Objective: To observe the clinical efficacy and mechanism of Kangyanling (KYL) in treating patients with systemic inflammatory reaction syndrome and multi-organ dysfunction syndrome (SIRS/MODS) after abdominal surgery. Methods: Eighty-two patients of SIRS/MODS after abdominal surgery were divided into two groups according to admission time, the KYL treated group (n=35) and the control group (n=47). The levels of serum C-reactive protein (CRP), plasma tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) were measured at the 1st, 3rd and 7th days post-operationally. Results: The levels of CRP, TNFα and IL-6 decreased gradually after surgical operation in both groups, but the reducing velocity was shorter in the KYL group than that in the control group, so the comparison of the levels in the two groups showed significant difference on the 3rd day after operation. Conclusion:KYL could inhibit the release of inflammatory mediator and relieve the inflammatory response so as to treat post-operational SIRS/MODS effectively.

肿瘤坏死因子-α及一氧化氮对暴发性肝衰竭肝损伤的作用

目的:研究肿瘤坏死因子-α(tumor necrosisfactor-α,TNF-α)及一氧化氮(nitric oxide,NO)在暴发性肝衰竭(fulminant hepatic failure,FHF)中对肝损伤的作用及相互关系.方法:采用脂多糖(LPS)和D-氨基半乳糖(D-GalN)构建FHF小鼠模型,采用ELtSA方法和RT-PCR法检测血清TNF-α水平及肝组织TNF-αmRNA表达,采用硝酸还原酶法和RT-PCR法检测血清NO水平及肝组织iNOSmRNA,在小鼠用药后不同时期动态观察TNF-α、NO及肝损伤的变化,并对模型鼠分别给予TNF-α单抗和NO合成酶抑制剂L-NMMA,动态观察上述指标的变化.结果:在FHF小鼠中,用药后2～4h肝组织TNF-αmRNA表达显著增加(0.91±0.75→0.82±0.08,P＜O.01),伴血清TNF-α水平升高,给予TNF-α单抗后可阻断LPSD-GalN介导的肝损伤,用药后4～8 h肝组织iNOSmRNA表达及血清NO水平亦显著升高(0.87±0.08→0.85±0.08,P＜0.01),给予L-NMMA后使肝损伤反而加重.FHF小鼠用药后8～12 h血清总胆红素(TBiL)和ALT明显异常,肝组织切片可见肝组织大块状出血和坏死.结论:在LPS/D-GalN所致的FHF中,TNF-α的产生与肝损伤成正相关,而NO在此模型中似有保肝和肝损伤的双重作用,TNF-α和NO在FHF模型鼠的肝损伤中起协同作用.

AIM To investigate the effect of recombinant human tumor necrosis factor (rbTNF) on telomerase activityin hepatoma cell line HepG2 and HepG1-6.METHODS TRAP-ELISA method was used to determine the telomerase activity in HepG2 and HepG1-6cells which were treated by different concentrations of rhTNF. In addition, the TERTLuc (800) plasmid wastransiently transfected, which was inserted 800 bp of the human telomerase reverse transcriptase (hTERT)promoter, into HepG2 cells by Lipofect. Different concentrations of rhTNF were added into the culturemedia 2 hours later, and the activity of the hTERT promoter was detected 48 hours after transfection.RESULTS The telomerase activity of HepG2 was suppressed by rhTNF in a dose-dependent manner. Theresults also revealed that the activity of hTERT promoter was inhibited linearly with rhTNF at the dose of 10- 1000 IU/mL.CONCLUSION Inhibition of the hTERT promoter expression by rhTNF may contribute to its anti-tumoractivity.

AIM To observe the effect of herbs-partition moxibustion on IL-1β and TNF-c in UC rats.METHODS The animal models were created by immunological method. They were divided into 5 groups atrandom, after treated by different methods, IL-1β and TNF-α in colon tissue of UC rats were detected withimmunologic technique.RESULTS In control group, there was a little or no IL-1β positive cell in colon mucosa. Compared withthat in rats of control group, the number of IL-1 positive cell in model group was much larger, and IL-1βcells with brown granules were mainly expressed in cytoplasm of macrophage in lamina propria of colon.Compared with model group, IL-1β positive cells in mild moxibustion group markedly decreased (P < 0.05),and those in electro-acupuncture group and herbs-partition moxibustion group decreased even more markedly(P < 0.01). The difference between the last two groups is evident (P < 0.05). TNF-α positive cells are not or seldomly found in UC rats, but in model group, these cells increasedevidently, which were mainly the macrophages in lamina propria of colon. Compared with those in modelgroup, the positive cells decreased markedly in electro-acupuncture group (P<0.05), and decreased moremarkedly in mild moxibustion group and in herbs-partition moxibustion group (P<0.01). There werestatistically significant differences between herbs-partition moxibustion group and electro-acupuncture group(P<0.05).CONCLUSION The mechanism of acupuncture and moxibustion may be that inhibited macrophageactivation, reduced expression of IL-1β and TNF-a and thereby blocking their further activation and thencontrolled, the initiated inflammation and its immunity cascade reaction and resulted in restoring the normalimmunity function and benefited in healing of ulcer.

危重感染患儿血清可溶性肿瘤坏死因子受体的变化

有研究发现,可溶性肿瘤坏死因子受体（soluble tumor necrosis factor receptors, STNFRs）在重症肺炎患儿中明显升高，且能反应疾病的严重程度。许多实验发现，细菌感染如化脓性脑膜炎、败血症、尿路感染等均有STNFRs升高，并且与感染严重程度及疾病预后相关［1-4］。STNFRs系肿瘤坏死因子膜受体的胞外段脱落形成，共有两类，为STNFRⅠ和STNFRⅡ。本实验通过观察STNFRs在儿科感染性疾病中的变化，以评价STNFRs在儿科危重感染中的应用价值。

不同病期儿童哮喘患儿峰流速值、血清ECP、TNFα测定观察

目的探讨不同病期儿童哮喘患儿峰流速值(PEF)、血清ECP和TNFα水平对疾病的影响.方法对急性发作组、治疗组及缓解组的哮喘息儿各30例和30例对照组,用瑞典Pharmacia CAP试剂盒检测血清ECP;以放射免疫分析法测定血清TNFα;峰流速仪测定PEF,并计算占预计值的百分比(PEF%).结果血清ECP在急性发作组明显高于其余3组(P＜0.01),血清TNFα在急性发作组高于缓解组、对照组(P＜0.01),治疗组高于缓解组及对照组(P＜0.05);PEF%在发作组明显低于其余3组(P＜0.01).结论血清ECP、TNFα均参与了哮喘发病,ECP较敏感,PEF测定更方便,可作为监测病情和指导治疗的有效指标.

Objective: hTe results of a previous study showed that a clear dysregulation was evident in the global gene expression of the BCL11A-suppressed B-lymphoma cells. In this study, the bone morphogenetic protein receptor, type II (BMPR2), E1A binding protein p300 (EP300), transforming growth factor-β2 (TGFβ2), and tumor necrosis factor, and alpha-induced protein 3 (TNFAIP3) gene expression patterns in B-cell malignancies were studied.
Methods:The relative expression levels ofBMPR2,EP300,TGFβ2, andTNFAIP3 mRNA in B-lymphoma cell lines, myeloid cell lines, as well as in cells from healthy volunteers, were determined by real-time quantitative reverse transcript-polymerase chain reaction (qRT-PCR) with SYBR Green Dye. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as reference.
Results:hTe expression level ofTGFβ2 mRNA in B-lymphoma cell lines was signiifcantly higher than those in the cells from the healthy control (P<0.05). However, the expression level ofTNFAIP3 mRNA in B-malignant cells was signiifcantly lower than that of the healthy control (P<0.05). hTe expression levels ofBMPR2 andEP300 mRNA showed no signiifcant difference between B-malignant cell lines and the healthy group (P>0.05). In B-lymphoma cell lines, correlation analyses revealed that the expression ofBMPR2 andTNFAIP3 (r=0.882,P=0.04) had signiifcant positive relation. hTe expression levels ofBMPR2,EP300, andTNFAIP3 mRNA in cell lines from myeloid leukemia were significantly lower than those in the cells from the healthy control (P<0.05). hTe expression levels ofTGFβ2 mRNA showed no signiifcant difference between myeloid leukemia cell lines and the healthy control or B-malignant cell lines (P>0.05). hTe expression levels of BMPR2,EP300, andTNFAIP3 mRNA in B-lymphoma cells were signiifcantly higher than those of the myeloid leukemia cells (P<0.05).
Conclusion:Different expression patterns ofBMPR2,EP300,TGFβ2, andTNFAIP3 genes in B-lymphoma cells exist.

神经根性疼痛与肿瘤坏死因子相关性研究

Objective To study the correlation between TNF and nerve root pain,and try to find out its significance.Methods 45 cases who had cervical syndrome,lumbar disc protrusion and lumbar spine stenosis were studied .TNF in blood serum was determined with subsequence saturation liquid phase competitive radio- immunity,and the results were further statistically processed. Results TNF value in 45 cases was higher than normal value(P<0.01). T- check- out was made between pain degree,we gained P<0.01. Conclusion There is notable correlation between TNF and nerve root pain,which is benifit to guide clinical diagnosis and treatment .

肉毒素和肿瘤坏死因子对大白鼠肝功能的影响

Objective To investigate the effect of endotoxin and tumor necrosis factor (TNF) on hepatic function of rats. Method Prepare hepatic cell suspension by filling male SD rats' livers with collagenaseⅠ ,culture in DMEM medium, and add endotoxin and TNF in it. After 24 hours detect GPT, GOT in supernatant fluid. Result The activity of GPT and GOT in supernatant fluid increased after adding endotoxin and TNF . Conclusion The system of hepatic cell membrane could be damaged severely after acted by endotoxin and TNF.

同化激素对S180实体瘤小鼠生存期及血浆TNF-α的影响

目的:探讨同化激素对荷瘤小鼠生存期的影响,以期为临床采用同化激素疗法增加蛋白质合成及增加体质量、改善癌性恶病质状态提供理论依据. 方法:建立 S180实体瘤小鼠模型,给予康力龙灌胃,用放免法测定血中肿瘤坏死因子( TNF-α)水平,观察小鼠生存期. 结果 :S180实体瘤小鼠康力龙实验组平均生存天数为( 28± 5) d,而对照组平均生存时间为 (24± 6) d,两组间比较无显著差异( t=1.814,P >0.05).正常小鼠组血浆 TNF-α水平为 (1.66± 0.20) μ g/L, 对照组为 (1.73± 0.26) μ g/L,实验组为 (1.73± 0.24) μ g/L,各组水平相似,统计学上无显著差异. 结论 :在本实验条件下,同化激素康力龙对 S180荷瘤小鼠生存期未见显著影响. TNF-α与 S180小鼠恶病质发生、发展关系不突出,同化激素也未见显著影响 S180小鼠循环中 TNF-α的水平.

Objective :To develop an agent that is more active against receptor-bearing target cells without increasing the toxic effect on non-target cells. Methods :By the use of molecular biology techniques,we designed and constructed a fusion protein 5＇IL6-TNF△ by connecting the human interleukin-6 (hIL-6) gene and a human tumor necrosis factor α derivative (TNF△) gene througha synthetic linker sequence followed by subsequent expression in E. Coli. Results: In cytotoxicity assay with myeloma cell line U266, the normal type of 5＇ IL6-TNF△ showed an antitumor activity 3 times higher than that of TNF△;and the antitumor activity of 5＇IL6-TNF△ blocked by IL-6Rwas only 1/30 of that of normal type of 5＇ IL6-TNF△. Meanwhile,the 5＇IL6-TNF△ blocked by an ti-TNF antibody did not show any cytotoxicity to U266 cells. In activity assay with L929 cells ,the toxic effect of the fusion protein was found 1/22 of that of TNF△. Conclusion: The 5＇IL6-TNF△fusion protein might be a useful cytotoxic agent in cancer treatment.

复方甘草酸苷对斑秃患者外周血单一核细胞中y干扰素、肿瘤坏死因子β表达的调节作用

目的 探讨甘草酸苷对斑秃患者外周血单一核细胞(PBMC)γ干扰素(IFN-γ)、肿瘤坏死因子β(TNF-β)表达的调节作用.方法 轻度斑秃患者18例、重症斑秃患者24例及正常人20例为检测对象,用密度梯度离心法常规分离PBMC,用逆转录-聚合酶链反应检测PBMC经植物血凝素和复方甘草酸苷共同刺激后IFN-γ和TNF-β的表达水平.结果 重症斑秃组患者IFN-γ及TNF-β水平均明显高于轻度斑秃组及正常人对照组(P值均＜ 0.05),轻度斑秃组高于正常人对照组(P值均＜0.05).甘草酸苷与植物血凝素共同刺激斑秃患者PBMC后可下调IFN--γ及TNF-β表达水平(P值均＜0.05).结论 甘草酸苷可抑制斑秃患者Th1型细胞因子表达,逆转Th1型反应.

兔脑出血灶周围脑组织bFGF,VEGF及TNF-α的表达

Intracerebral hemorrhage frequently occurs in nervous system diseases, and le ads to secondary cerebral lesion, such as ischemia, edema of perihematomal brain r egions and the biochemical change of the cell. Recent studies have confirmed tha t cytokines such as basic fibroblast growth factor(bFGF), vascular endothelial g r owth factor(VEGF) and tumor necrosis factor(TNF-α) are involved in the pathoge n esis of cerebral hemorrhage. In nervous system, positive expressions of bFGF and TNF-α are in neurons and astrocytes, and that of VEGF is in vascula r endothelial cells. The content of bFGF protein in brain regions is different a t different time after brain injuries. There was no literature about detectin g the expressions of bFGF, VEGF and TNF-α protein in the perihematomal brain r egion s after intracerebral hemorrhage. Using immunohistochemical technique,the author detected the expressions of bFGF,VEGF and TNF-α in the perihematomal brain re g ions in order to research the pathological mechanism of intracerebral hemorrhage.

花生四烯酸代谢物与肝损伤

花生四烯酸(arachidonic acid,AA)代谢物为一类20碳不饱和脂肪酸,主要包括前列腺素(prostaglandins,PGs)、血栓素(thromboxanes,TXs)和白三烯(leukotrienes,LTs)等3大类.近年来研究表明,花生四烯酸代谢物作为脂类介质在调节肝脏生理和病理生理过程中起着重要作用;肝脏不仅是花生四烯酸代谢物产生的重要部位,也是它们的靶器官以及代谢失活的主要场所;根据花生四烯酸代谢物在血液、尿和胆汁中的变化,以及选择干扰它们合成和作用的药物的大量资料,可以肯定肝损伤与这类物质有关[1,2].

AIM:Increasing evidence indicates that inflammation contributes to the initiation and perpetuation of atrial fibrillation ( AF) .Al-though tumor necrosis factor ( TNF)-αlevels are increased in patients with AF , the role of TNF-αin the pathogenesis of AF remains unclear.Recent research has revealed that T-type Ca2+currents ( ICa,T ) play an important role in the pathogenesis of AF .METH-ODS:In this study , we used the whole-cell voltage-clamp technique and biochemical assays to explore the role of TNF-αin the regula-tion of ICa,T in atrial myocytes.RESULTS:We found that compared with sinus rhythm (SR) controls, T-type calcium channel (TCC) subunit mRNA levels were decreased , while TNF-αexpression levels were increased , in human atrial tissue from patients with AF .In murine atrial myocyte HL-1 cells, after cultured for 24 h, 12.5, 25 and 50 μg/L TNF-αsignificantly reduced the protein expression levels of the TCC α1G subunit in a concentration-dependent manner .The peak current was reduced by the application of 12.5 or 25μg/L TNF-αin a concentration-dependent manner [from ( -15.08 ±1.11) pA/pF in controls to ( -11.89 ±0.83) pA/pF and (-8.54 ±1.55) pA/pF in 12.5 and 25 μg/L TNF-αgroups, respectively].TNF-αapplication also inhibited voltage-dependent inactivation of ICa,T shifted the inactivation curve to the left .CONCLUSION:These results suggest that TNF-αis involved in the path-ogenesis of AF, probably via decreasing ICa,T function in atrium-derived myocytes through impaired channel function and down -regula-tion of channel protein expression .This pathway thus represents a potential pathogenic mechanism in AF .

X线照射肝癌细胞株HepG2对可溶性肿瘤坏死因子受体-p55的影响

目前,肝癌的治疗已由单一手术变成放、化疗和手术治疗相结合的综合治疗.光子刀是一种能提高肿瘤组织对放射治疗敏感性,同时减轻周围正常组织损伤的先进的射线设备.为进一步了解照射对肿瘤细胞产生的生物学效应,本研究应用一定剂量X线照射肝癌细胞株HepG2,分析其可溶性肿瘤坏死因子受体-p55(soluble tumor necrosis factor receptor-p55,sSTNFR-p55)变化情况,以期为临床治疗提供可靠依据.

肿瘤坏死因子基因多态性与动脉血栓性疾病关系的研究进展

肿瘤坏死因子(tumor necrosis factor,TNF)是一类具有多种生物学活性的前炎性细胞因子.它不仅有抗肿瘤、抗病毒与免疫调节的作用,而且可以直接或间接损伤血管内皮细胞,产生促炎症、促凝血、抗纤溶反应,从而在血栓形成、动脉粥样硬化、DIC等许多疾病发病机制中起重要作用.近年来,通过对血栓患者重要炎性介质进行基因型分析,发现TNF基因多态性可能与血栓性疾病的的易感性有关.

乳腺癌患者血清过氧化物酶及肿瘤坏死因子测定的临床意义

重组改构人肿瘤坏死因子联合化疗治疗晚期非小细胞肺癌三例报告

重组改构人肿瘤坏死因子(recombinant mutant human tumor necrosis factor,rmhTNF)是利用蛋白质工程技术改造天然TNF而成的高活性、低毒性的基因工程TNF.多中心随机对照Ⅲ期临床试验已经证实rmhTNF联合化疗治疗肺癌等实体瘤有一定疗效[1].我们在2004年2月至4月间采用rmhTNF联合化疗治疗3例难治进展的晚期非小细胞肺癌(NSCLC),现将结果报道如下.

CMV-hFasL转基因小鼠容易被小剂量的链尿菌素诱导至糖尿病

AIM: To investigate the role of Fas-FasL pathway in the pathogenesis of streptozotocin (STZ)-induced type I diabetes mellitus. METHODS: Low dose injections of STZ were used to induce type I diabetes mellitus in the CMV-hFasL transgenic mice. Blood glucose concentration was measured with Glucotrand Plus blood glucose test strips. Expression of hFasL was detected by RT-PCR and Western blotting. The severity of insulitis was determined by histologicalexamination. Expressions of IL- 1 β and TNF-α mRNA in the pancreas were detected by semi-quantitative RT-PCR analysis. Fas expression in apoptotic RIN-5F cells was also confirmed by RT-PCR in vitro. RESULTS: hFasL was expressed in the islets of CMV-hFasL transgenic mice. The transgenic mice were sensitive to diabetic induction than the control WT mice. IL-1 β and TNF-α expressions in the pancreas of CMV-hFasL transgenic mice were far more than that in WT mice. We also found STZ and IL-1β could both induce higher expression of Fas in RIN-5F. The combining of Fas-FasL could lead to the apoptosis of β cells in the CMV-hFasL transgenic mice. CONCLUSION: Fas-FasL interaction plays a significant role in the pathogenic mechanism of type I diabetes mellitus.