Changes of Tumor Necrosis Factor, Surfactant Protein A, and Phospholipids in Bronchoalveolar Lavage Fluid in the Development and Progression of Coal Workers＇ Pneumoconiosis

Objective To evaluate the alterations of biomarkers in the development and progression of coal workers＇ pneumoconiosis （CWP）. Methods The type and number of cells, and the levels of tumor necrosis factor-alpha （TNF-α）, pulmonary surfactant protein, phospholipids and fibronectin in bronchoalveolar lavage fluid were assayed in 14 health active coal miners, 21 coal miners without CWP and 13 miners with CWP of 0/1 to 1/1. Results Compared to active coal miners without CWP （8,23μg/mL）, TNF-α concentration was gradually decreased when dust exposure was stopped （5.90 μg/mL）. Elevated surfactant protein A （SP-A） level and phosphatidylglycerol （PG） to phosphatidylinositol （PI） ratio were found in miners actively exposed to coal dust （6528 μg/mL for SP-A and 10. for PG/P1）, and both parameters decreased when CWP progressed from CWP （0/1） （3419μg/mL for SP-A and 5.9 for PG/PI） to CWP （1/1） （1654 μg/mL for SP-A and 5.5 for PG/PI）. Conclusion Biomarkers in bronchoalveolar lavage fluid can be used to screen coal miners at high risk of developing coal workers＇ pneumoconiosis.     

Effect of Mifepristone on Transforming Growth Factor-β and its Receptor Transcription in Decidua, Villi and Serum Tumor Necrosis Factor -α Level in Early Human Gestation

Mifepristone is a progesterone antagonist which acts at the level of the receptor. Itbinds the progesterone receptor with a high affinity and antagonises progesterone biologicalaction. It has been applied in clinical use for multiple therapeutic purposes. In obstetrics andgynecology, mifepristone has been effective in medical termination of pregnancy in the firsttrimester. Mifepristone followed approximately 48 h later by a prostaglandin analog hasbeen reported to effect complete abortion in 9…     

Changes of Tumor Necrosis Factor-α and the Effects of Ulinastatin Injection during Cardiopulmonary Cerebral Resuscitation

The changes of tumor necrosis factor-a (TNF-a) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into.control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate,30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-a were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated, The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-a among different time points (P＞0.05). In resuscitation group, the level of TNF-a was increased obviously after resuscitation (P＜0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-a showed in UTI group. There were no differences in TNF-a among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-a was expressed rapidly and kept increasing. It indicated that TNF-a might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-a and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.     

Tumor necrosis factor（TNF） superfamily ligands and rrceptors

1　TNF ligand and receptor superfamily membersTumor Necrosis Factor (TNF) supergene family and its cognate family of rel ated r eceptors (TNF-R) have expanded in the past few years to include at least 17 lig ands and 22 receptors (The New TNF Nomenclature Scheme, http://www.gene.ucl.ac.uk/users/nomenclature/genefamily/tnfinfo.html)[1]. With the exception of LTα,whichlacks a hydro phobic transmembrane region, allof the ligands are type Ⅱintegral membrane pro teins that may also function as soluble proteins. Many of the TNF superfamily ligands pair with a single, although some specific receptor, including TNFα, LT α, TRAIL, FasL, LIGHT and TRANCE/RANKL, bind to multiple receptors (Tab 1).     

Effect of Tumor Necrosis Factor-α Antagonism in Asthma： a Meta-analysis of the Published Literature

It remains controversial whether tumor necrosis factor(TNF)-α antagonism is effective for asthma.This meta-analysis was performed to evaluate efficacy of TNF-α antagonism in treatment of patients with asthma.MEDLINE,EMBASE,LILACS,and CINAHL databases were searched for English-language studies published through January 3,2010.Randomized-controlled trials comparing TNF-α antagonism with control therapy were selected.For each report,data were extracted in relation to the outcomes analyzed:asthma exacerbation,asthma quality of life questionnaire scores,and forced expiratory volume in 1 second.Four assessable trials were identified including 641 patients with asthma.TNF-α antagonism therapy was superior to control therapy in preventing exacerbations in asthmatics [pooled odds ratio 0.52(95% confidence interval 0.29-0.88),P=0.02];however,there was a nonsignificant reduction in asthma quality of life questionnaire scores [0.23(0 to 0.47),P=0.05],forced expiratory volume in 1 second [0.03,(-0.14 to 0.10),P=0.74] when analyzed using standardized mean differences.TNF-α antagonism was superior to control chemotherapy in terms of asthma exacerbation,but not asthma quality of life questionnaire scores or forced expiratory volume in 1 second.     

Effects of Yixin Jiangya Capsules on Insulin Resistance and Tumor Necrosis Factor-a in Cases of Primary Hypertension with Left Ventricular Hypertrophy

To observe the effects of Ftxin Jiangya Capsules （益心降压胶囊capsules for nourishing the heart and lowering blood pressure） on insulin resistance （IR） and tumor necrosis factor-a （TNF-a） in patients with primary hypertension with left ventricular hypertrophy （LVH）. Methods： Totally 93 cases were randomly divided into a control group of 31 cases taking Enalapril and a treatment group of 62 cases taking Enalapril and Irtxin Jiangya Capsules. Results： Fasting serum insulin （FSI） and TNF-a obviously increased and insulin sensitive index （ISI） significantly decreased in both groups before treatment as compared to those of a healthy group. After treatment, FSI, TNF-a and fasting blood glucose （FBG） obviously decreased and ISI remarkably increased in the treatment group, while ISI significantly increased and TNF-a obviously decreased in the control group. The curative effect in the treatment group was remarkably superior to that in the control group. FSI was positively related to TNF-a before treatment in both groups. Conclusion： FSI and TNF-a obviously increase and ISI significantly decreases in patients with primary hypertension with LVH. FSI and TNF-a influencing each other are involved in the generation and development of hypertension. Irtxin Jiangya Capsules can improve IR and decrease TNF-a.     

Tumor Necrosis Factor-related Apoptosis Ligand Induces Apoptosis in Prostate Cancer PC-3M Cell Line

Summary： To study the effect of tumor necrosis factor-related apoptosis inducing ligand （TRAIL） on PC-3M cell line, PC-3M cell line was incubated with gradient concentrations of TRAIL for 4-24 h. Annixin-V fluorescence staining and TUNEL method were employed to detect the apoptosis of PC-3M cells. The morphology of apoptotic PC-3M cells was observed by electron microscopy. The relationship between TRAIL concentrations and the percentage of apoptotic cells was evaluated by flow cytometry. The proliferation inhibitory ratio was calculated by using MTT colorimetry. Our results showed that apoptosis of PC-3M cells could be induced by treatment with TRAIL for at most 4 h. The results of flow cytometry and MTT colorimetry demonstrated a time-and concentration-dependent relationship between cell apoptosis rate and TRAIL concentration. It is concluded that apoptosis of PC-3M cells can be induced by TRAIL. Because of the selective killing effect of TRAIL on tumor cells, it may become a potential alternative for the treatment of advanced prostate cancer.     

Tumor Necrosis Factor α, Interleukin-6, Interluikin-8,and Interferon α in Children with Viral Hepatitis

To investigate the cellular immunological changes in children with viral hepatitis, interleukin 6 (IL-6), interleukin 8 (IL-8), interferon a (IFN_a), and tumor necrosis factor a (TNF_a) in supernatant of cultured peripheral blood mononuclear cells (PBMCs) of 49 children with hepatitis A, B or C were measured. The levels of IL-6, IL-8, TNF_a in PBMCs of the 3 viral hepatitis groups were increased and the level of IFN_a decreased as compared with those of normal control group. But there were no significant differences among the 3 viral hepatitis groups. It was concluded that cellular immunological disorders were related to the onset and the induced damage of the viral hepatitis in children.     

Experimental Study on Inhibitory Effect of Niacinamide on Tumor Necrosis Factor-alpha-induced Matrix Degradation of Annulus Fibrous Tissue in vitro

The inhibitory effect of niacinamide on tumor necrosis factor-α （TNF-α） induced annulus fibrous （AF） degradation was assessed, and the mechanism of the inhibition was investigated. Chiba＇s intervertebral disc （IVD） culture model was established. Forty-eight IVDs from 12 adult Japanese white rabbits were randomly divided into 4 groups （12 IVDs in each group）, and various concentrations of niacinamide and TNF-α were added to the medium for intervention： negative control group, niacinamide control group （0.5 mg/mL niacinamide）, degeneration group （10 ng/mL TNF-α）, and treatment group （0.5 mg/mL niacinamide and 10 ng/mL TNF-α）. After one week＇s culture, AFs were collected for glycosaminoglycan （GS） content measurement, safranin O-fast green staining, and immunohistochemical staining for type Ⅰ , Ⅱ collagen and cysteine containing aspartate specific prote- ase-3 （Caspase-3）. It was found that the GS content in treatment group was increased by about 48% as compared with degeneration group （t=16.93, P〈0.001）, and close to that in niacinamide control group （t=0.71, P=0.667）. Safranine O-fast green staining exhibited higher staining density and better histological structure of AF in the treatment group as compared with the degeneration group. Immunohistochemical staining for both TypeⅠ and Ⅱ collagen demonstrated that lamellar structure and continuity of collagen in treatment group were better reserved than in degeneration group. Positive staining rate of Caspase-3 in AFs of negative control group, niacinamide control group, degeneration group and treatment group was 3.4%, 4.3%, 17.9% and 10.3% respectively. The positive rate in treatment group was significantly lower than in degeneration group （P〈0.01）. It was concluded that niacinamide could effectively alleviate TNF-α induced destruction and synthesis inhibition of matrix ingredients in AFs. The inhibition may be related with reduction of expression of Caspase-3. Thus, niacinamide is of potential f     

Morphological Study on the Mechanism of Tumor-selective Cytocidal Action of Tumor Necrosis Factor

Using light microscopy and electron microscopy, we observed the morphological changes inheuman hepatocellular carcinoma cell line (SMMC-7721) treated with tumor necrosis tumor necrosis factor (TNF)and the cytocidal effect of TNF on the heterotransplanted human hepatocellular carcinoma. It wasfound that the changes of the injury occurred earlier in the cell membranes than in the nuclei duringthe course of TNF killing of SMMC-7721 cells and there were similar lesions around the necroticarea in the heterotransplanted human hepatocellular carcinoma in the nude mice as compared withthose produced in SMMC-7721 cells. In addition, the determination of the DNA content in TNF-treated SMMC-7721 cells and controls revealed no significant difference between them. On the basisof these results and Darzynkiewicz's proposals, it is suggested that TNF exerts its tumor-selectivekilling effect by binding to a specific to a specific plasma membrane receptor to disturb synthesis or assembly ofcell membrane components, thus causing the plasma membrane injury and finally cell lysis.     

Effect of Wenhua Juanbi Recipe (温化蠲痹方) on Expression of Receptor Activator of Nuclear Factor Kappa B Ligand, Osteoprotegerin, and Tumor Necrosis Factor Receptor Superfamily Member 14 in Rats with Collagen-Induced Arthritis

Objective: To study the effect of Wenhua Juanbi Recipe(温化蠲痹方, WJR) on expression of receptor activator of nuclear factor kappa B ligand(RANKL), osteoprotegerin(OPG), and tumor necrosis factor receptor superfamily member 14(TNFRSF14, also known as LIGHT) in rats with collagen-induced arthritis(CIA). Methods: CIA rats were generated by subcutaneous injection of bovine collagen type-Ⅱ at the tail base. Sixty CIA rats were randomly assigned(10 animals/group) to: model, methotrexate(MTX)-treated(0.78 mg/kg body weight), and WJR-treated(22.9 g/kg) groups. Healthy normal rats(n=10) were used as the normal control. Treatments or saline were administered once daily by oral gavage. Rats were sacrificed at day 28 post-treatment and knee synovium and peripheral blood serum were collected. Toe swelling degree and expression of RANKL, OPG, and LIGHT were determined by Western blot and immunohistochemistry. Results: Compared with the normal group, toe swelling degree was significantly increased in the model group(P0.01). After treatment, toe swelling degree decreased significantly in the WJR and MTX groups compared with the model group(P0.01). Compared with the normal group, expression of RANKL and LIGHT were significantly increased and OPG significantly decreased in peripheral blood and synovium of the model group(P0.01). Conversely, RANKL and LIGHT expression were significantly reduced and OPG increased in the WJR and MTX groups compared with the model group(P0.01). No statistically significant difference existed between WJR and MTX groups. Conclusion: WJR likely acts by reducing RANKL expression and increasing OPG expression, thus inhibiting RANKL/RANK interaction and reducing LIGHT expression, thereby inhibiting osteoclast formation/activation to block bone erosion.     

Effect of Xuezhikang Capsule(血脂康胶囊)on Serum Tumor Necrosis Factor-αand Interleukin-6 in Patients with Nonalcoholic Fatty Liver Disease and Hyperlipidemia

<正>Objective:To evaluate the effect of Xuezhikang Capsule(血脂康胶囊) on the serum levels of inflammatory factors such as tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in patients with nonalcoholic fatty liver disease(NAFLD) and hyperlipidemia,and to explore whether it has anti-inflammatory effect.Methods:A total of 84 patients were randomly assigned to two groups with stratified block randomization, the treatment group(42 cases) and the control group(42 cases).They were treated with Xuezhikang Capsule and polyene phosphatidylcholine capsule for twenty-four weeks,respectively.The changes in serum TNF-αand IL-6 were measured by enzyme linked immunosorbent assay before treatment and at the 12th and 24th week. Results:Compared with those before treatment,the serum levels of TNF-αand IL-6 significantly decreased in both groups after treatment(P0.01).There was no significant change between the two groups for the treatments at different time points(P0.05) and between the two groups for treatments at the same time points (P0.05).Conclusion:Xuezhikang Capsule can inhibit the serum inflammatory factor in patients with NAFLD and hyperlipidemia.     

烧伤患者血清IL—6,IL—8,TNF—α测定及其临床意义

目的 探讨细胞因子白介素－６（ＩＬ－６）,白介素－８（ＩＬ－８）,肿瘤坏死因子－α（ＴＮＦ－α）与烧伤的关系。方法 应用ＥＬＩＳＡ法检测４２例烧伤患者及２０例正常人血清ＩＬ－６,ＩＬ－８,ＴＮＦ－α水平。结果 入院时患者的血清ＩＬ－６,ＩＬ－８,ＴＮＦ－α明显高于正常对照组,烧伤后第３天与入院时比较,ＩＬ－６无明显变化（Ｐ〉０．０５）,ＴＮＦ－α增高（Ｐ〈０．０１）,而ＩＬ－８在烧伤面积≤３０％者     

肿瘤坏死因子相关凋亡诱导配体的克隆,表达及重新折叠

目的：人的肿瘤坏死因子相关凋亡诱导配体（ＴＮＦ－ｒｅｌａｔｅｄ ａｐｏｐｔｏｓｉｓ ｉｎｄｕｃｉｎｇ ｌｉｇａｎｄ,ＴＲＡＩＬ）基因经扩增后,克隆在大肠杆菌中表达并重新折叠并获得有活性的ＴＲＡＩＬ蛋白。方法：用ＰＣＲ的方法从人胎盘ｃＤＮＡ库中扩增ＴＲＡＩＬ基因,经序列分析鉴定,再克隆到原核表达载体ｐＥＴ１１ａ,经Ｅ．ｃｏｌｉ ＢＬ２１（ＤＥ３）表达,电泳鉴定后,柱层析纯化,重新折叠,流式细胞术等     

肿瘤坏死因子（TNF）对流行性出血热,甲型肝炎病毒的作用研究

流行性出血热和甲型肝炎严重危害人民健康。目前对流行性出血热病毒和甲肝病毒还暂无特效药物,近年报道肿瘤坏死因子具有抗病毒活性,本文报告用在国内分离、克隆并表达的人重组肿瘤坏死因子(rhTNF-2)在体外对流行性出血热病毒及甲型肝炎病毒的抗感染作用进行了研究,现将结果报告如下。材料与方法     

鼻咽癌组织中VEGF,TNF-α及其受体蛋白表达及相关性研究

目的：观察探讨VEGF,TNF-α及受体蛋白VEG-FR1,VEGFR2,P55,P75在鼻咽癌组织的表达情况及VEGF,TNF-α与其受体表达的相关关系.方法：采用组化免疫方法,对60例鼻咽癌组织标本进行染色,观察VEGF,TNF-α与其受体VEGFR1,VEGFR2,P55,P75阳性率及表达强度,并对VEGF,TNF-α与其受体VEGFR1,VEGFR2,P55,P75表达进行相关性分析.结果：鼻咽癌组织中VEGF,TNF-α及受体蛋白VEGFR1,VEGFR2,P55,P75鼻咽癌组织中过度表达,VEGF同VEGFR1表达呈正相关（r=0.440,P=0.010）、同VEGFR1表达呈正相关（r=0.440,P=0.010）,TNF-α同P55表达呈正相关（r=0.442,P=0.002）.结论：VEGF,TNF-α及受体蛋白VEGFR1,VEGFR2,P55,P75在鼻咽癌组织中过度表达,其可能通过VEGF、TNF-α与受体的相互调控在肿瘤的发展中发挥作用.