Increase of tumor necrosis factor receptor 1 expression in women with unexplained early spontaneous abortion

Objective: To investigate membrane tumor necrosis factor receptor 1 protein expression level in decidua and concentration of soluble tumor necrosis factor receptor 1 in serum in women with unexplained early spontaneous abortion, threatened abortion, and compare the levels with healthy pregnant women. Methods: Thirty-seven women with unexplained early spontaneous abortion, 27 women with threatened abortion, and 34 healthy pregnant women undergoing artificial abortion of pregnancy at 6 - 10 weeks of gestation were selected. Decidual samples were collected when women were undergoing artificial abortion, and blood samples were collected at the same time. The level of membrane tumor necrosis factor receptor 1 in decidua was detected by flow cytometer, and the concentration of soluble tumor necrosis factor receptor 1 in sera was measured with an enzyme-linked immunosorbent assay. Results: The percentages of membrane tumor necrosis factor receptor 1 positive decidual cells were 16.42 ± 7.10 Mean ± SD for wome     

Knockout of the tumor necrosis factor α receptor 1 gene can up-regulate erythropoietin receptor during myocardial ischemia-reperfusion injury in mice

Background Tumor necrosis factor a receptor 1 （TNFaR1） plays an important role in the signal pathway of apoptosis. The objective of this study was to investigate the effects of TNFaR1 knockout on the up-regulation of erythropoietin receptor （Epo-R） and the coordinated anti-apoptosis functions during myocardial ischemia-reperfusion injury in mice. Methods The ischemia-reperfusion injury model for cardiomyocytes was performed by ligating the left circumflex branch artery of TNFaR1 knockout （P55/） C17 B6 mice, as well as wild-type （P55^＋/^＋） C17 B6 mice. Triphenyltetrazolium chloride （TTC） staining was performed to observe the damaged area of the heart. TUNEL staining and DNA fragmentation were used to identify apoptosis. Mitochondrial Bcl-2 and Bax as well as expression of Epo-R and its downstream genes （Jak-2, stat-5, Akt, lkB-a, HIF-1a） were measured by Western blotting. The gene knockout mice were assigned into those undergoing the apoptosis surgical model group （KO group）, and those subjected to sham operation （KOs group）. Similarly, wild-type mice were either exposed to the surgical model （WT group） or subject to a sham operation （WTs group）. Results The myocardial damage ratio of the wild-type group after the operation was significantly higher than that of the knockout group, （50.5±6.4）% vs （36.9±6.9）%, P 〈0.01. Similarly, TUNEL positive ratio of the wild-type group was significantly higher than that of the knockout group, （63.1±5.6）% vs （42.1±4.7）%, P〈0.01. The gray value ratios of Epo-R, Jak-2, stat-5, Akt, IkB-a, HIF-1 and mitochondrial Bcl-2 in the KO group were significantly higher than those of the WT group, P 〈0.05; however, mitochondrial Bax was significantly lower than that of the WT group significantly （P 〈0.05）. Conclusions Using the ischemia-reperfusion injury model in mice, cardiomyocytes of TNFaR1 knockouts exhibited anti-apoptotic characteristics. This information could be used to coordinate the prevention of myocardial apoptosis by up-regulating and activating the Epo-R pathway.     

Effects of Novel recombination human tumor necrosis factor on tumor cell growth and NF-KB activity

Objective: To investigate the relationship among the TNFRp55 and TNFRp75 expression in tumor cell lines in vitro, the suppression of nrhTNF on the tumor cell lines growth and the changing of NF-kB activity in the tumor cell lines. Methods:The expressions of TNFRs are studied by immunohistochemistry. The inhibition of nrhTNF to tumor cells was investigate by crystal violet assay. The changing of activity of NF-icB was evaluated by using immunohistochemistry and Western blot methods. Results: In tumor cell lines, positive rates of expression of TNFRp55 and TNFRp75 were 99% and 98. 8% respectively. There was no significant difference among various types of tumor cells (P>0. 05). nrhTNF could inhibit the growth of SW480, SGC7901, 8910, SMMC7721 and BEL-7402 cell lines in which NF-icB translocated into cytonuclei slightly. However, nrhTNF has no effects on A549, PLA801, Hela, Ecal09 and GRC-1 cell lines in which NF-kB translocated into cytonuclei obviously. Conclusion: The low degree of activating of NF-kB m     

Correlation research between child pneumonia and nitric oxide and tumor necrosis factor

ＯｂｊｅｃｔｉｖｅＴｏｃｌａｒｉｆｙｔｈｅａｃｔｉｏｎｌｉｎｋｏｆｌｕｎｇｔｉｓｕｅｄａｍａｇｅｃａｕｓｅｄｂｙｎｉｔｒｉｃｏｘｉｄｅ（ＮＯ），ｗｅｄｙｎａｍｉｃａｌｙｏｂｓｅｒｖｅｄｔｈｅｃｈａｎｇｅｓｏｆｓｅｒｕｍＮＯａｎｄｔｕｍｏｒｎｅｃｒｏｓ...     

The relationship between gut-derived endotoxemia and tumor necrosis factor, neopterin: experimental and clinical studies.

Ｔｈｅｒｅｌａｔｉｏｎｓｈｉｐｂｅｔｗｅｎｇｕｔｄｅｒｉｖｅｄｅｎｄｏｔｏｘｅｍｉａａｎｄｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒ，ｎｅｏｐｔｅｒｉｎ：ｅｘｐｅｒｉｍｅｎｔａｌａｎｄｃｌｉｎｉｃａｌｓｔｕｄｉｅｓＳｈｅｎｇＺｈｉｙｏｎｇ盛志勇，Ｙａｏ...     

Inhibitory effect of matrine on tumor necrosis factor production and protein kinase C activity

ＩｎｈｉｂｉｔｏｒｙｅｆｆｅｃｔｏｆｍａｔｒｉｎｅｏｎｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒｐｒｏｄｕｃｔｉｏｎａｎｄｐｒｏｔｅｉｎｋｉｎａｓｅＣａｃｔｉｖｉｔｙＺｈａｎｇＪｕｎｐｉｎｇ（张俊平）；ＨｕＺｈｅｎｌｉｎ（胡振林）；ＬｉｎＷｅｎ（林文）；...     

Correlation between tumor necrosis factor a gene promoter polymorphisms and acute rejection following renal transplantation

Objective To study the significance of cytokine tumor necrosis factor α ( TNF -α) gene promoter 308 position polymorphisms in predicting acute graft rejection following renal transplantation. Methods In 35 preoperative recipients, TNF-α produced by peripheral blood cells was measured by enzyme-linked immmunosorbent assay, and their TNF- α gene promoter 308 position polymorphisms were determined by FOR restriction fragment length polymorphisms(PCR-RFLP). The assocication between TNF-α gene promoter polymorphisms and production of them was studied. Furthermore, the correlation between their polymorphisms and acute rejection in the first 3 months after renal transplantation was discussed. Results The recipients with A/A or A/G genotype in TNF-α promoter 308 position secreted more cytokine (624.96 ± 177.78) pg/ml and (544.32 ± 13.242)pg/ml than those with G/G(233.16 ± 25.37)pg/ml,P<0.01. When HLA-DR was mismatched, the recipients with high production of TNF - α genotype showed higher incidence rat     

Effects of removing circulatory tumor necrosis factor by immunoadsorption on experimental endotoxin shock animals.

ＥｆｅｃｔｓｏｆｒｅｍｏｖｉｎｇｃｉｒｃｕｌａｔｏｒｙｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒｂｙｉｍｍｕｎｏａｄｓｏｒｐｔｉｏｎｏｎｅｘｐｅｒｉｍｅｎｔａｌｅｎｄｏｔｏｘｉｎｓｈｏｃｋａｎｉｍａｌｓＺｈａｎｇＸｕｎ张训，ＨｏｕＦａｎｆａｎ侯凡凡，Ｌｉ...     

The effects of tumor necrosis factor on cultured hepatocytes and non-parenchymal liver ceils in the mouse

The effects of tumor necrosis factor(TNF)on the cultured mouse hepa-tocytes and non-parenchymal liver cells were observed.It was found that therewere no significant changes of the morphological integrity and viability of thehepatocytes and the aspartate transferase level in the culture supernate after theaddition of TNF into the culture medium as compared with those of the normalcontrol,which indicates that TNF exerts no obvious cytotoxocity on the culturedmouse hepatocytes. In addition,there were also no significant changes of theabove mentioned parameters after TNF was added to the cocultures of hepato-cytes and non-parenchymal liver cells,which implies that the unactivated non-parenchymal liver cells are not involved in the TNF-related hepatocyte injury.     

Construction of murine interleukin－3 and murine tumor necrosis factor－α hepatoma－specific retroviral vectors and specific exp

Ｃｏｎｓｔｒｕｃｔｉｏｎｏｆｍｕｒｉｎｅｉｎｔｅｒｌｅｕｋｉｎ－３ａｎｄｍｕｒｉｎｅｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒ－αｈｅｐａｔｏｍａ－ｓｐｅｃｉｆｉｃｒｅｔｒｏｖｉｒａｌｖｅｃｔｏｒｓａｎｄｓｐｅｃｉｆｉｃｅｘｐｒｅｓｓｉｏｎｉｎｔｈｅｈｅ...     

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).     

Tumor necrosis factor (TNF) superfamily ligands and receptors

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).     

The influence of Paeoniflorin and recombinant human type Ⅱ tumor necrosis factor receptor-antibody fusion protein on human synovial cells and part mechanism

目的 观察重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rhTNFR:Fc)与芍药苷(Pae)联合应用对人成纤维样滑膜细胞(FLS)增殖的影响,探讨其对肿瘤坏死因子受体(TNFR)信号通路的调节作用.方法 经知情同意,收集行髋关节置换术患者正常滑膜组织,采用组织块培养法对人滑膜细胞进行培养.取第3代人FLS,用肿瘤坏死因子α(TNF-α,20 μg/L)刺激,分别用rhTNFR:Fc(10 mg/L)、Pae(10-5 mol/L)及二者联合干预.MTT法检测人FLS的增殖反应,免疫组化法半定量分析肿瘤坏死因子受体1(TNFR1)、肿瘤坏死因子受体相关因子2(TRAF2)、肿瘤坏死因子受体相关死亡结构蛋白(TRADD)在FLS中的表达情况.结果 rhTNFR:Fc与Pae联合用药对FLS增殖的抑制作用优于rhTNFR:Fc和Pae单独给药组.rhTNFR:Fc、Pae及联合用药均能明显下调FLS 中TNFR1和TRAF2表达,上调TRADD表达;与单独用药相比,联合用药能进一步上调TRADD表达,而对TNFR1和TRAF2的表达无明显影响.结论 rhTNFR:Fc和Pae联合用药对人FLS增殖的抑制作用优于单独给药,其作用机制可能与调节TRADD有关.     

Variations of tumor necrosis factor-α, leptin and adiponectin in mid-trimester of gestational diabetes mellitus

Background Many cytokines have been found to increase the insulin resistance during pregnancy complicated by glucose metabolism disorder. This study aimed to investigate which comes first, the changes of some cytokines or the abnormal glucose metabolism.
Methods This nested case-control study was undertaken from January 2004 to March 2005. Twenty-two women with gestational diabetes mellitus （GDM）, 10 with gestational impaired glucose tolerance （GIGT）, and 20 healthy pregnant women were chosen from the women who had visited the antenatal clinics and had blood samples prospectively taken and kept during their visit. The levels of tumor necrosis factor-α （TNF-α）, leptin and adiponectin were determined. One-way ANOVA analysis and bivariate correlation analysis were used to assess the laboratory results and their relationship with body mass index （BMI）. Results Women with GDM have the highest values of TNF-α and leptin and the lowest value of adiponectin compared with those with GIGT and the healthy controls （P 〈0.01） at 14-20 weeks of gestation. This was also found when these women progressed to 24-32 weeks. The significantly increased levels of TNF-α and leptin and the decreased level of adiponectin were found at the different periods of gestation within the same group. Positive correlation was shown between the levels of TNF-α and leptin at the two periods of gestation with the BMI at 14-20 weeks, while adiponectin was negatively correlated （P 〈0.05）.
Conclusions The concentrations of TNF-α, leptin and adiponectin may change before the appearance of the abnormal glucose level during pregnancy. Further studies are required to verify the mechanism of this alteration and whether the three cytokines can be predictors for GDM at an early staqe of preqnancy.     

Serum tumor necrosis factor (TNF) in the pathogenesis of clinical hepatic failure of HCV and/or HBV infection.

Serum TNF and IL-6 levels were measured in 48 patients with liver disease positive for anti-HCV only or concurrent HBV infection. High serum TNF levels were observed in patients with liver disease positive for anti-HCV and/or HBV infection (P < 0.001). Serum TNF levels varied with the severity of liver disease. Serum TNF levels of anti-HCV positive patients with hepatic failure were higher than those with CAH (P < 0.01). Serum TNF levels of patients infected with HCV or concurrent HBV were also significantly higher than those with HBV infection alone (P < 0.001). However, no difference in serum IL-6 levels was observed in either group of patients. Serum TNF in the deceased patients with hepatic failure induced by HBV and HCV infection was higher than in those who survived (P < 0.05), and it also seemed significantly different in patients with and without multiple organ failure (P < 0.05). In vitro, HSS showed marked inhibitory activity on TNF production from PBM induced by endotoxin, but had no significant effect on the TNF cytotoxicity of L929 cells. It seems that high serum TNF level is an important mediator in the pathogenesis of liver necrosis and failure of microcirculation in HCV and/or HBV infection. These observations favor the attempt to treat hepatic failure with HSS or anti-TNF. Encouraging results were achieved using HSS in the treatment of subacute liver necrosis in our institute.(ABSTRACT TRUNCATED AT 250 WORDS)

     

Impact of genetic variation of tumor necrosis factor-α on gestational hypertension

Background The mechanisms responsible for the pathogeneses of gestational hypertension and preeclampsia are unclear. Tumor necrosis factor-1α （TNF-1α） is a pro-inflammatory Th1-type cytokine. TNFA gene is located in the human leukocyte antigen （HLA） class Ⅲ region of the major histocompatibility complex （MHC） on chromosome 6. The high TNF-1α mRNA expression may be associated with the TNF2 （A） allele, which is the polymorphism of TNF-1α at position - 308 in promoter region. This study assessed whether the TNF2 （A） allele at position -308 plays a role in the alteration of blood pressure （BP） and urinary protein excretion during pregnancy. Methods The original prospective cohort study comprised 1623 pregnant women from January 2000 to October 2001. The G/A polymorphism was done by restriction fragment length polymorphism （RFLP） analysis with Nco I enzyme. Results The distributions of the G/A polymorphism of TNF-1α in the promoter region at position -308 were wild-type 72.4% and variant 27.6%, respectively. The frequency of TNF2 （A） allele was approximately 0.15 for Caucasian pregnant women in the study. It was not significantly different in the distributions of genotypes and G/A allele frequencies among the three groups of pregnant women with gestational hypertension, preexisting hypertension and normal blood pressure （P〉0.05）. The maternal blood pressure in the third trimester was significantly higher in the group of women possessing the TNF2 （A） allele compared to homozygous for the TNF1 （G） allele （systolic BE P〈0.01 and diastolic BE P〈0.05）. The elevated blood pressure in the TNF2 （A） group was accompanied by higher urinary protein excretion in the third trimester （P〈0.05）. The blood pressure and urinary protein excretion did not change apparently between the two groups in the first and second trimesters （P〉0.05）. Conclusions Maternal TNF2 （A） allele of TNF-1α promoter region at position -308 could play a role in the alteration of blood pressures and/or enhancement of urinary protein excretion during pregnancy, and might play an important role in the development of both gestational hypertension and preeclampsia.     

The relationship between tumor necrosis factor-a gene polymorphisms and acute severe pancreatitis

Objective To investigate the relationship between the presence of the TNF2 allele and plasma concentrations of tumor necrosis factor-α (TNFα) and soluble TNF receptor (sTNF-R) with the development of acute severe pancreatitis (ASP) and severe sepsis.Methods Genomic DNA was prepared from peripheral blood leukocytes. The TNF1 and TNF2 biallelic polymorphisms were identified by analyzing Ncol-digested DNA fragments obtained from PCR products. Plasma levels of TNFa and sTNF-R were measured by EASIA.Results The overall TNF2 allele frequency in ASP patients was comparable to that found in healthy volunteers (29. 2% vs. 29. 3% , P>0. 05). Severe sepsis occurred in 26 of 72 patients. Patients with severe sepsis showed a significantly higher prevalence of TNF2 than those without (46. 2% vs. 19.6%, P<0. 05). Plasma TNFα, sTNF-R Ⅰ, and sTNF-R Ⅱ levels were (36± 31) pg/ml, (5. 4± 3.5) ng/ml, and (11.2±7.8) ng/ml, respectively, in patients with severe sepsis, and (31 ±25) pg/ml, (4.6±3.8) ng/ml, and (8.8