In order to observe activity of tumor necrosis factor (TNF) in the serum, pancreatic histopathological damage, as well as their relationships in acute necrotizing pancreatitis (ANP), thirty five SD rats were randomly divided into 7 groups according to their sampling time with 5 in each group. ANP was induced by retrograde infusion of 5% sodium taurocholate through biliopancreatic duct in 6 experimental groups (Group B1～B6).Blood and pancreatic tissue samples were obtained at hour 0,0.5,2,4,6 or 8 respectively when the animals were sacrificed.Results showed that serum level of TNF activity rose significantly in Group B2,and reached the maximal value in Group B4.The pancreatic histopathological damage in ANP rats was getting worse along with time. Serum TNF activity had close relation to pancreatic histopathological score (r=0.63, Ｐ＜0.01),suggesting that serum TNF may play an important role in the process of deterioration of pancreatic tissue damage during ANP.
Objective To detect the effects of cytokines on the expression of early growth response gene-1 (Egr-1) in cultured human retinal pigment epithelial (RPE) cells. Methods Immunofluorescence staining, Western blotting and reverse transcription polymerase chain reaction (RT-PCR) were used to detect and quantitatively analyze the expression of Egr-1 protein and mRNA in cultured human RPE cells which were exposed to stimulants, including 20 mu;g/ml lipopolysaccharide (LPS), 40 ng/ml tumor necrosis factor (TNF)-alpha;, 10 U/ml interferon (IFN)gamma;, 30% supernatant of monocyte/macrophage strain (THP1 cells) and the vitreous humor from healthy human eyeballs, for 0, 10, 20, 30, 40 and 60 minutes, respectively. Results The RPE cells stimulated for 0 minute revealed faint green fluorescence of Egr-1 in the cytoplasm. With exposure to the stimulants, the expressionof Egr-1 increased obviously and b green fluorescence was found in cytoplasm in some nuclei of RPE cells. Compared with the untreated RPE cells, after stimulated by 20 mu;g/ml LPS, 40 ng/ml TNFalpha;, 10 U/ml IFNgamma;, 30% supernatant of THP-1 cells and the vitreous humor, the approximate ultimate amplitudes of Egr-1 mRNA enhanced 1.9, 1.3, 14, 1.2, and 1.4 times, respectively; the greatest amplitudes of Egr-1 protein increased 3.4, 1.2, 1.7, 32, and 1.3 times, respectively. Conclusion LPS, TNF-alpha;, IFN-gamma;, supernatant of THP-1 cells and the vitreous humor can upregulate the expression of Egr-1 mRNA and protein in cultured human RPE cells, and induce its nuclear transposition, which suggests the activation of Egr-1.
Objective To investigate the expressions of tumor necrosis factor related apoptosis inducing ligand （TRAIL） and its receptors (DR4, DcR1) in human rectal cancer tissues and normal rectal tissues. MethodsThe expressions of TRAIL and its receptors (DR4, DcR1) in 31 cases of human rectal cancer tissues and 20 cases of normal rectal tissues were detected by immunohistochemical staining. ResultsThe positive expression rates of TRAIL, DR4 and DcR1 （32.26%， 29.03%， 0） were lower than those of normal rectal tissues （55.00%， 70.00%， 65.00%）, the difference was statistically significant(P=0.015， P=0.000， P=0.000). There were no relation between the expressions of TRAIL, DR4 and DcR1 and clinicopathologic characteristics (Pgt;0.05). ConclusionThe expressions of TRAIL and its receptors (DR4, DcR1) in human rectal cancer tissues were lower than those of normal rectal tissues, which may suggest that the apoptotic effect induced by the interaction between TRAIL and its receptors has attenuated in human rectal cancer.
Interleukin-1 (IL-1), interleukin-2(IL-2) and interleukin-6(IL-6) activities and tumor necrosis factor (TNF) contents in plasma from patients with different sites of cancers as well as controls using bioassay technique were studied. The results showed that the levels of IL-1,IL-2,IL-6 s from patients with different sites of cancer were decreased remarkably in comparision with controls and the contents of TNF from patients with different sites of cancers increased significantly. But the difference between different sites of cancer was not statistically significant. The data suggest that the variations in the contents of TNF and the levels of interleukins may be related to the development of these caner patients.
ObjectiveTo observe the expression of vascular endothelial growth inhibitor (VEGI, TL1A), vascular endothelial growth factor (VEGF), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in diabetes rats' serum, vitreous and retina, and discuss the role of VEGI in the pathogenesis of diabetic retinopathy (DR). MethodsA total of p70 adult male Wistar rats were randomly divided into 4 groups, the control group (10 rats), the diabetes mellitus (DM) 1 month group (20 rats), the DM 3 month group (20 rats) and the DM 6 month group (20 rats). Cytokines of serum and vitreous were determined by enzyme-linked immunosorbent assay (ELISA), and the concentrations of the cytokines in the retina were determined by immunohistochemistry on paraffin retinal sections. Hematoxylin-eosin (HE) staining of retina was used to estimate the pathological change of DR. The results were analyzed by one-way analysis of variances, independent samples t-test and LSD test. ResultsThe serum TL1A levels of the control group, the DM 1 month group, the DM 3 month group and the DM 6 month group rats were (92.09±2.05), (118.36±8.30), (85.90±7.51) and (78.90±4.88) ng/L respectively, the level of TL1A in serum of the DM 1 month group, the DM 3 month group and the DM 6 month group were significantly lower than that of the control group (F=77.405, P < 0.05). The concentration of serum TNF-α and IL-1β increased after DM model was established (F=3.508, 15.416; P < 0.05); the VEGF level in serum showed no difference between the groups (F=1.242, P > 0.05). The vitreous TL1A levels of the control group, the DM 1 month group, the DM 3 month group and the DM 6 month group were (91.50±8.18), (67.03±6.74), (47.44±4.92) and (46.01±4.62) ng/L respectively, every DM groups showed significant difference with the control group (F=114.777, P < 0.05); VEGF level in vitreous increased from 1 month after DM model was established (F=8.816, P < 0.05); TNF-α and IL-1β level in vitreous also showed an upward tendency (F=4.392, 3.635; P < 0.05). Paraffin section immunohistochemistry showed that the absorbance (also called optical density) of TL1A of the DM 1 month group and the DM 3 month group were significantly lower than that of the control group (t=6.851, 6.066; P < 0.05), but the DM 6 month group showed no difference with the control group (t=1.401, P > 0.05); the level of VEGF and TNF-α in DM groups were higher than that of the control group (tVEGF=-4.709, -16.406, -9.228; tTNF-α=-4.703, -6.583, -17.762; P < 0.05); the level of IL-1β were significantly higher in the DM 1 month group and the DM 6 month group (t=-4.108, -3.495; P > 0.05); but the DM 3 month showed no difference with the control group (t=-0.997, P > 0.05). HE staining of retina showed that the retina of the control group and the DM 1 month group had normal retinal structures, the DM 3 month group had retinal edema and disorganization, the DM 6 month group had severe retinal edema, deep stain of ganglion cells, and more neovascularization in inner plexiform layer. ConclusionVEGI is involved in the pathogenesis of DR, and it might interacts with VEGF, TNF-α and IL-1β to affect the development of DR.
Purpose To investigate the expression of the interleukin-6(IL-6)and tumor necrosis factor alpha(TNF-alpha;) in epiretinal membranes(ERM) of eyes with proliferative vitreoretinopathy(PVR). Methods Nineteen epiretinal membranes were obtained form eyes undergoing vitrectomy for retinal detachment complicated with PVR and observed by immunohistochemical methods. Results Expression of IL-6 and TNF-alpha; were observed in 12 and 15 membranes respectively with positive staining mostly in extracellular matrix of epiretinal membranes.Only one membrane showed positive to IL-6 intracellularly,and expression for IL-6 and TNF-alpha; simultaneously in membranes. Conclusion The findings indicate that IL-6、and TNF-alpha;might be involved in the development of PVR. (Chin J Ocul Fundus Dis,1998,14:219-221)
Objective To investigate the effects of methylprednisolone on airway inflammation of chronic bronchitis in rats, and to explore its possible mechanism. Methods Forty SD rats were randomly divided into five groups, ie. a blank control group, amethylprednisolone control group, a model group, and two methylprednisolone intervention groups. Chronic bronchitis model was established by cigarette inhalation in the model group and two intervention groups. Methylprednisolone was injected intraperitoneally in the two intervention groups before exposing to cigarette smog ( at the dose of 1 mg/ kg and 10 mg/ kg, qd,respectively) . The protein expression of phosphodiesterase 4D ( PDE4D ) in trachea and lung samples was determined by immunohistochemical staining. The average optical density of positive staining of PDE4D was determined by image analysis technique and gray scale scanning. Bronchoalveolar lavage fluid ( BALF) was collected for total and differential cell counts, and the concentrations of TNF-αand interleukin-8 ( IL-8) in BALF were detected by ELISA. Results Cigarette smoking induced obvious airway inflammation in themodel group, and the inflammation was alleviated in the two methylprednisolone intervention groups.Compared with the two control groups, the expression of PDE4D was obviously elevated in tracheal and lungs in the model group( P lt; 0. 05) . Moreover, the increased expression of PDE4D was positively related with theincreased release of TNF-αand IL-8 in BALF. The expression of PDE4D and the release of TNF-αand IL-8 in BALF were decreased after the treatment with methylprednisolone in a dose-dependent manner ( P lt;0. 05) . Compare with the low dose intervention group, there was no markedly difference related to PMNnumber and TNF-α release in the high dose intervention group ( P gt; 0.05) . Conclusions Methylprednisolone may alleviate airway inflammation of chronic bronchitis by inhibiting the expression of PDE4D in rats. Inhibition of PDE4D may down-regulate TNF-αactivity, which may further reduce IL-8 release and alleviate airway inflammation.
Objective To investigate the effects of ginkgo biloba extract （GBE） on expressions of IL-1β, IL-6,and TNF-α in the pancreas and brain tissues of rats with severe acute pancreatitis （SAP）, and further to explore the pathogenesis of SAP and the efficacy of GBE on brain injury. Methods Fifty-four Winstar rats were randomly divided into normal control group, model group, and treatment group, with 18 rats for each group. For rats in the normal control group, only conversion of pancreas was performed by abdomen opening , followed by wound closure immediately. For rats in the model group and treatment group, 5% sodium taurocholate hydrate were injected under pancreatic capsule to establish SAP model, and then GBE and normal saline were infected into intra-abdomen repeatedly every 8 hours, respectively. At 6 h, 12 h, and 24 h after the model establishment, experimental samples were extracted and serum amylase was detected. Pathogenic scoring for pancreas tissues was performed under light microscopy, and immunohistochemistry method was employed to detect the expression levels of IL-1β, IL-6, and TNF-α in pancreas and brain tissues. Results For the treatment group, both serum amylase and pancreas scoring were significantly lower than those of the model group （P＜0.01）. At 24 h after model establishment, the expressions of IL-1β, IL-6, and TNF-α of pancreas tissues in model group were significantly higher than those at 6 h and 12 h （P＜0.05 or P＜0.01）, but no significant differences wereobserved in treatment group （P＞0.05）. The expressions of IL-1β, IL-6, and TNF-α of brain tissues in model group were significantly higher than those at 6 h and 12 h （P＜0.05 or P＜0.01）, but in treatment group decreased （P＜0.05 or P＜0.01）. The expressions of IL-1β, IL-6, and TNF-α in the treatment group were significantly lower than those of the model group at same time （P＜0.01）. Conclusions During SAP, the expressions of IL-1β, IL-6 and TNF-α in pancreas and brain tissues increased obviously. GBE showed suppressing and scavenging effects on IL-1β, IL-6 and TNF-α in pancreas and brain tissues.
PURPOSE:To measure the concentration changes of tumor necrosis factor a (TNF-alpha;)in vitreous during the development of experimental PVR induced by macrophages and explore the initial and mediated factors which stimulate the cellular proliferation. METHODS:Rabbit PVR model was induced by macrophages and the vitreous was taken at the 7th,14th,21st and 28th day and 4 eyes in each group. The TNF-alpha; levels in vivreous of the above examinated and control eyes were measured with an ELISA kit. RESULTS:The TNF-alpha; level in the vitreous reached its peak 434mu;g/ml at 21st day in the mod-el, then rappidly decreased to 122mu;g/ml at 28th day. CONCLUSION:The changes of TNF-a in the vitreous of the PVR model were parallel to the natrual phases of the development of PVR,indicating TNF-alpha; may play an important role in initiating and mediating the inflammation and cellular proliferation in the vitreous. （Chin J Ocul Fundus Dis,1997,13: 231-233）
Objective To summarize the role of inflammatory cytokines in the pathogenesis of acute pancreatitis (AP) and gut barrier dysfunction in recent years. Methods Literatures on cytokines and experimental pancreatitis as well as clinical pancreatitis were collected and reviewed. Results Tumor necrosis factor-α and other inflammatory cytokines were elevated significantly during pancreatitis in many tissues, especially in pancreas and alimentary tract, in a fashion independent of the animal model used. Anti-cytokine therapy could decrease the concentration of the cytokines in experimental animal. Conclusion Inflammatory cytokines are believed to be primarily responsible for the pathogenesis of acute pancreatitis and its associated distant organ dysfunction. Further study of the nature of these cytokines may provide a new approach to treating this disease.