人类白细胞介素-24基因在肿瘤联合治疗中的应用

人类白细胞介素-24基因（hIL-24）是一个既抑制肿瘤生长又调节免疫系统功能的细胞因子类的抑癌基因,可以特异性地抑制多种肿瘤细胞生长并诱导其凋亡,同时与其他基因治疗、放疗、化疗、细胞因子治疗等方式联合应用有抗肿瘤协同效应,能显著提高杀伤肿瘤的效果,为肿瘤治疗的研究提供了新的思路。     

肝硬化患者血清IL-6、TNF和尿液IL-6、IL-8检测的临床意义

目的 探讨细胞因子在肝硬化发病中的作用。方法 采用双抗体夹心Elisa法对54例肝硬化患和35例正常人血清白细胞介素－6（IL-6)、肿瘤坏死因子（TNF）和尿液IL－6、IL－8进行检测。结果 肝硬化患血清中IL－6、TNF和尿液IL－6、IL－8含量较对照组明显升高（P＜0．01）,血IL－6、TNF含量GN与尿液量白蛋白呈高度正相关：尿液IL－6、IL－8呈显正相关（r=0．5728,P＜0．05）。结论 肝硬化患病程中TNF、IL－6、IL－8均处于高活性状态,IL－6与体液免疫反应亢进所致的免疫病理损伤有关,IL－6、IL－8、TNF参与肾脏的免疫损伤、可作为判定患预后和转归指标。     

重症肌无力患者胸腺AChR特异反应性IL-4,IL-10和IFN-γ分泌细胞数的检测

目的：探讨重症肌无力（MG）患者的乙酰胆碱受体（AChR）特异性T细胞免疫应答。方法：利用酶联免疫斑点技术（Elispot）检测32例MG患者胸腺AchR特异反应性白细胞介素-4(IL-4)、白细胞介素-10（IL-10）和干扰素-γ（IFN-γ）分泌细胞数。结果：MG患者胸腺AchR特异反应性IL-4，IL-10和IFN-γ分泌细胞数均增高，其中胸腺增生组AChR特异反应性IL-4，IL-10和IFN-γ分泌细胞数明显高于胸腺瘤组。结论：MG胸腺Th1和Th2细胞存在免疫功能紊乱，胸腺AChR特异反应性IL-4，IL-10和IFN-γ分泌细胞数可作为判断胸腺Th细胞免疫功能紊乱的指标。     

白细胞介素与支架内再狭窄

支架置入术后的支架内再狭窄是困扰动脉粥样硬化性心脑血管病微侵袭介入治疗发展的主要问题.支架置入术后的血管内炎症反应是再狭窄的重要原因之一.其中,以白细胞介素为代表的细胞因子起着复杂和多变的作用.文章综述了白细胞介素表达水平对血管内皮增生的作用以及对支架内再狭窄发生率的影响.     

抑肽酶对体外循环中细胞因子的作用及影响

目的研究体外循环(CPB)心脏直视手术中细胞因子如肿瘤坏死因子TNF-α、白介素IL-6、白介素IL-8的变化,观察抑肽酶对体外循环炎性反应的抑制作用。方法20例心脏瓣膜手术患者随机分为抑肽酶组(A组)和对照组(C组),每组10例:对照组不给药,抑肽酶组给抑肽酶总量300万KIU,其中50万KIU为麻醉诱导前给予,250万KIU预充体外循环机内。分别于CPB前(T1)、升主动脉阻断半小时(T2)、CPB结束(T3)、停CPB后2h(T4)各时间点抽取静脉血,采用酶联免疫试剂盒测定TNF-α、IL-6和IL-8的水平。结果两组患者血浆TNF-α、IL-6、IL-8水平有明显增加(P<0.05或P<0.01),但与对照组相比,抑肽酶组血清中TNF-α、IL-6、IL-8的浓度明显受到抑制(P<0.01),升高的幅度明显低于对照组。结论在CPB过程中,抑肽酶可能通过降低TNF-α、IL-6、IL-8等细胞因子水平,从而减轻炎性反应达到减轻缺血再灌注损伤的目的。     

乌司他丁和地塞米松对心肺脑复苏早期大鼠脑组织含水量及IL-1β水平等的影响

目的探讨乌司他丁、地塞米松以及两者联合应用对心肺脑复苏早期大鼠脑组织含水量及脑组织IL-1β、外周血肿瘤坏死因子α（TNF-α）含量的影响。方法将40只SD大鼠随机分为假手术对照组、心肺脑复苏（CPCR）组、地塞米松组、乌司他丁组、乌司他丁＋地塞米松组，每组各8只大鼠。采用夹闭气管法建立大鼠心肺脑复苏模型。于自主呼吸循环恢复后2h，采用干湿法检测各组大鼠脑组织含水量，采用放射免疫法检测大鼠脑组织IL-1β和外周血TNF-α水平。结果①脑组织含水量：CPCR组为（80．4±2．0）％，较对照组（76．7±1．3）％显著增加（P〈0．01）；乌司他丁组、地塞米松组、乌司他丁＋地塞米松组，3组间差异无统计学意义（P〉0．05），但均较CPCR组显著减少（P〈0．01）。②脑组织IL-1β含量：CPCR组为（0．235±0．051）ng／mg，较对照组（0．108±0．020）ng／mg明显增高（P〈0．01）；地塞米松组、乌司他丁组与CPCR组比较，差异无统计学意义；乌司他丁＋地塞米松组IL-1β含量为（Q（365±Q021）ng／mg，明显低于CPCR组（0．235±0．051）ng／mg（P〈0．001）。③外周血TNF-α水平：CPCR组为（3．07±0．74）ng／ml，较对照组（1．03±0．51）ng／ml明显增高（P〈0．01）；乌司他丁组、地塞米松组、乌司他丁＋地塞米松组均比CPCR组显著降低（P〈0．01），但3组间差异无统计学意义（P〉0．05）。结论CPCR早期即可发生脑水肿，脑组织IL-1β及外周血TNF-α水平显著增加；应用乌司他丁、地塞米松能有效降低脑组织含水量、IL-1β和外周血中TNF-α水平。     

Study of pro-inflammatory (TNF-α, IL-1α, IL-6) and T-cell-derived (IL-2, IL-4) cytokines in plasma and synovial fluid of patients with juvenile chronic arthritis: Correlations with clinical and laboratory parameters

Acute phase proteins, synovial fluid (SF) cellular infiltrates, pro-inflammatory (TNF-, IL-1, IL-6) and Th1 (IL-2) and Th2 (IL-4) derived cytokine levels both in plasma and SF were examined in pauciarticular and polyarticular juvenile chronic arthritis (JCA) patients during the active (n=22) and inactive (n=14) period in order to determine pathogenic mechanisms and correlations between cytokines and laboratory parameters showing disease activity. The erythrocyte sedimentation rate (ESR), serum C-reactive protein (CRP) and IgG concentrations were found to be significantly elevated in the active period of JCA. In pauciarticular JCA patients, when compared with their peripheral blood lymphocyte subpopulations, SF CD3+ cells (73.1%) and HLA-DR+ active T cells (22.5%) were found to be significantly increased. In the active period of JCA, plasma TNF- and IL-6 concentrations were significantly elevated. Plasma IL-2 and IL-4 levels were not elevated and were found to be similar to those in the inactive phase and in healthy controls. SF IL-6, TNF- and IL-1 levels were extremely high in all the patients. SF IL-4 and IL-2 levels were all undetectable. There was a significant correlation between ESR values and plasma IL-6 levels and between serum CRP levels and plasma IL-6 and TNF- concentrations. In conclusion, increased local production of pro-inflammatory cytokines appears to account for the articular manifestations of JCA. The impaired production of anti-inflammatory Th2-derived cytokines (IL-4) seems to cause increased production of inflammatory cytokines acting on the balance between them. The deficit in IL-2 production was not suggested to be primarily involved in the pathogenesis. In addition, not only CRP and ESR values, but also plasma IL-6 and TNF- concentrations may be used as markers of disease activity.     

Interferon gamma and interleukin 8 gene polymorphisms in patients with hepatitis C virus related oral lichen planus

ObjectivesThis study aimed to determine the association of rs2430561 and rs4073 polymorphisms in the Interferon gamma (IFN-ɤ) and Interleukin 8 (IL-8) genes, respectively, with hepatitis C virus-related oral lichen planus and disease severity.DesignThis is a case-control study. 60 subjects were equally divided into patients with and without oral lichen planus. They were further subdivided into hepatitis C virus seropositive and seronegative patients. All patients were genotyped for IFN-γ rs2430561 thymine to adenine (T > A) and IL-8 rs4073 adenine to thymine (A > T) polymorphisms. All patients with oral lichen planus had their lesions measured and documented using the Escudier scoring system.ResultsDisease activity was significantly higher in the "oral lichen planus/hepatitis C virus-positive" patients than in the "oral lichen planus/hepatitis C virus-negative" patients (P = 0.003). IFN-γ rs2430561 T > A and IL-8 rs4073 A > T genotypes and allele frequencies were not associated with the oral lichen planus group or the normal group. Stratification of the two groups into HCV and non-HCV-infected patients or into erosive and non-erosive types revealed no significant associations. The “A-allele-containing" genotypes of IL-8 rs4073 A > T were significantly more prevalent in the patients with oral lichen planus than in those without.ConclusionHepatitis C virus infection is associated with the development of erosive oral lichen planus. The A-allele of IL-8 rs4073 A > T may have a role in the development and progression of oral lichen planus.     

N-乙酰半胱氨酸对急性胰腺炎模型大鼠的保护作用

背景：急性胰腺炎是由胰腺腺泡细胞损伤介导的常见炎性疾病,白细胞浸润是其主要的发病特征。近来发现N-乙酰半胱氨酸能够控制白细胞游走并在一些严重的炎症疾病中发挥调节炎症反应的作用。
　　目的：观察N-乙酰半胱氨酸在体内对牛黄胆酸盐诱导的急性胰腺炎大鼠模型的保护作用。
　　方法：90只SD大鼠随机等分为正常对照组、急性胰腺炎组和N-乙酰半胱氨酸组,后2组以十二指肠大乳头逆行注射牛黄胆酸盐制备急性大鼠胰腺炎模型。N-乙酰半胱氨酸组大鼠由尾静脉给予N-乙酰半胱氨酸治疗。结果与结论：急性胰腺炎模型诱导后大鼠血浆淀粉酶活性较正常对照组大鼠显著升高(P<0.05)。急性胰腺炎组白细胞介素1β,6,10和肿瘤坏死因子α表达水平明显高于正常对照组(P<0.05)。免疫荧光化学显示N-乙酰半胱氨酸主要表达在胰岛细胞上,急性胰腺炎组织 N-乙酰半胱氨酸的表达从 mRNA 水平到蛋白水平都明显低于正常组织。N-乙酰半胱氨酸治疗显著降低了大鼠血清淀粉酶水平,髓过氧化物酶活性以及促炎性细胞因子产物生产和胰腺及肺组织损伤,但N-乙酰半胱氨酸治疗并没有明显抑制胰腺组织核因子κB的激活。提示N-乙酰半胱氨酸能改善急性胰腺炎大鼠胰腺和肺脏的组织损伤,并发挥抗炎症的作用。