血小板源性生长因子(PDGF)、血清反应因子(SRF)和波形蛋白在人脑胶质瘤中表达的临床意义

 目的 研究血小板源性生长因子(platelet derived growth factor,PDGF)、血清反应因子(serum response factor,SRF)和波形蛋白(vimentin)在人脑胶质瘤中的表达及其临床意义。方法 采用免疫组化染色法检测13例正常脑组织和70例人脑胶质瘤组织中PDGF-B、SRF和波形蛋白的表达并分析其临床意义。结果 PDGF B、SRF和波形蛋白在人脑胶质瘤组织中高表达,阳性表达率分别为67.14%、48.57%和81.43%,差异有统计学意义(P<0.05);三者在脑胶质瘤中的表达与患者性别、年龄、肿瘤发生部位、肿瘤大小无关(P>0.05)。随着胶质瘤恶性程度增加,三者表达逐渐上调,其中PDGF B、波形蛋白在脑胶质瘤中的表达与肿瘤分级相关;相关性分析显示PDGF-B与SRF、波形蛋白在脑胶质瘤中的表达有相关性(P<0.05)。结论 PDGF B、SRF和波形蛋白在脑胶质瘤的发生、发展中可能起到重要的调节作用,与肿瘤恶性程度具有一定的相关性。     

Platelet-Derived Growth Factor A-Chain Homodimer Stimulated Growth of Cultured Smooth Muscle Cells from Spontaneously Hypertensive Rats

Vascular smooth muscle cells from spontaneously hypertensive rats (SHR) were growth stimulated when cocultured with bovine aortic endothelial cells whereas myoctyes from normotensive, Wistar Kyoto rats (WKY) were growth inhibited. The responsiveness of cells from the two rat sources to the two homodimeric forms of plateletderived growth factor (PDGF-AA or-BB) was different; SHR-derived cells responding equally well to both PDGF forms whereas cells from WKY responded to the B-chain homodimer only. The responses measured included S₆ kinase activation, phospholipase C mediated phosphoinositide catabolism and cell growth. Saturation binding experiments using [¹²⁵ I]-labelled PDGF homodimers (AA or BB) indicated that smooth muscle cells from hypertensive rats possess similar numbers of cell-surface A-chain receptors (α subunits) as Swiss 3T3 cells which have been used to characterize the mitogenic effects of the two PDGF homodimeric forms. The differences in responsiveness of SHR vs WKY cells to PDGF-AA and to the influence of endothelial cells may reside in their differential expression of PDGF receptors.     

Octopamine-mediated circuit mechanism underlying controlled appetite for palatable food in Drosophila

The easy accessibility of energy-rich palatable food makes it difficult to resist food temptation. Drosophila larvae are surrounded by sugar-rich food most of their lives, raising the question of how these animals modulate food-seeking behaviors in tune with physiological needs. Here we describe a circuit mechanism defined by neurons expressing tdc2-Gal4 (a tyrosine decarboxylase 2 promoter-directed driver) that selectively drives a distinct foraging strategy in food-deprived larvae. Stimulation of this otherwise functionally latent circuit in tdc2-Gal4 neurons was sufficient to induce exuberant feeding of liquid food in fed animals, whereas targeted lesions in a small subset of tdc2-Gal4 neurons in the subesophageal ganglion blocked hunger-driven increases in the feeding response. Furthermore, regulation of feeding rate enhancement by tdc2-Gal4 neurons requires a novel signaling mechanism involving the VEGF2-like receptor, octopamine, and its receptor. Our findings provide fresh insight for the neurobiology and evolution of appetitive motivation.The adaptive control of foraging decisions is crucial to survival and reproduction and is mediated by complex brain mechanisms. For example, in hungry animals, feeding behaviors can be modulated by diverse neural systems including those responsible for receiving and processing sensory properties and assigning reward and motivational significance of food stimuli (1–3). At present, elucidation of molecular and circuit mechanisms underlying the adaptive control of feeding behavior remains highly challenging.Our previous studies have shown that Drosophila larvae, like mammals, display diverse adaptive foraging strategies in response to appetizing odors or satiety state and food quality (4–6). For example, larvae fed for ad libitum intake tend to prefer soft, liquid sugar media that contain readily ingestible sugar solution but decline solid media in which sugar solution is embedded in gelled agar and is less accessible (5). However, as food deprivation is prolonged, larvae will become increasingly persistent in extracting the sugar solution from solid media (7). We have also shown that an evolutionarily conserved signaling cascade, involving neuropeptide F (NPF, the fly homolog of neuropeptide Y, or NPY) and insulin-like peptides (dILPs), selectively integrates motivational state (hunger) with persistence to pulverize solid food (5, 7).The observation that the conserved NPY-like system selectively promotes food acquisition behaviors that require high energetic cost has led us to postulate that fly larvae may use other conserved neural mechanisms to regulate acquisition of readily accessible palatable food. In this work, we provide evidence which supports this hypothesis. We show that an octopamine (OA)/β-adrenergic-like receptor (Octß3R)-dependent circuit mechanism selectively regulates appetite for soft sugar media. This circuit mechanism seems to involve two subsets of tdc2-Gal4 neurons in the subesophogeal ganglia (SOG). One of them mediates the hunger-driven increase of feeding and is modulated by a novel activity of the VEGF2-like receptor pathway (8). The other is required for preventing excessive appetite in fed larvae. This and our previous findings provide fresh mechanistic insights into how brain mechanisms differentially organize appetitive motivations in responses to high- and low-quality food sources under different energy states.     

糖肾宁对糖尿病肾病模型大鼠PDGF免疫组化表达的影响

目的：观察以健脾补肾解毒活血通络为治法组方的糖肾宁对糖尿病肾病模型大鼠肾组织血小板源生长因子（PDGF）免疫组化表达的影响。方法：采用三联造模法（单侧肾摘除＋高糖高脂＋小剂量STZ注射）制备糖尿病肾病大鼠模型,药物干预12周后,观察糖肾宁对糖尿病。肾病模型大鼠肾组织中PDGF免疫组化表达的影响。结果：糖肾宁可显著降低STZ大鼠的PDGF表达水平,并成一定的剂量相关性。结论：通过健脾补肾解毒活血通络法对糖尿病肾病进行早期干预效果明显,糖肾宁有很好的调节PDGF表达水平的作用,提示糖肾宁可能通过抑制PDGF在肾脏中的异常表达起到保护肾小球、延缓糖尿病肾病病变进程的作用。     

加味四妙勇安油治疗大鼠急性放射性皮肤损伤机制

目的:探讨加味四妙勇安油在治疗放疗导致的急性放射性皮肤损伤过程中的抗炎、保护胶原纤维及促血管新生作用.方法:将75只大鼠随机分为对照组、B12组、四妙勇安组,每组25只,暴露于直线加速器下,经6MeV-X电子射线照后产生10％Ⅱ度放射性皮炎模型,观察照射野皮肤淋巴细胞浸润、胶原纤维排列和完整性,血管内皮生长因子(VEG...     

PDGF/PDGFR信号通路在纤维化疾病中的作用研究进展

纤维化是机体受到有害因子刺激造成的成纤维细胞过度激活导致的细胞外基质过度沉积。血小板衍生生长因子（PDGF）是纤维化疾病重要介质之一,PDGF/PDGFR通路参与调控心、肝、肾和皮肤等多器官纤维化。综述PDGF/PDGFR信号通路在纤维化疾病中的作用研究进展,以期为纤维化疾病的治疗提供参考。     

脑外伤后胰岛素样生长因子-Ⅰ及血小板衍生生长因子对骨折愈合的影响

目的研究大鼠股骨骨折合并脑外伤时血清胰岛素样生长因子-Ⅰ(IGF-Ⅰ)和血小板衍生生长因子(PDGF)水平,探讨IGF-Ⅰ和PDGF与骨折合并脑外伤时愈合加快的关系。方法将152只大鼠分为4组:A组(正常对照组)、B组(脑外伤组)、C组(骨折组)和D组(骨折合并脑外伤组),其中A组8只,B、C、D组各48只。建立大鼠脑外伤和骨折模型,分别于术后1d、4d、1周、2周、3周和4周取血清,酶联免疫吸附法(ELISA)测血清中IGF-Ⅰ和PDGF浓度。结果实验期间C组IGF-Ⅰ的血清浓度无明显变化,围绕A组IGF-Ⅰ的血清浓度水平上下波动,B组和D组的变化趋势趋于一致,两组在各个时间点上相比较差异无统计学意义。1d时,B组和D组IGF-Ⅰ的血清浓度较其余两组明显增加(P<0.01),4d时达到峰值,B、D两组与其余两组比较差异有统计学意义(P<0.01),1周和2周时B、D两组IGF-Ⅰ的血清浓度逐渐下降,与其余两组比较差异有统计学意义(P<0.01),3周和4周时B、D两组IGF-Ⅰ的血清浓度基本降至A组水平,各组相比差异无统计学意义(P>0.05)。在1d至1周时间段内,各时间点B组、C组和D组PDGF的血清浓度均较A组降低,以D组降低最为明显,与其余各组相比差异均有统计学意义(P<0.01),B组和C组与A组相比降低(P<0.01),在2周和4周时间点上,B组和C组PDGF的血清浓度基本回升至A组水平,与A组比较差异无统计学意义(P>0.05),D组与其他3组比较差异有统计学意义(P<0.01)。结论IGF-Ⅰ和PDGF可能是脑外伤后骨折愈合加快的原因之一,且两者之间可能有协同作用。     

部分背根切断对备用背根节神经元CNTF、PDGF表达的影响

目的　研究部分去背根对备用背根节神经元睫状神经营养因子 (CNTF)和血小板源性生长因子(PDGF)表达的影响。方法　制作猫备用背根模型 ,分别在 3d、7d及 14 d时取备用背根节用 CNTF抗血清、PDGF抗血清行免疫组织化学 ABC法染色。分别计数各组阳性神经元总数以及大、中小阳性神经元的数量。结果　两因子在备用背根节的大、中小神经元均有表达。 CNTF阳性神经元总数及中小阳性神经元数均在 3d时明显减少 (P<0 .0 5 ) ,7d、14 d时与正常比较无差异 ,大阳性神经元在各个时间段与正常相比无差异。PDGF阳性神经元总数及中小阳性神经元数在 3d、7d时均较正常显著减少 (P<0 .0 5 ) ,14 d时与正常无差异 ,大阳性神经元数各个时间段均无差异。结论　部分背根切断对备用背根节内不同神经元表达 CNTF、PDGF有不同的影响。     

骨康含药血清对成骨细胞PDGF-AA表达影响的实验研究

目的 观察中药骨康含药血清对新生大鼠成骨细胞血小板衍生生长因子-AA（PDGF—AA）基因表达的调控作用。方法 将实验动物随机分成中药组、罗盖全组和蒸馏水组3组，通过体外分离和培养成骨细胞体系，运用逆转录法测定含药血清对成骨细胞PDGF-AA mRNA表达的影响。结果 用10％的血清培养成骨细胞第7d时，与空白血清组相比，骨康含药血清组和罗盖全含药血清组对成骨细胞PDGF—AA mRNA表达的平均影响率分别为149．4％和177．7％。结论 中药骨康含药血清能明显增强成骨细胞PDGF—AA mRNA的表达。     

Chronic rejection in lung allografts: immunohistological analysis of fibrogenesis

Abstract  In ongoing chronic rejection after lung transplantation, alveolar interstitial fibrosis develops. However, little is known about the mechanisms involved. In order to investigate these mechanisms, expression of extracellular matrix molecules (ECM) (undulin, decorin, tenascin, laminin, and fibronectin) and cytokines [transforming growth factor(TGF)-β1, TGF-β3, platelet-derived growth factor(PDGF), and PDGF receptor] were semiquantita-tively evaluated in chronically rejected lung allografts, using standard immunohistochemical techniques. Additionally, the presence of mac-rophages was analysed. The present study demonstrates an increased infiltration of macrophages with a concomitant upregulation of cytokines (TGF-β1, TGF-β3, and PDGF) and an increased deposition of ECM in chronic lung rejection. These cytokines have an important role in the stimulation of fibroblasts which are a major source of ECM. Upregulated expression of ECM in the alveolar interstitial space leads to alveolar malfunction by thickening of the wall and, thus, is one of the causative factors of respiratory dysfunction in chronic lung graft rejection.