白表达水平;应用小干扰RNA（siRNA）降低成纤维细胞中PTTG1基因表达,通过 Real-time PCR 方法检测细胞中 PTTG1 及与细胞纤维化密切相关的几个基因α-SMA、COL1A1、COL1A2、COL3A1的表达变化;通过细胞实时增殖检测系统检测细胞增殖。结果 与正常对照相比,SSc患者皮肤组织中PTTG1的表达水平明显升高,差异具有统计学意义（P<0.05）;与正常对照相比,SSc患者皮肤组织中阳性细胞增多,PTTG1蛋白表达明显升高;原代皮肤成纤维细胞中PTTG1表达水平和α-SMA、COL1A1、COL1A2、COL3A1均存在正相关,差异具有统计学意义（R²=0.8192,P<0.05;R²=0.6398,P<0.05;R²=0.316,P<0.05;R²=0.3723,P<0.05）;同时,原代皮肤成纤维细胞中PTTG1干扰后,细胞增殖被显著抑制,纤维化相关基因（COL1A1、COL1A2、PAI-1）表达下降,胶原蛋白的基因表达降低。结论 SSc患者中存在PTTG1过度表达,干扰PTTG1可降低成纤维细胞活性,提示PTTG1与SSc纤维化程度密切相关。