红霉素、阿仑膦酸钠抑制磨损颗粒对小鼠巨噬细胞分泌白细胞介素1,6及肿瘤坏死因子α的影响

背景:阿仑膦酸钠的抗骨吸收作用是通过其对破骨细胞的抑制作用完成的,近年亦有报道证实红霉素有直接抑制破骨细胞的作用。目的:观察阿仑膦酸钠和红霉素抑制钛颗粒刺激巨噬细胞分泌肿瘤坏死因子α、白细胞介素1,6的作用。方法:分离、培养小鼠腹腔巨噬细胞,14h后分为红霉素组及阿仑膦酸钠组,每组分为6个亚组。红霉素组:A组:仅为巨噬细胞;B组:巨噬细胞+钛颗粒;C组:巨噬细胞+钛颗粒+红霉素1μg/L;D组:巨噬细胞+钛颗粒+红霉素10μg/L;E组:巨噬细胞+钛颗粒+红霉素100μg/L;F组:巨噬细胞+钛颗粒+红霉素1000μg/L。阿仑膦酸钠组分组及剂量同红霉素组。培养24h后,用酶联免疫法检测细胞培养上清液中白细胞介素1,6及肿瘤坏死因子α的质量浓度。结果与结论:B组白细胞介素1,6及肿瘤坏死因子α的质量浓度明显高于其他组(P<0.05),F组白细胞介素1,6及肿瘤坏死因子α的质量浓度明显低于C组(P<0.05)。同剂量阿仑膦酸钠和红霉素组间差异无显著性意义(P>0.05)。提示钛颗粒可以刺激巨噬细胞分泌大量的白细胞介素1,6及肿瘤坏死因子α,红霉素、阿仑膦酸钠能够呈剂量依赖型地有效抑制钛颗粒诱导的巨噬细胞分泌白细...     

阿仑膦酸钠对髋关节假体周围界膜组织分泌肿瘤坏死因子α的影响

背景:目前肿瘤坏死因子α的研究有望成为防治假体周围骨丢失的新的切入点,但阿仑膦酸钠对界膜分泌肿瘤坏死因子α的影响及作用机制尚不清楚.目的:观察阿仑膦酸钠对髋关节假体周围界膜组织分泌肿瘤坏死因子α的影响.设计、时间及地点:随机分组设计,对比观察,实验于2006-02/03在广州中医药大学附属骨科医院骨科实验室完成.材料和对象:界膜组织(15 g)取自广州中医药大学第一附属医院(患者知情并同意);雄性新西兰白兔6只用于制备阿仑膦酸钠含药血清,阿仑膦酸钠为石家庄制药厂产品.方法:无菌条件下从人工髋关节假体周围股骨分离界膜组织(15 g),并将其放入RPMI培养液中培养,将界膜组织剪成约250 mg的碎块,计30块,随机分为3组:空白对照组、低浓度阿仑膦酸钠组(100 g/L)、高浓度阿仑膦酸钠组(200 g/L),每组10个样本.低浓度阿仑膦酸钠组和高浓度阿仑膦酸钠组分别加入1.8 mL和1.6 mL,空白对照组加入1.8 mL.然后在低浓度阿仑膦酸钠组、高浓度阿仑膦酸钠组的培养孔中分别加入入0.2 mL和0.4 mL的阿仑膦酸钠含药血清,空白对照组加入0.2 mL空白血清.添加血清后在37℃、含体积分数为5%CO2的饱和湿度条件下培养72 h.主要观察指标:酶联法检测各组界膜组织中肿瘤坏死因子α的表达.结果:低浓度阿仑膦酸钠组和高浓度阿仑膦酸钠组界膜组织分泌肿瘤坏死因子α的量分别为(3.93±0.03),(3.92±0.04)pg/g,与空白对照组(4.04±0.13)pg/g相比,差异有显著性意义(P<0.01).结论:阿仑膦酸钠能显著抑制髋关节假体周围界膜组织分泌肿瘤坏死因子α.     

阿仑膦酸钠对大鼠松质骨和密质骨影响的比较

目的：比较阿仑膦酸钠(固邦，ALN)对去卵巢大鼠胫骨上段和腰椎质松骨及胫骨中段密质骨的影响。方法：3月龄雌性SD大鼠，ALN1mg／(kg&;#183;d)，灌胃给药90d。骨标本行不脱钙骨制片，骨组织形态计量法钡5量。结果：松质骨：OVX组胫骨上段(PTM)和腰椎(LV)质松骨的骨量减少(P&;lt;0．001)，骨结构变差；ALN组PTM，LV骨量增加(P&;lt;0．001)，完全对抗OVX大鼠的骨高转换。密质骨：OVX组胫骨中段(TX)骨量减少(P&;lt;0．05)，骨内膜骨形成和骨吸收增加。ALN组骨量增加(P&;lt;0．05)，骨内膜骨形成减少而骨吸收有减少的趋势。结论：ALN能有效预防OVX后大鼠的骨质疏松，但不同部位有不同的骨转换速度。     

早期应用阿仑膦酸钠对脊髓损伤大鼠骨密度及生物力学特性的影响

目的探讨早期应用阿仑膦酸钠(ALN)对脊髓损伤(SCI)大鼠股骨骨密度及生物力学特性的影响。方法将36只3月龄雌性SD大鼠随机分为假手术组(sham组)、SCI组、SCI ALN组，假手术组仅行T10椎板切除，其余组行T10椎板切除、脊髓横断术。SCI ALN组于术后1周开始腹腔注射ALN，每周3次。术后8周取股骨，进行骨密度及生物力学检测。结果脊髓横断术后8周大鼠股骨骨密度及生物力学参数与Sham组相比发生了显著性改变；与SCI组相比，SCI ALN组股骨骨密度值显著升高(P＜0．01)；弹性载荷值、最大载荷值显著升高(P＜0．01)，最大应力值升高(P＜0．05)。结论脊髓横断术后8周的大鼠可用于SCI后骨质疏松的研究；早期应用ALN可减少SCI大鼠股骨的骨量丢失，改善SCI大鼠股骨的生物力学特性。     

脉冲电磁场及阿仑膦酸钠对脊髓损伤大鼠骨质量的影响

目的探讨早期应用脉冲电磁场（PEMFs）和／或阿仑膦酸钠（ALN）对脊髓损伤（SCI）后大鼠骨质量的影响。方法将62只3月龄雌性sD大鼠随机分为5组，其中假手术组仅行椎板切除术，SCI组、SCI＋ALN组、SCI＋PEMFs组及SCI＋PEMFs＋ALN组行脊髓完全横断术，后3组于术后1周时分别给予ALN和／或PEMFs治疗；于术后8周时取材，检测各组大鼠股骨骨密度值、生物力学指标以及胫骨近端骨组织形态计量学等指标。实验所得数据比较采用单因素方差分析及析因分析。结果早期应用ALN和／或PEMFs均可使股骨骨密度、股骨弹性载荷、最大载荷等生物力学指标增高，胫骨近端骨小梁面积百分比也同时增大，骨小梁宽度增加。结论早期应用ALN和／或PEMFs均可抑制SCI后骨量丢失，增强抗骨折能力，阻止胫骨近端微观结构的退变，提示早期应用ALN及PEMFs有助于防治SCI后骨质疏松，但其具体治疗机制还有待进一步研究。     

髓芯减压及阿仑膦酸钠治疗Ⅱ期股骨头坏死的早期观察

目的探讨髓芯减压术及阿仑膦酸钠治疗Ⅱ期股骨头坏死的临床疗效。方法 2007年1月2010年3月采用经皮斯氏针髓芯减压术联合阿仑膦酸钠治疗早期股骨头坏死23例37髋。结果 23例患者术后48h感觉疼痛明显缓解,自述疼痛缓解过半以上。门诊复查1年内髋关节疼痛复发或者加重7例,髋关节疼痛明显缓解1年以上的16例,临床满意率69.5%。视觉模拟评分法评分由术前4～5分下降1～2分。X线片、MRI显示股骨头坏死面积扩大的5例,伴股骨头轻微塌陷的3例。随访期内无患者行人工髋关节置换术,未发生股骨颈骨折。结论早期股骨头坏死采用经皮斯针髓芯减压术联合长期服用阿仑膦酸钠治疗有一定功效,可快速缓解髋关节疼痛,延迟股骨头坏死的发展,且具有创伤小、住院时间短、费用低等优点。     

降钙素配伍阿仑膦酸钠对骨质疏松症治疗的疗效价值

目的探讨降钙素配伍阿仑膦酸钠治疗骨质疏松症(OP)的临床疗效。方法选择2011年1月至2013年6月在我院骨科就诊的120例原发性OP患者,按照纳入顺序分为3组,对照Ⅰ组(40例,实际完成37例)肌注降钙素;对照Ⅱ组(40例,实际完成38例)口服阿仑膦酸钠;观察组(40例,实际完成38例)联用降钙素、阿仑膦酸钠,比较三组骨密度(BMD)、血骨钙素(BGP)、抗酒石酸酸性磷酸酶-5b(TRACP-5b)、疼痛症状、生活质量及不良反应。结果组内比较:较之治疗前,三组OP患者治疗后腰椎1⁴(L14(L1⁴)、股骨颈(NF)、全髋(TH)部位的BMD及生活质量评分均明显增加,BGP、TRACP-5b均明显减少,差异均有统计学意义(P<0.05)。组间比较:治疗前,三组OP患者L14)、股骨颈(NF)、全髋(TH)部位的BMD及生活质量评分均明显增加,BGP、TRACP-5b均明显减少,差异均有统计学意义(P<0.05)。组间比较:治疗前,三组OP患者L1⁴、NF、TH部位的BMD、BGP、TRACP-5b及生活质量评分差异均无统计学意义(P>0.05);治疗后,观察组L14、NF、TH部位的BMD、BGP、TRACP-5b及生活质量评分差异均无统计学意义(P>0.05);治疗后,观察组L1⁴、NF、TH部位的BMD及生活质量评分(除生理职能)均明显高于对照组Ⅰ组、对照Ⅱ组,BGP、TRACP-5b均明显低于对照组Ⅰ组、对照Ⅱ组,疼痛改善情况明显好,差异均有统计学意义(P<0.05);对照组Ⅰ组、对照Ⅱ组的BMD、BGP、TRACP-5b及疼痛、生活质量改善情况比较差异均无统计学意义(P>0.05)。三组不良反应、骨折发生率组间比较差异无统计学意义(P>0.05)。结论降钙素配伍阿仑膦酸钠治疗OP,有效且安全,值得推广应用。     

阿仑膦酸钠对长期服用糖皮质激素女性系统性红斑狼疮患者骨密度的影响

目的：评价联合阿仑膦酸钠和碳酸钙维生素D对非绝经期系统性红斑狼疮（SLE）患者长期应用糖皮质激素（GCS）所造成的骨量丢失的有效性和安全性。方法：116例绝经前期SLE患者随机分为观察组和对照组各58例,均每日2次给予碳酸钙维生素D300mg治疗,观察组同时加服阿仑膦酸钠70mg/周。结果：治疗6个月后,2组血钙、血磷含量与治疗前比较均差异无显著性意义;碱性磷酸酶及全段甲状旁腺激素含量均低于治疗前,且观察组明显低于对照组（P〈0.05）;腰椎和股骨颈骨密度检测2组均较治疗前上升,且观察组明显高于对照组（P〈0.05）。结论：女性SLE患者联合阿仑膦酸钠能有效改善GCS长期应用所造成的骨量丢失,增加骨密度,最大限度的预防骨质疏松的发生。     

构建创伤性股骨头塌陷坏死大鼠模型及阿仑膦酸钠预防的机制

背景：临床随访研究表明阿仑膦酸钠对于预防股骨头坏死塌陷有效,但尚缺乏其预防塌陷作用的机制研究。目的：分析阿仑膦酸钠预防股骨头坏死塌陷的效果及其作用机制。方法：将45只SD大鼠随机分成3组,每组15只。安慰剂组在建立股骨头坏死模型后给予生理盐水治疗;阿仑膦酸钠组建立股骨头坏死模型后给予药物阿仑膦酸钠治疗;假手术组给予同样剂量的生理盐水治疗。造模后5周处死大鼠,取造模侧股骨标本分别行大体标本观察,X射线、Micro-CT及组织学检测。结果与结论：大体标本观察安慰剂组股骨头明显塌陷畸形,阿仑膦酸钠组股骨头轻度变形。股骨头高度与宽度的比值假手术组〉阿仑膦酸钠组〉安慰剂组,差异均有显著性意义。Micro-CT扫描结果显示阿仑膦酸钠组骨小梁平均数量多于安慰剂组,少于假手术组,差异均有显著性意义。阿仑膦酸钠组骨小梁平均厚度小于安慰剂组,但和假手术组比差异无显著性意义。阿仑膦酸钠组骨小梁平均间距小于安慰剂组,但大于假手术组,差异均有显著性意义。阿仑膦酸钠组股骨头骨组织体积、骨表面积、骨矿盐密度均大于安慰剂组,小于假手术组,差异均有显著性意义。组织学检测结果显示,阿仑膦酸钠组存在明显的死骨,破骨细胞明显受到抑制,破骨细胞数量较安慰剂组明显减少,成骨细胞和新生血管也受到了一定程度的抑制。结果表明阿仑膦酸钠可通过全面抑制破骨细胞、成骨细胞及血管新生而抑制骨坏死的修复反应,减慢坏死骨的吸收,保存骨量及股骨头形态,对大鼠创伤性股骨头坏死早期塌陷具有一定的预防作用。     

阿法骨化醇联合阿仑膦酸钠治疗老年骨质疏松症的效果及对患者骨代谢的影响

目的分析阿法骨化醇联合阿仑膦酸钠治疗老年骨质疏松症(OP)的效果及对患者骨代谢的影响。方法选取我院2018年11月至2020年5月收治的118例老年OP患者,将其随机分为对照组(59例,阿法骨化醇)和试验组(59例,阿法骨化醇联合阿仑膦酸钠)。比较两组治疗效果。结果治疗后,试验组S-Ca、S-P、BMD、TGF-β1及IGF-1水平均明显高于对照组(P<0.05),OC、BALP、TRACP-5b、TNF-α水平及VAS、ODI评分均明显低于对照组(P<0.05)。试验组治疗总有效率显著高于对照组(P<0.05)。结论阿法骨化醇联合阿仑膦酸钠治疗老年OP的临床效果显著,能够有效改善患者体内骨代谢指标和细胞因子水平,减轻患者疼痛,提高患者活动能力。     

C5a stimulates secretion of tumor necrosis factor from human mononuclear cells in vitro. Comparison with secretion of interleukin 1 beta and interleukin 1 alpha

We have demonstrated that purified C5a is a potent stimulus to human PBMC secretion of TNF-alpha, IL-1 beta, and IL-1 alpha, which proceeds in a dose-dependent fashion. At a given concentration of C5a, TNF-alpha and IL-1 beta secretion did not differ significantly; both were secreted in significantly greater quantity than IL-1 alpha. Clinical conditions such as Gram-positive and Gram-negative bacterial infections, trauma, and immune complex diseases activate complement. Through the mediation of TNF and IL-1 secreted in response to C5a, these diverse disorders can share common features of fever, coagulopathy, acute phase protein production, and disordered metabolism.     

Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis

In spontaneous inflammatory arthritis of K/BxN T cell receptor transgenic mice, the effector phase of the disease is provoked by binding of immunoglobulins (Igs) to joint surfaces. Inflammatory cytokines are known to be involved in human inflammatory arthritis, in particular rheumatoid arthritis, although, overall, the pathogenetic mechanisms of the human affliction remain unclear. To explore the analogy between the K/BxN model and human patients, we assessed the role and relative importance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficient recipients. Interleukin (IL)-1 proved absolutely necessary. Tumor necrosis factor (TNF)-alpha was also required, although seemingly less critically than IL-1, because a proportion of TNF-alpha-deficient mice developed robust disease. There was no evidence for an important role for IL-6. Bone destruction and reconstruction were also examined. We found that all mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/BxN arthritis, with no evidence of any particular requirement for TNFalpha for bone destruction. The variability in the requirement for TNF-alpha, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes.     

Human neutrophils produce high levels of the interleukin 1 receptor antagonist in response to granulocyte/macrophage colony-stimulating factor and tumor necrosis factor alpha

Neutrophils, an abundant cell type at sites of inflammation, have the ability to produce a number of cytokines, including interleukin 1 (IL-1), IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor alpha (TNF-alpha). In this study, we have examined the ability of human neutrophils to produce the IL-1 receptor antagonist (IL-1Ra), a 17-23-kD protein recently isolated and cloned from macrophages. Since IL-1Ra has been shown to inhibit both the in vitro and in vivo effects of IL-1, its production by large numbers of tissue-invading neutrophils might provide a mechanism by which the effects of IL-1 are regulated in inflammation. Using antibodies that are specific for IL-1Ra and a cDNA probe encoding for this protein, we were able to show that neutrophils constitutively produce IL-1Ra. However, after activation by GM-CSF and TNF-alpha, IL-1Ra was secreted into the extracellular milieu where it constituted the major de novo synthesized product of activated neutrophils. None of a large array of other potent neutrophil agonists were found to affect the production of IL-1Ra by neutrophils. Quantitative measurements by enzyme-linked immunosorbent assay revealed that intracellular IL-1Ra is in eightfold excess of the amount secreted in supernatants when studying nonactivated neutrophils. However, in GM-CSF- and TNF-alpha-activated cells, this difference was reduced to values between four- and fivefold, as virtually all of the de novo synthesized IL-1Ra was secreted. In activated cells, the intracellular content of IL-1Ra was found to be in the 2-2.5-ng/ml range per 10(6) neutrophils, whereas levels reached the 0.5-ng/ml range in supernatants. This would imply that IL-1Ra is produced in excess of IL-1 by a factor of at least 100, an observation that is in agreement with the reported amounts of IL-1Ra needed to inhibit the proinflammatory effects of IL-1. Neutrophils isolated from an inflammatory milieu, the synovial fluid of patients with rheumatoid arthritis, were found to respond to GM-CSF and TNF-alpha in terms of IL-1Ra synthesis, indicating that the in vitro observations made in this study are likely to occur in an inflammatory setting in vivo.     

Nystatin induces secretion of interleukin (IL)-1beta, IL-8, and tumor necrosis factor alpha by a toll-like receptor-dependent mechanism

Nystatin is an antifungal compound with potent proinflammatory properties. Herein, we demonstrate that nystatin induces interleukin (IL)-1beta, IL-8, and tumor necrosis factor alpha secretion through its activation of toll-like receptor 1 (TLR1) and TLR2. Hence, a TLR-dependent mechanism could serve as the molecular basis for the proinflammatory properties of nystatin.     

Local production of tumor necrosis factor alpha, interleukin 1, and interleukin 6 in meningococcal meningitis. Relation to the inflammatory response

We examined the cerebrospinal fluid (CF) taken on admission from 60 patients with infections caused by Neisseria meningitidis for presence of TNF-alpha, IL-1, and IL-6. TNF-alpha was detected in CF in 55 and 19% (p = 0.03), IL-1 in 50 and 15% (p = 0.05), and IL-6 in 98 and 100% of patients with meningitis and septic shock/bacteremia, respectively. The median IL-6 concentration in CF in patients with meningitis was 154 ng/ml, and in patients with septic shock/bacteremia it was 42 ng/ml (p = 0.001). The level of LPS in CF correlated with the level of TNF-alpha (r = 0.91, p less than 0.001), but not with the level of IL-1 and IL-6. CF levels of TNF-alpha, IL-1, and IL-6 correlated with each other (r = 0.34-0.54, p less than 0.01), with the protein concentration (r = 0.34-0.62, p less than 0.01) and inversely with the CF/blood glucose ratio (r = -0.34 to -0.67, p less than 0.01). Only the Il-6 level correlated with the leukocyte count (r = 0.37, p less than 0.01). In rabbits TNF-alpha, IL-1, and IL-6 activities sequentially appeared in CF within 3 h of injection of meningococcal LPS or viable meningococci, whereas the main infiltration of granulocytes started after 4 h. TNF-alpha was detected in serum at concentrations less than 1/100 of those in CF after administration of LPS into the subarachnoid space, and conversely, TNF-alpha was detected in CF at concentrations 1/100 of those in serum after intravenous injection of LPS. The results demonstrate that TNF-alpha, IL-1, and IL-6 are sequentially produced in the initial phase of the local inflammatory response caused by meningococci, and that the subarachnoid space and systemic circulation are separate compartments with respect to production of TNF-alpha, IL-1, and IL-6.     

Inhibition of secretion of interleukin-1alpha and tumor necrosis factor alpha by the ketolide antibiotic telithromycin

The antibiotic telithromycin was examined for its effect on secretion of interleukin-1α (IL-1α), IL-1β, IL-6, IL-10, and tumor necrosis factor alpha (TNF-α) by lipopolysaccharide (LPS)-stimulated monocytes of eight human donors. Secretion of each cytokine was significantly increased by LPS alone, whereas treatment with telithromycin significantly inhibited secretion of IL-1α and TNF-α but not secretion of IL-1β, IL-6, and IL-10. Telithromycin had immunomodulatory effects as a result of alteration of secretion of IL-1α and TNF-α by monocytes.     

五种生物材料对大鼠巨噬细胞肿瘤坏死因子α和白细胞介素1 β表达的影响

背景：生物材料的免疫学研究主要包括免疫球蛋白、血清总补体及补体降解产物的血生化定量测定等方面，主要通过细胞学和组织学的检测手段，其评价指标比较单一，无特异性。 目的：以细胞因子（肿瘤坏死因子α和白细胞介素1β）为研究对象，从mRNA水平上对5种生物材料介导的炎症反应进行相关免疫学评价。 设计、时间及地点：对比观察实验，于2004—01／2005—03在上海生物材料研究测试中心完成。 材料：清洁级SD大鼠3只用于原代培养大鼠巨噬细胞。阳性材料：含8％有机锡的聚氟乙烯。阴性材料：聚苯乙烯。实验材料：美国NPG黄合金块、β-磷酸三钙、固化的磷酸钙骨水泥、聚丙交酯乙交酯及聚四氟乙烯。 方法：参照ISO 10993-12标准，用RPMI—1640按1g／5mL比例，37℃72h制备材料的浸提液。将大鼠腹腔巨噬细胞分别给予脂多糖刺激和无脂多糖刺激，脂多糖的终浓度为1．0mg／L，再用不同生物材料的浸提液予以刺激，作用2h后收集细胞，进行反转录-聚合酶链反应检测。 主要观察指标：大鼠巨噬细胞肿瘤坏死因子α和白细胞介素1β的表达强度。 结果：未经脂多糖诱导的大鼠腹腔巨噬细胞与阳性材料及聚四氟乙烯、NPG接触后肿瘤坏死因子α和白细胞介素1β的表达均高于阴性材料，差异均有非常显著性意义（P〈0．05）；聚丙交酯乙交酯中肿瘤坏死因子α的表达与阴性材料相比无明显升高（P〉0．05），白细胞介素1β的表达高于阴性材料，差异有显著性意义（P〈0．05）；β-磷酸三钙和固化的磷酸钙骨水泥中肿瘤坏死因子α和白细胞介素1β的表达与阴性材料比较差异无显著性意义（P〉0．05）。经脂多糖诱导的大鼠腹腔巨噬细胞与阳性材料及聚四氟乙烯、NPG、聚丙交酯乙交酯、β-磷酸三钙及固化的磷酸钙骨水泥接触后肿瘤坏死因子α和白细胞介素1β的表达均高于阴性材料，差异均有非常显著性意义（P〈0．01）。 结论：肿瘤坏死因子α、白细胞介素1β是在分子水平上衡量不同生物材料诱导免疫刺激反应的理想指标。聚四氟乙烯和NPG的生物相容性程度较差，β-磷酸三钙和固化的磷酸钙骨水泥的相容性较好，尤其是固化的磷酸钙骨水泥。     

组织工程皮肤移植过程中白细胞介素10和肿瘤坏死因子α的表达

背景:白细胞介素10和肿瘤坏死因子α在异体异种皮肤移植局部免疫与排斥反应中发挥了重要作用.但在组织工程人工皮肤移植过程中局部皮肤组织内白细胞介素10和肿瘤坏死因子α的表达情况目前尚不清楚.目的:采用表皮干细胞联合脱细胞真皮构建人工皮肤并移植修复兔全层皮肤缺损创面,观察创面修复效果和局部皮肤组织白介素10与肿瘤坏死因子α的表达变化.方法:将体外培养的人表皮干细胞或角质细胞接种到脱细胞真皮支架中,构建组织工程人工皮肤;取新西兰白兔常规制作背部全层皮肤缺损创面随机分为4组,表皮干细胞组、角质细胞组用含表皮干细胞或角质细胞的组织工程皮肤移植于皮肤缺损创面;脱细胞真皮组移植单纯脱细胞真皮;对照组创面空置.观察刨面修复情况,局部炎症反应,创面愈合时间.各组分别于术后7d在部分创而取材观察组织形态和白细胞介素10与肿瘤坏死因子α表达.结果与结论:含表皮干细胞的人工皮肤移植后创面愈合良好,局部炎症反应轻微,无出血、积脓、坏死,创面愈合时间较角质细胞组明显缩短.白细胞介素10在各组均有表达,其中表皮干细胞组表达最强,角质细胞组次之,脱细胞真皮组和对照组最弱.肿瘤坏死因子α在各组也均有表达,其中角质细胞组表达最强,表皮干细胞组次之,脱细胞真皮组和对照组较弱.说明以表皮干细胞作为种子细胞联合脱细胞真皮构建人工皮肤可用有效促进皮肤缺损创面的修复治疗,创面修复过程中局部皮肤组织内白细胞介素10和肿瘤坏死因子的表达变化可能是其取得较好效果的主要机制之一.     

腰椎间盘突出症患者血清白细胞介素1β、白细胞介素6、肿瘤坏死因子α表达与其疼痛的相关性

目的:分析腰椎间盘突出症患者血清细胞因子的表达及其与疼痛的关系,深化对其病变的认识。方法:于2005-02/12选择中国中医科学院望京医院及骨伤科研究所门诊和住院的腰椎间盘突出症患者43例,为试验组。腰椎间盘突出症根据临床症状结合CT和/或MRI影像学检查确诊。同期选择成年健康体检者30例,为正常组。应用放免法测定血清中白细胞介素1β、白细胞介素6、肿瘤坏死因子α的含量,采用目测类比评分法测定患者疼痛程度。结果:纳入患者43例和健康体检者30例,均进入结果分析。①试验组血清白细胞介素1β、白细胞介素6、肿瘤坏死因子α含量高于正常组,差异有显著性意义[分别为(0.40±0.17),(0.19±0.06)μg/L;(131.78±32.06),(108.85±41.48)μg/L;(1.84±0.49),(1.14±0.40)μg/L,P<0.01]。②疼痛和白细胞介素6依存性不显著(P>0.05),疼痛和白细胞介素1β、肿瘤坏死因子α呈数值依存性(P<0.01)。结论:腰椎间盘突出症患者血清白细胞介素1β、白细胞介素6、肿瘤坏死因子α异常升高,白细胞介素1β、肿瘤坏死因子α是导致疼痛的重要因素。