支气管哮喘急性发作期血清干细胞因子的变化

目的:探讨支气管哮喘急性发作期患者治疗前后血清干细胞因子(Stem cell factor,SCF)水平变化及意义.方法:选择入住我院呼吸科的支气管哮喘急性发作期患者33例作为研究对象,采用酶联免疫吸附试验(ELISA)检测其治疗前后的血清SCF水平,同时测定25例正常对照者血清SCF水平.结果:急性发作期患者血清中S...     

支气管哮喘患者急性发作期血清干细胞因子的测定及其临床意义

目的:探讨支气管哮喘患者急性发作期血清干细胞因子(SCF)的水平及意义,以及该细胞因子与血清中嗜酸粒细胞计数(EOS)、血清总免疫球蛋白E(T-IgE)、第1秒钟用力呼气容积实测值/预计值比值(FEV1实/预％)、呼出气一氧化氮(FeNO)之间的关系.方法:将65例支气管哮喘急性发作患者按病情严重程度分为轻、中、重度组(均为哮喘组),以同期37例健康体检者作对照,分别测定并比较各组血清SCF、EOS、T-IgE、FEV1实/预％及FeNO,并将哮喘组SCF浓度与实际测得患者各组血清T-IgE、FEV1实/预％、FeNO作相关分析.结果:哮喘各组的SCF、FEV1实/预％、FeNO差异有统计学意义(均P＜0.01),中、重度组血清SCF水平明显高于对照组及轻度组(P＜0.01),轻度组与对照组SCF差异无统计学意义(P＞0.05).哮喘组血清SCF与FeNO呈正相关(rs=0.447,P=0.004).结论:血清SCF的水平可较准确反映气道炎症变化,可能与哮喘急性发作的严重程度有关.     

炎症,细胞因子与哮喘

随着哮喘研究的不断深入,近年来对哮喘本质的认识已发生重大变化。传统观念认为哮喘是因为支气管平滑肌痉挛引起的气道阻塞性疾病,现已证明哮喘是一种慢性气道炎性疾病,表现在支气管上皮损伤、炎性细胞浸润、微血管扩张、通透性增加和渗出物增多[1,2]。支气管炎症引起管壁增厚,平滑肌收缩导致可逆性支气管阻塞,而上皮损伤、上皮细胞剥脱引起支气管平滑肌痉挛。导致哮喘炎症反应的细胞包括嗜碱性粒细胞、嗜酸性粒细胞、肥大细胞Ｔ淋巴细胞及Ｂ淋巴细胞、红细胞、中性粒细胞、单核细胞、血小板等多种细胞成分[3],尤以嗜酸性粒细胞居于主导作用…     

小鼠干细胞因子基因以脂质体介导转染脐血细胞

目的小鼠干细胞因子 (SCF)以脂质体介导转染脐血细胞并表达。方法采用PCR技术从 pRC/CMV(含SCFcDNA)中钓取SCFcDNA膜外段活性区 ,克隆入真核表达载体 pcDNA3 ,转染传 2代的脐血细胞 ;用RT PCR方法检测mRNA表达水平及通过协同刺激集落形成来检测转染细胞上清的生物活性。结果转染SCFcDNA的脐血细胞SCFmRNA水平表达量高于对照组 ,其细胞培养上清协同GM CSF刺激骨髓细胞形成集落数比GM CSF单独作用高两倍左右。结论脂质体介导质粒载体转染培养富集的脐血细胞并表达 ,且转染上清具有生物学活性 ,为进一步研究转染基因的表达特性及持续时间提供依据。     

支气管哮喘患者急性发作期血清中干细胞因子的测定及其临床意义

摘要 目的：探讨支气管哮喘患者急性发作期血清干细胞因子（SCF）的水平及意义,以及该细胞因子与血清中嗜酸粒细胞计数（EOS）、血清总免疫球蛋白E（T-IgE）、第1秒用力呼气流量（FEV1%）、呼出气一氧化氮（FeNO）之间的关系。方法：将65例支气管哮喘急性发作患者按病情严重程度分为轻、中、重度组,同时与同期37例健康人作对照,分别测定病例各组血清SCF、EOS,并随机测得病例各组血清T-IgE、FEV1%、FENO。结果：中、重度组治疗前血清SCF水平明显高于对照组及轻度组（P〈0.05）,病例组治疗前血清SCF水平明显高于对照组（P〈0.05）。病例组血清SCF与EOS、T-IgE、FEV1%无明显相关性,与FeNO成正相关（r=0.447,P=0.004）。结论：血清SCF的水平可较准确反应气道炎症变化,可能与哮喘急性发作的严重程度有关。     

CpG-ODN对哮喘小鼠Th1/Th2相关细胞因子表达的影响

目的：探讨CpG-ODN对哮喘小鼠Th1/Th2相关细胞因子的调节作用及气道炎症的抑制作用。方法：采用酶联免疫中附法（ELISA）分别检测CpG-ODN对哮喘小鼠抗原首次激发后24小时和抗末次激发后24小时血清及支气管肺泡灌洗液（BALF）中Th2细胞因子IL－4和Th1细胞因子IFNγ水平的影响，并与激素治疗组和哮喘组对照。结果：（1）抗原末次激发后24小时，CpG-ODN 血清及BALF中IFNγ水平高于哮喘组及地塞米松组（P＜0．001）。（2）抗原首次激发后24小时及抗原末次激发后24小时血清和BALF中IL－4水平低于哮喘组（P＜0．05），与地塞米松组比较无显著性差异（P＞0．05）。（3）抗原末次激发后24小时，CpG-ODN组外周血和BALF中嗜酸性粒细胞计数均低于哮喘组（P＜0．001）。结论：CpG-ODN不仅有具有与地塞米松相同的下调Th2细胞因子表达和抑制嗜酸性粒细胞的作用，而且还具有地塞米松所没有的诱导Th1细胞因子表达的作用。说明其可能通过调节Th1/Th2平衡而达到在早期抑制哮喘发病的目的。     

舒利迭对支气管哮喘患儿细胞因子的影响研究

目的研究及观察舒利迭对支气管哮喘患儿细胞因子的影响程度。方法 56例支气管哮喘患儿随机分为对照组（丙酸氟替卡松组）28例和观察组（舒利迭组）28例,然后将两组患儿治疗前后的血清白介素5（IL-5）、肿瘤坏死因子-α（TNF-α）及白介素6（IL-6）水平进行比较。结果观察组治疗后6周与12周时的血清IL-5、TNF-α及IL-6水平均低于对照组,P均〈0.05。结论舒利迭对支气管哮喘患儿细胞因子的影响较大,更有助于患儿支气管哮喘状态的改善。     

康复新对小鼠结肠炎细胞因子表达量的抑制作用

目的研究康复新对恶唑酮诱导的小鼠实验性肠炎的影响,并探讨其机制。方法健康昆明小鼠24只分为3组:正常组、模型组和康复新组。除正常组外,其余小鼠均以恶唑酮灌肠造模。3 d后处死,提取外周血单个核细胞(PBMC)和肠黏膜固有层单个核细胞(LPMC)进行给药培养之后用荧光定量PCR检测IL-4、IL-5、IFN-γ和TNF-α。结果①模型组的LPMC和PBMC中的IL-4、IL-5、IFN-γ和TNF-α表达量均明显高于正常组(P<0．01);②康复新组的各指标均低于模型组(P<0．05);③康复新组的LPMC中的IFN-γ表达量以及PBMC中的IL-4表达量高于正常组(P<0．01)。结论康复新具有调节细胞因子表达量的作用。     

扎鲁司特对哮喘患者外周血细胞因子及IgE的调节作用

目的 探讨扎鲁司特对哮喘患者外周血IL-10、TNF-α、IL-6及IgE的含量是否有调节作用.方法 支气管哮喘成人患者80例随机分两组,治疗组和对照组各40例.对照组予以茶碱缓释片、酮替芬等常规治疗.治疗组患者在对照组治疗的基础上,再给予口服扎鲁司特20mg,每天2次,4周为一疗程.结果 两组患者治疗前气道反应性基本相当(P＞0.05).治疗一疗程后,两组患者气道对组胺的反应阈值Dmin都较治疗前有明显提高(P＜0.05或P＜0.01),两组患者气道对组胺的反应性Rrsc都较治疗前有明显降低(P＜0.05或P＜0.01),但治疗组改善较对照组更明显(P＜0.05).两组患者治疗前外周血的TNF-α、IL-6、IL-10、IgE含量水平基本一致(均P＞0.05).治疗一疗程后,两组患者外周血TNF-α、IL-6、IgE含量水平都明显下降(均P＜0.05),IL-10含量水平都明显升高(P＜0.05);但两组比较,治疗组患者的改变更明显(均P＜0.05).结论 扎鲁司特不仅通过阻断白三烯与受体结合途径缓解病情,并且还可能通过调节支气管哮喘患者外周血的TNF-α、IL-6、IL-10、IgE含量水平,来降低患者的气道高反应性,从而改善患者的病情.     

Chrysin inhibited stem cell factor (SCF)/c-Kit complex-induced cell proliferation in human myeloid leukemia cells

Stem cell factor (SCF) has important roles in the proliferation and differentiation of hematopoietic stem cells. The complex of c-Kit and its ligand SCF induce hematopoiesis, melanogenesis, and gametogenesis. However, the mechanism by which SCF induces cell proliferation in the human megakaryoblastic leukemia cell line, MO7e, and the signaling molecules involved, especially in downstream signaling of c-Kit, remain unclear. Here, we show that pharmacological inhibition of the PI3K pathway inhibits SCF/c-Kit signaling and cell proliferation. In addition, we find that the Shc/PDK1/PKC/Akt/c-raf signaling cascade is essential for SCF/c-Kit signal pathway. Our results also suggest that ERK5 is activated and translocated to the nucleus, activating CREB and STAT3. Interestingly, chrysin shuts down the SCF/c-Kit complex-induced signaling cascade. Taken together, these studies give additional insight into the molecular mechanism of SCF/c-Kit-induced cell proliferation and its inverse agonist, chrysin. Finally, these findings enhance our understanding of MO7e cell proliferation.     

Inhibitory effect of tributyltin on expression of steroidogenic enzymes in mouse testis

Tributyltin (TBT) is known to disrupt the development of reproductive organs, thereby reducing fertility. The aim of this study was to evaluate the acute toxicity of TBT on the testicular development and steroid hormone production. Immature (3-week-old) male mice were given a single administration of 25, 50, or 100 mg/kg of TBT by oral gavage. Lumen formation in seminiferous tubule was remarkably delayed, and the number of apoptotic germ cells found inside the tubules was increased in the TBT-exposed animals, whereas no apoptotic signal was observed in interstitial Leydig cells. Reduced serum testosterone concentration and down-regulated expressions of the mRNAs for cholesterol side-chain cleavage enzyme (P450scc), 17alpha -hydroxylase/C(17-20) lyase (P450(17alpha)), 3beta -hydroxysteroid-dehydrogenase (3beta -HSD), and 17beta -hydroxysteroid-dehydrogenase (17beta -HSD) were also observed after TBT exposure. Altogether, these findings demonstrate that exposure to TBT is associated with induced apoptosis of testicular germ cells and inhibition of steroidogenesis by reduction in the expression of steroidogenic enzymes in interstitial Leydig cells. These adverse effects of TBT would cause serious defects in testicular development and function.     

糖皮质激素对哮喘大鼠肺组织IL-8表达的抑制作用

目的研究地塞米松(DXM)对哮喘大鼠肺组织IL-8mRNA及蛋白表达的影响。方法以1%卵蛋白(OVA)致敏并激发,建立大鼠哮喘模型。30只♂SD大鼠随机分为正常组,哮喘组,DXM干预组。在末次激发后24 h,将肺组织经脱水透明、石蜡包埋等处理后制作成肺标本切片。观察各组大鼠肺组织病理学改变。RT-PCR方法对肺组织IL-8 mR-NA表达检测,免疫组织化学方法技术测定大鼠肺组织标本IL-8表达。结果哮喘组肺组织IL-8 mRNA及蛋白的表达水平明显高于正常组(P<0.01),DXM组IL-8 mRNA及蛋白的表达与哮喘组相比明显减少(P<0.01)。结论哮喘大鼠肺组织IL-8水平增高,并且DXM可通过抑制IL-8的表达,减弱其对炎性细胞的趋化与激活,是激素减轻气道炎症重要机制之一。     

Inhibitory effect of genistein on osteoclast-like cell formation in mouse marrow cultures.

The effect of genistein on osteoclast-like cell formation in mouse marrow culture in vitro was investigated. The bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a well-known bone resorbing agent [parathyroid hormone (1-34) (PTH), prostaglandin E2 (PGE2), 1,25 dihydroxyvitamin D3 (VD3), or lipopolysaccharide (LPS)] with an effective concentration. Osteoclast-like cell formation was estimated by staining for tartrate-resistant acid phosphatase (TRACP), a marker enzyme of osteoclasts. The presence of PTH (10(-8) M), PGE2 (10(-6) M), VD3 (10(-8) M), or LPS (1 microg/mL) induced a remarkable increase in osteoclast-like multinucleated cells. These increases were inhibited significantly in the presence of genistein (10(-7) to 10(-5) M). The inhibitory effect of genistein (10(-5) M) was equal to that of 17 beta-estradiol (10(-8) M), calcitonin (10(-9) M), or zinc sulfate (10(-5) M). Genistein (10(-5) M) significantly inhibited dibutyryl cyclic adenosine monophosphate (10(-5) M)-induced osteoclast-like cell formation. However, genistein (10(-5) M) did not inhibit phorbol 12-myristate 13-acetate-induced osteoclast-like cell formation. The present study demonstrated that genistein has a potent inhibitory effect on osteoclast-like cell formation in mouse marrow culture. The inhibitory action of genistein may involve in cyclic AMP signaling.     

Inhibitory effect of dexamethasone palmitate-low density lipoprotein complex on low density lipoprotein-induced macrophage foam cell formation

We used low density lipoprotein (LDL) as a carrier of site-specific delivery of drugs to atherosclerotic lesions, prepared a dexamethasone palmitate (DP)-LDL complex, and examined the effect of the DP-LDL complex on foam cell formation of macrophages in vitro. LDL was isolated from human plasma and the DP-LDL complex was prepared by incubation in the presence of Celite 545. The complex contained about 50 mol of DP in 1 mol of LDL. When macrophages were incubated with LDL for 48 h, cholesterol ester was accumulated in the macrophages, indicating foam cell formation. This accumulation of cholesterol ester was significantly inhibited by incubation with the DP-LDL complex. The potency of the DP-LDL complex was similar to that of dexamethasone alone. The DP-LDL complex also significantly attenuated the accumulation of cholesterol ester induced by incubation with LDL prior to the incubation with the DP-LDL complex. These findings indicated that the DP-LDL complex showed similar characteristics to LDL, and the DP-LDL complex inhibited the foam cell formation of macrophages in in vitro experiments. This DP-LDL complex has a possibility as a drug-carrier complex for use in atherosclerosis.     

复方茵陈片对乙肝病毒HBsAg和HBeAg表达的影响

目的:研究复方茵陈片对HBsAg和HBeAg表达的抑制作用。方法:分别以不同浓度含药培养基培养2.2.15细胞,运用放射性免疫测定方法检测乙型肝炎表面抗原和e抗原。结果:复方茵陈片药液最大无毒浓度为600 g·mL-1。在此浓度基础上以培养基递减稀释药液,给药组的2.2.15细胞HBsAg和HBeAg cpm值明显低于细胞对照组。结论:复方茵陈片可以抑制HBV的复制和表达。