Association of heparin with basic fibroblast growth factor, epidermal growth factor, and constitutive nitric oxide synthase on healing of gastric ulcer in rats.

The healing effect of heparin on gastric ulcer and its underlying mechanisms were studied. The influences of protamine on these effects were also investigated. Gastric ulcer was induced by acetic acid in rats. Heparin (100-1000 U/kg i.v.) was given once daily for 4 or 7 days. Ulcer area was measured; gastric mucosal regeneration, proliferation, and angiogenesis were determined by histological or immunohistochemical methods. Gastric mucosal basic fibroblast growth factor (bFGF) level was assessed by an enzyme-linked immunosorbent assay, and the mucosal epidermal growth factor (EGF) level and nitric oxide synthase (NOS) activity were measured by radioimmunoassay. The anticoagulant action of heparin was determined by the duration of bleeding time. The results showed that heparin given for 4 or 7 days significantly accelerated gastric ulcer healing in a dose-dependent manner. The three doses of heparin significantly stimulated mucosal regeneration and proliferation as well as angiogenesis but not the contraction of ulcer base. Similar effects were observed in gastric mucosal bFGF and EGF levels and constitutive NOS activity. Protamine not only abolished the anticoagulant action of heparin but also significantly potentiated its effects on ulcer healing, gastric mucosal proliferation, angiogenesis, and constitutive NOS activity. These findings indicate that heparin can accelerate gastric ulcer healing, which is associated with mucosal regeneration, proliferation, and angiogenesis. These actions are likely to be stimulated by bFGF, EGF, and constitutive NOS activity in the gastric mucosa. Protamine potentiates the ulcer-healing effect of heparin, which is probably acting through constitutive NOS activation.     

Phenytoin-induced lymphocytic chemotaxis, angiogenesis and accelerated healing of decubitus ulcer in a patient with stroke

We studied the effect of topically applied phenytoin on the healing of a decubitus ulcer in the sacral region of an immobile patient with stroke. Another similar, but smaller, ulcer was treated with conventional treatment only and served as a control. The ulcers were measured once a week and biopsies were taken from the margins before, 1 week and 2 weeks after commencing treatment with phenytoin. Clinically, phenytoin substantially accelerated the rate of healing. Microscopic examination of the biopsies showed increased lymphocytic infiltration of the phenytoin-treated lesion. Anti-CD31 immunohistochemistry revealed dense CD31+ lymphocytic infiltration and increased angiogenesis only in the phenytoin-treated lesion. Our findings suggest that phenytoin enhances wound healing by stimulating lymphocytic chemotaxis and up-regulation of angiogenesis.     

bFGF对大鼠创面血管生成及愈合的影响

【目的】观察重组碱性成纤维细胞生长因子(bFGF)对创面血管生成及愈合的促进作用。【方法】采用大鼠全层皮肤切除模型(以下称创伤),实验组创面用bFGF,对照组用生理盐水处理后,观察其愈合时间及创面血管的变化,测定创面愈合率,并进行组织学检查及免疫组化分析。【结果】外用bFGF后,创面愈合时间缩短(2.4±0.55) d,创面血管新生、肉芽组织的形成加速。【结论】bFGF不仅刺激成纤维细胞生长,而且刺激内皮细胞分裂,引起血管新生,促进肉芽组织的形成,加速创面的愈合。     

宫颈癌IGF—IR的表达及与肿瘤血管生成、癌细胞增殖关系

目的探讨宫颈癌组织中胰岛素样生长因子-I受体（insulin—likegrowthfactor-Ireceptor，IGF-IR）表达及其与肿瘤血管生成、癌细胞增殖的关系。方法采用免疫组织化学SP法检测93例宫颈癌和21例正常宫颈上皮组织中IGF．IR蛋白表达，并检测微血管密度（CD34标记）和癌细胞增殖指数（Ki-67标记）。结果宫颈癌组织中IGF-IR、微血管密度、Ki．67指数明显高于正常宫颈上皮组织（P〈0．01），IGF-IR高表达与宫颈癌淋巴结转移和浸润深度有关，而与患者年龄、宫颈癌组织学类型和临床分期无明显相关性。结论IGF．IR过度表达者，宫颈癌血管生成能力显著增强、癌细胞增殖活跃，检测宫颈癌中IGF-IR表达对进一步了解宫颈癌生物学行为和判断其预后有一定的价值。     

宫颈癌血管生成与癌细胞增殖及浸润转移的关系

目的　探讨早期宫颈癌血管生成与癌细胞增殖及浸润转移的关系。方法　采用免疫组织化学 SP法检测75例早期宫颈癌、18例宫颈上皮内瘤样病变 (CIN)和 15例癌旁正常宫颈上皮中微血管密度 (MVD,CD34 标记 )及 Ki- 6 7抗原的表达情况 ,探讨宫颈癌血管生成与癌细胞增殖及浸润转移的关系。结果　 CD34 主要表达于宫颈癌巢间质血管内皮细胞 ,而 Ki- 6 7主要表达于宫颈癌细胞核。从正常宫颈上皮→ CIN→宫颈浸润癌 ,MVD和 Ki- 6 7表达均显著升高 (P<0 .0 5 )。宫颈癌 MVD与盆腔淋巴结转移、脉管浸润、间质浸润和 Ki- 6 7表达有关 (P<0 .0 5 ) ;而与年龄、FIGO分期、组织学分级和组织学类型无关 (P>0 .0 5 )。有盆腔淋巴结转移、脉管浸润、≥深层间质浸润及 Ki- 6 7呈高度表达者 ,其 MVD分别显著高于无盆腔淋巴结转移、无脉管浸润、<深层间质浸润及 Ki- 6 7<高度表达者 (P<0 .0 5 )。结论　肿瘤血管生成可能在宫颈癌发生发展、癌细胞增殖和浸润转移中起重要作用。宫颈癌伴 MVD显著升高者 ,其癌细胞增殖活跃 ,易发生浸润转移 ,但并非唯一决定因素。检测宫颈癌 MVD对进一步了解宫颈癌生物学行为具有一定的临床应用价值。     

Gene therapy with adenoviral plasmids or naked DNA of vascular endothelial growth factor and platelet-derived growth factor accelerates healing of duodenal ulcer in rats

After we demonstrated that daily intragastric administration of angiogenic growth factors like basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), or vascular endothelial growth factor (VEGF) accelerated the healing of chronic duodenal ulcers in rats, we hypothesized that a single dose of gene therapy related to these growth factors may be enough to accelerate the healing of duodenal ulcers through enhancement of synthesis of endogenous angiogenic growth factors. Thus, we compared the effects of intraduodenal or intravenous adenoviral vectors and naked DNA transducing the genes for either VEGF or PDGF in experimental duodenal ulcers induced by cysteamine in rats. Sprague-Dawley female rats with confirmed duodenal ulcers were randomly divided into control and treatment groups. The controls received either intraduodenal injection of buffer or the beta-galactosidase-transducing adenoviral vector. Rats treated with a single or double dose of adenoviral vector or naked DNA of VEGF or PDGF had significantly smaller ulcers than the controls. Histologic analysis demonstrated that reepithelized granulation tissue with prominent angiogenesis replaced the ulcers. Western blotting, immunohistochemistry, and enzyme-linked immunosorbent assay of duodenal mucosa confirmed that the expression of VEGF or PDGF proteins was enhanced by the transgenes, whereas beta-galactosidase staining in multiple organs identified that the transgenes, especially after local administration were only localized in the duodenum, stomach, and jejunum. These results suggest that gene therapy with either VEGF or PDGF may be a rapid approach to achieve duodenal ulcer healing.     

Paracrine Factors of Mesenchymal Stem Cells Recruit Macrophages and Endothelial Lineage Cells and Enhance Wound Healing

Bone marrow derived mesenchymal stem cells (BM-MSCs) have been shown to enhance wound healing; however, the mechanisms involved are barely understood. In this study, we examined paracrine factors released by BM-MSCs and their effects on the cells participating in wound healing compared to those released by dermal fibroblasts. Analyses of BM-MSCs with Real-Time PCR and of BM-MSC-conditioned medium by antibody-based protein array and ELISA indicated that BM-MSCs secreted distinctively different cytokines and chemokines, such as greater amounts of VEGF-α, IGF-1, EGF, keratinocyte growth factor, angiopoietin-1, stromal derived factor-1, macrophage inflammatory protein-1alpha and beta and erythropoietin, compared to dermal fibroblasts. These molecules are known to be important in normal wound healing. BM-MSC-conditioned medium significantly enhanced migration of macrophages, keratinocytes and endothelial cells and proliferation of keratinocytes and endothelial cells compared to fibroblast-conditioned medium. Moreover, in a mouse model of excisional wound healing, where concentrated BM-MSC-conditioned medium was applied, accelerated wound healing occurred compared to administration of pre-conditioned or fibroblast-conditioned medium. Analysis of cell suspensions derived from the wound by FACS showed that wounds treated with BM-MSC-conditioned medium had increased proportions of CD4/80-postive macrophages and Flk-1-, CD34- or c-kit-positive endothelial (progenitor) cells compared to wounds treated with pre-conditioned medium or fibroblast-conditioned medium. Consistent with the above findings, immunohistochemical analysis of wound sections showed that wounds treated with BM-MSC-conditioned medium had increased abundance of macrophages. Our results suggest that factors released by BM-MSCs recruit macrophages and endothelial lineage cells into the wound thus enhancing wound healing.     

胃肠间质瘤中Ki-67、血管内皮细胞生长因子表达及其与微血管密度和细胞增殖的关系

目的:探讨Ki-67和血管内皮细胞生长因子(VEGF)在胃肠间质瘤 (GIST)中的表达及与临床病理因素的关系,VEGF、微血管密度(MVD)和细胞增殖的之间的相关性。方法:采用免疫组化S-P法检测44例胃肠间质瘤组织中Ki-67、VEGF表达及计数MVD值和Ki-67增殖指数(PI)。结果:VEGF、Ki-67在GIST组织中阳性表达分别为77.3%、 63.6%,VEGF、Ki-67表达在不同大小的肿块之间有统计学差异(P<0.01);MVD值和Ki-67 PI在VEGF阳性和阴性组的比较有统计学差异(P<0.01);VEGF、MVD和Ki-67 PI之间呈显著性正相关(相关系数分别为0.26、0.44和0.84,P<0.01)。结论:VEGF促进GIST组织中的新生血管形成和肿瘤细胞的增殖、肿瘤的生长、发展和转移,Ki-67PI为GIST的预后判断提供了比较客观的依据。     

溃疡性结肠炎合并结肠多发性锯齿状息肉的临床病理分析

目的 探讨溃疡性结肠炎(UC)合并结肠多发性锯齿状息肉的临床病理特点及免疫组化表型. 方法报告2例分别有10年和8年溃疡性结肠炎病史、合并多发性结肠锯齿状息肉病的临床、内窥镜及病理组织学改变.行AE1/AE3、CK7、CK20、CEA、CD34、SMA、p53和Ki-67免疫组化染色,并结合文献进行复习讨论. 结果 2名患者均为中年女性,间断腹泻10年和8年,分别多次行内窥镜检查发现结直肠黏膜多处糜烂、浅表溃疡.例1,降、乙状结肠可见密集分布、大小不等的息肉,最大直径3cm;例2,全结肠可见10余枚息肉.镜检:结直肠溃疡糜烂处符合溃疡性结肠炎病变;息肉处腺体大部分呈锯齿状扩张增生,部分细胞核增生呈复层,可见异型增生.免疫组化:息肉部腺体CEA(+),Ki-67阳性细胞位于锯齿状隐窝基底及中1/3;例2局部p53(+).结论 UC相关锯齿状息肉/腺瘤病具有肿瘤性病变特征,UC合并锯齿状息肉或腺瘤可能更易癌变.     

低氧诱导因子-1α、Ki67和微血管密度在弥漫浸润性星形细胞瘤中的表达及意义

目的探讨低氧诱导因子-1α（HIF-1α）、增殖指标（Ki67）及微血管密度（MVD）在人弥漫浸润性星形细胞瘤中的表达与临床病理指标及预后的关系。方法用免疫组织化学法检测10例正常人脑组织和76例弥漫浸润性星形细胞瘤中HIF-1α、Ki67和CD34的表达,并以CD34平均阳性血管数作为微血管密度（MVD）。结果 76例弥漫浸润性星形细胞瘤中HIF-1α阳性表达59例（77.6%）,Ki67平均核阳性率为8.22%,平均MVD为（43.7±11.3）,与正常对照组比较差异均有统计学意义（P〈0.05）。HIF-1α、Ki67的表达率和MVD计数均随弥漫浸润性星形细胞瘤级别的升高而增加,并与患者的预后负相关,各组间差异显著（P〈0.01）;HIF-1α和K i67的表达与MVD计数呈正相关。结论 HIF-1α、Ki67和MVD计数在弥漫浸润性星形细胞瘤中的表达与级别及预后有关,提示缺氧及微血管的增殖在弥漫浸润性星形细胞瘤的发生和演进中发挥作用。     

Combination of Caspy2 and IP-10 Gene Therapy Significantly Improves Therapeutic Efficacy Against Murine Malignant Neoplasm Growth and Metastasis

Abstract It has been shown that Caspy2, a zebrafish active caspase, can efficiently suppress the growth of malignant tumor. The present study was designed to test whether combined gene therapy with IP-10, a potent antitumor chemokine, and Caspy2 would improve therapy efficacy. Recombinant plasmid expressing both Caspy2 and IP-10 genes was mixed with DOTAP-cholesterol nanoparticles. Immunocompetent mice bearing CT26 colon carcinoma, B16-F10 melanoma, and 4T1 breast carcinoma were treated with the complex. We found that the combined gene therapy more efficiently inhibited tumor growth, while efficiently prolonging the survival of tumor-bearing animals, compared with monotherapy. Moreover, a significant reduction in spontaneous lung metastasis could be observed in the 4T1 breast carcinoma model. Infiltration of CD8(+) T lymphocytes was also observed. In addition, apoptotic cells were widely detected by TUNEL assay and caspase-3 immunostaining in coadministered tumor tissues. The combination treatment also successfully inhibited angiogenesis and tumor cell proliferation as assessed by CD31 and Ki-67 immunostaining, respectively. Furthermore, depletion of CD8(+) T lymphocytes could significantly abrogate the antitumor activity, whereas the depletion of CD4(+) cells or natural killer cells showed partial abrogation. Rechallenged CT26 tumors were rejected in all of the surviving mice treated by combination therapy. Our results suggest that combined therapy with Caspy2 and IP-10 can significantly enhance antitumor activity by acting as an immune response initiator, apoptosis inducer, and angiogenesis inhibitor, which may be important for further applications in clinical cancer therapy.     

Basic fibroblast growth factor enhances the coupling of intimal hyperplasia and proliferation of vasa vasorum in injured rat arteries.

Basic fibroblast growth factor (bFGF) is mitogenic for smooth muscle cells (SMC) and angiogenic. We examined the in vivo effects of bFGF in balloon denuded carotid arteries of laboratory rats. bFGF was administered continuously from polymer-based devices at 34 ng/d into the periadventitial space of rat carotid arteries for 2 wk. Intimal hyperplasia was not observed in the absence of injury or with lipopolysaccharide induced endothelial dysfunction. Different degrees of vascular injury produced proportionally more intimal hyperplasia. bFGF increased the intimal hyperplastic response 1.3-fold with severe vascular injury, and 2.4-fold with more mild injury. Increased cell proliferation, not extracellular matrix production, accounted for these effects. Cell density was unchanged for the control and bFGF-treated groups, and the number of proliferating intimal cells at 2 wk rose to an amount equivalent to the increase in mass; 1.9- and 4.0-fold for severe and lesser injury, respectively. The relative ability of heparin to reduce SMC proliferation was not altered by the presence of bFGF.bFGF also induced profound angiogenesis within and surrounding the polymeric releasing device, and in the vasa vasorum immediately around the injured arteries. bFGF's effect on vasa was linearly related to the amount of SMC proliferation within the blood vessel. Thus, the in vivo mitogenic and angiogenic potential of bFGF are coupled, and may be similarly modulated by the products of local injury and/or factors in the vessel wall.     

Interferon-alpha and interleukin 2 synergistically enhance basic fibroblast growth factor synthesis and induce release, promoting endothelial cell growth.

To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/inflammatory disorders, the effects of interferon-alpha (IFN-alpha) and interleukin 2 (IL-2) on endothelial cell (EC) growth in vitro and angiogenesis in vivo were studied. Preincubation of cultured human ECs with IFN-alpha, followed by exposure to IL-2, resulted in effective stimulation of cell growth, whereas either cytokine alone had only a slight effect. The combination of IFN-alpha/IL-2 induced an angiogenic response in the rabbit cornea. IL-2 receptor expression was enhanced on IFN-alpha-treated ECs: p55 was increased and p70 was induced. 125I-IL-2 binding to ECs treated with IFN-alpha was enhanced (Kd from approximately 7 nM to approximately 260 pM with IFN-alpha), and anti-p55 IgG blocked 125I-IL-2/EC interaction as well as IL-2-mediated EC proliferation. Consistent with these findings in cell culture, immunohistologic studies demonstrated p55 and p70 antigen in the vasculature of rheumatoid joints, but not in normal joint tissue. Exposure of cultured ECs to IFN-alpha increased levels of intracellular EC basic fibroblast growth factor (bFGF), and subsequent addition of IL-2 led to bFGF release into the medium. The observation that anti-bFGF IgG largely blocked EC proliferation in response to IFN-alpha/IL-2 suggested that bFGF was a critical agent in this setting. These data suggest a mechanism rendering ECs responsive to IL-2 which may be relevant in immune/inflammatory disorders: IFN-alpha-mediated induction of functional EC receptors for IL-2, which drives cell proliferation by a mechanism dependent on increased synthesis and release of bFGF.     

Survivin、Ki-67核抗原在涎腺基底细胞腺瘤、癌中的意义

目的探讨涎腺基底细胞腺瘤、癌中survivin表达与Ki-67核抗原表达的相关性,了解其在肿瘤恶性增殖及良恶性肿瘤鉴别诊断中的意义。方法应用免疫组织化学方法检测15例正常涎腺组织、28例涎腺基底细胞腺瘤、23例基底细胞腺癌组织中survivin及Ki-67核抗原的表达;RT-PCR分析2例涎腺基底细胞腺瘤及2例涎腺基底细胞腺癌survivin、Ki-67的mRNA表达水平。结果 Survivin及Ki-67核抗原在正常涎腺组织、基底细胞腺瘤、基底细胞腺癌中的表达依次递增,差异有统计学意义(P0.01);Ki-67核抗原的表达随survivin表达增加而上升(P0.05)。涎腺基底细胞腺癌survivin mRNA表达水平高于基底细胞腺瘤。结论 Survivin、Ki-67核抗原的过度表达可能参与涎腺基底细胞腺瘤的恶性增殖过程,并且可作为基底细胞腺瘤、癌的鉴别诊断分子指标之一。     

电针结合经颅磁刺激对脑缺血大鼠碱性成纤维细胞生长因子和血管生成素及其受体表达的影响

目的:观察电针结合经颅磁刺激对急性脑缺血大鼠血管新生的影响。方法:将25只雄性Wistar大鼠随机分成5组:正常组、模型组、电针组、磁刺激组和电针加磁刺激组。复制急性大脑中动脉缺血模型,分别施以电针、磁刺激和电针加磁刺激方法处理,采用免疫组织化学方法,检测碱性成纤维细胞生长因子(bFGF)和血管生成素2(Ang-2)及其受体(Tie-2)的表达。结果:电针组、磁刺激组和电针加磁刺激组梗死灶周围bFGF、Ang-2表达增强,尤以电针加磁刺激组明显(P<0.01),而Tie-2的表达虽较正常组增高,但各治疗组之间比较差异无显著性意义。结论:电针结合磁刺激可以增强急性脑缺血大鼠梗死灶周围bFGF和Ang-2的表达,促进了急性脑缺血大鼠梗死灶周围的血管新生。     

胃肠道间质瘤34例临床病理学分析

目的 探讨胃肠道间质瘤的临床表现、病理组织形态学和免疫组织化学特点及良恶性参考指标.方法 对34例胃肠道间质瘤患者的手术标本采用免疫组化PV-9000法进行CD117、CD34、S-100、SMA、Des、Ki-67标记、分析.结果 34例胃肠道间质瘤免疫组化CD117阳性率95％,CD34阳性率70％,S-100、SMA、Des局灶弱阳性或阴性表达,Ki-67表达不一.临床表现为腹部不适、腹痛、腹胀、上消化道出血及腹部包块.结论 胃肠道间质瘤多发于中老年,肿瘤细胞形态多样,结构多样,免疫组化CD117和CD34阳性表达是确诊胃肠道间质瘤最有诊断价值的依据,但胃肠道间质瘤良、恶性诊断须结合肿瘤大体、组织学形态及生物学行为等综合考虑.     

CD31和Ki-67在大肠癌组织中的表达和相关性研究

目的 :探讨 CD31和 Ki- 6 7在大肠癌组织中的表达的意义和二者之间的相关性。方法 :采用免疫组化染色检测 CD31和 Ki- 6 7在 4 8例大肠癌标本中的表达。结果 :1CD31随着大肠癌分化程度的降低其表达率呈上升趋势。 2CD31表达与大肠癌的分化程度浆膜浸润和淋巴结转移有关。 3Ki- 6 7的表达与大肠癌的分化程度有关。 4 CD31和 Ki-6 7表达呈显著正相关。结论 :检测 CD31和 Ki- 6 7在大肠癌中的表达有助于了解病变的发展阶段和预后评估 ;CD31和Ki- 6 7表达呈正相关 ,CD31过度表达区域 ,Ki- 6 7表达率也增高 ,推测两者在大肠癌的增殖调控以及发生、发展中有协同作用。     

双龙丸对大鼠实验性心肌梗死血管新生的影响与分子学机制

目的 探讨双龙丸对缺血心肌血管新生的影响和分子学机制。方法 63只Wistar大鼠参照Drexler法结扎冠状动脉左前降支，制成急性心肌梗死(AMI)模型。随机分为双龙丸大剂量组(6．72g／kg)、双龙丸小剂量组(3．36g/kg)、AMI对照组(生理盐水灌胃)，另取11只大鼠为正常对照组(生理盐水灌胃)，各组治疗观察半数至2w、半数至4w结束。应用免疫组化两步法检测AMI大鼠缺血心肌新生血管数量、免疫组化SP法检测缺血心肌血管内皮生长因子(VEGF)和碱性成纤维细胞生长因子(bPGF)的表达、逆转录多聚酶链反应(RT—PCR)法检测缺血心肌VEGF mRNA和bFGF mRNA的表达。结果 双龙丸大、小剂量组各期的缺血心肌新生血管数均比AMI对照组增多，且第4w比第2w更显著；第2w时，大剂量组VEGF较AMI对照组、bFGF较小剂量组和AMI对照组均增高，大剂量组4w时VEGF较2w降低；大、小剂量组各期VEGF mRNA的表达均比AMI对照组增高，其第4w均较第2w为低；而bFGF mRNA的表达则仅见大剂量组第2w时高于其他组；以上各组比较均具有显著性差异(P＜0．05—0．01)。结论 双龙丸能够促进缺血心肌血管新生；大剂量应用对VEGF、bFGF及其mRNA均有明显的上调作用。     

碱性成纤维细胞生长因子对增生性瘢痕与正常皮肤成纤维细胞胶原、纤维连接蛋白表达的影响

背景:碱性成纤维细胞生长因子能促进愈合伤口产生胶原蛋白、纤维连接蛋白和基质酶的基质成分.然而,细胞增殖、细胞外基质及新生血管的形成或伤口基质重塑过程失调,会导致瘢痕组织过度增殖.目的:观察碱性成纤维细胞生长因子在正常皮肤创面愈合和增生性瘢痕形成中的作用.方法:从5例进行瘢痕修复手术患者身上同时取正常皮肤和增生性瘢痕组织,分离培养正常人皮肤成纤维细胞和增生性瘢痕成纤维细胞.应用RT-PCR和酶联免疫吸附法检测两种成纤维细胞胶原、纤维连接蛋白基因表达和蛋白合成.采用JC-1染色和流式细胞术测定成纤维细胞线粒体膜电位改变,采用化学发光法检测细胞内ATP水平改变.观察碱性成纤维细胞生长因子对两种细胞的上述指标的影响.结果与结论:不同浓度碱性成纤维细胞生长因子可减慢增生性瘢痕成纤维细胞生长,抑制增生性瘢痕成纤维细胞Ⅰ型胶原表达和合成(P<0.05).碱性成纤维细胞生长因子对正常皮肤和增生性瘢痕成纤维细胞Ⅲ型胶原表达和合成均无影响.然而可上调正常皮肤成纤维细胞表达纤维连接蛋白(P<0.05).此外,10,100 μg/L碱性成纤维细胞生长因子处理后增生性瘢痕成纤维细胞线粒体膜电位呈去极化趋势,正常皮肤成纤维细胞中ATP水平显著增高(P<0.05).结果表明,碱性成纤维细胞生长因子在正常皮肤创面愈合和增生性瘢痕形成中可能有不同的作用和机制.