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.
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 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.
Objectve To measure the serum levels of human IL-32 and explore the clincal implication in patients with chronic obstructive pulmonary disease( COPD) at acute exacerbation or stable stage. Methods 120 patients with COPD were recruited, including 60 patients with acute exacerbation COPD and 60 patients with stable COPD from October 2010 to May 2011. Thirty healthy nonsmoking volunteers were included as controls. The concentrations of interleukin-8 ( IL-8) , tumor necrosis factor alpha ( TNF-α) , and IL-32 in serum were measured by enzyme-linked immunosorbent assay ( ELISA) . The correlations among IL-32, IL-8, TNF-αand lung functions were investigated. The datas were analyzed using a statistical software package ( SPSS13. 0) . Variables were compared with one-way ANOVA . The correlations between variables were analyzed using Pearson’s correlation coefficient or Spearman correlation coefficient. Results SerumIL-32 level was significantly higher in AECOPD patients [ ( 174. 56 ±88. 15) ng/L] than that in healthy subjects [ ( 59. 41 ±20. 98) ng/L] and in stable COPD patients [ ( 89. 40 ±33. 84) ng/L]( P lt;0. 05) while serum IL-32 level was also significantly higher in stable COPD patients than in healthy subjects( P lt;0. 05) . The serumIL-32 1evel in patients with acute exacerbation COPD and stable COPD was positively correlated with the serumIL-8 level, TNF-αlevel ( respectively P lt;0. 01) . The serumIL-32 level was negatively correlated with FEV1 /predicted value, FEV1 /FVC and PaO2 ( respectively, P lt;0. 01) . There was no statistical significance of the serum IL-32, IL-8 or TNF-α levels in COPD patients with different severity ( all P gt;0. 05) . Conclusion The serumlevel of IL-32, a newpro-inflammatory cytokine is elevated in COPD patients, which may be involved in the pathogenesis of inflammation in COPD.
Objective To study the role of hydrogen sulfide （H2S） in prophase of acute peritoneal cavity infection. Methods NaHS was taken as a donor of H2S. Seventy-two Sprague-Dawley rats were divided into 4 groups randomly：control group， cecal ligation and puncture （CLP） and treated with natural saline group，CLP and treated with NAHS group， and CLP and treated with DL-propargylglycine （PAG， an inhibitor of H2S formation） group. Selected 6 rats at 2h， 6h， and 12h after treatment in each group. The contents of TNF-αand H2S in serum and the content of MPO in intestinal tissue were measured， respectively. The histopathological change of ileum tissues were observed at 6 h after treatment in each group. Results The H2S could alleviate CLP-induced inflammation obviously， decrease the content of TNF-α in serum when inflammation，and attenuate the infiltration of neutrophilic granulocyte in small intestine. Conclusion The H2S has anti-inflammation effect in prophase of acute peritoneal cavity infection.
Objective To examine the levels of interferon-gamma; (INF-gamma;), tumor necrosis factor-alpha; (TNF-alpha;) and interleukin-6(IL-6) in serum of patients with acute uveitis before and after treatment, and to explore the possible roles of those cytokines in the initiation and progression of the uveitis. Methods A series of 75 patients with acute uveitis,and 30 healthy persons from our hospital were investigated. The levels of INF-gamma;, TNF-alpha; and IL-6 in acute phase and convalescent phase were measured by the enzymelinked immunosorbent assay. Result The serum levels of INF-gamma;, TNF-alpha; and IL-6 in acute phase were significantly higher than that of the convalescent phase and the healthy controls (F=65.805/50.418/155.381, P=0.000). A significant negative correlation was found between the serum levels of INF-gamma;, TNF-alpha; and IL-6 in acute phase with their initial visual acuity(r=-0.656, -0.592 and -0.653, Plt;0.01). There was also a positive correlation among the serum levels of INF-gamma;, TNF-alpha; and IL-6(r=0.340, 0.467 and 0.338, Plt;0.05). Conclusions There are high serum levels of INF-gamma;, TNF-alpha; and IL-6 in patients with acute uveitis, and the cytokines levels were decreased after the treatment. The results suggested that the INF-gamma;, TNF-alpha; and IL-6 involved in initiation and progression of uveitis.
ObjectiveTo investigate the effects of transforming growth factor-β (TGF-β) in choroidal neovascularization (CNV) induced by laser in mice. Methods Eighty male C57BL/6J mice at the age of 6-8 weeks old were randomly divided into the normal control, photocoagulation model, photocoagulation with phosphate buffered saline (PBS control group) and photocoagulation with TGF-β receptor inhibitor groups (TGF-β receptor inhibitor group), twenty mice of each group. Fundus argon laser photocoagulation was performed in the photocoagulation model group, PBS control group and TGF-β receptor inhibitor group to induce CNV. One week, two, three and four weeks after the laser procedure, fundus fluorescein angiography (FFA) was carried out in the normal control or photocoagulation model groups to observe CNV formation dynamically. Western blot was used to analyze the expressions of TGF-β in the retina from the mice of normal control or photocoagulation model groups, and VEGF or TNF-α in the retina of normal control, PBS control or TGF-β receptor inhibitor groups. The CNV areas of each group were evaluated by using fluorescein stain on retinal pigment epithelium (RPE)/choroid flat mounts after two weeks of photocoagulation. ResultsThe FFA results showed the retinal vessels centered on the optic disc and arranged radially, while the choroidal vascular present network distribution in the normal control mice. Significant leakage of fluorescein showed discoid strong fluorophore in photocoagulation sites of retina at one week after photocoagulation. The quantitative analysis results of Western blot demonstrated that the TGF-β protein expression levels in retina of photocoagulation model mice gradually increased with time passing. The protein expression levels of TGF-β were significant differences in the photocoagulation model group comparing with the normal control group (F=13.042, P < 0.05). The protein expression levels of TNF-α (F=14.721, 17.509) and VEGF (F=18.890, 11.251) increased significantly in retina of PBS control or TGF-β receptor inhibitor groups when compared with that of normal control group at one week, two, three and four weeks after photocoagulation, and the differences were both statistically significant (P < 0.05). Compared with PBS control group, the protein levels of TNF-α and VEGF in retina from TGF-β receptor inhibitor group were significantly reduced, the differences was statistically significant (F=21.321, 16.160, P < 0.05). Two weeks after laser photocoagulation, a distinct reduction in CNV lesion size in the TGF-β receptor inhibitor group mice when compared to PBS or normal control groups, the differences was statically significant (F=4.482, P < 0.05). ConclusionTGF-β may promote CNV formation by up-regulating both TNF-α and VEGF protein expressions, the application of its specific inhibitor is able to reduce CNV progression.
Objective To determine the concentration of int erleukin-12(IL-12),interleukin-2(IL-2) and tumor necrosis factor(TNF)and the irpossible role in the pathogenesis of proliferative vitreoretinopathy(PVR) ． Methods Patients were divided into 3 groups:18 with PVR,7 with simples retinal detachment caused by macular hole and 4 samples from normal eyes were used as control.Sample s of vitreous were obtained by aspiration through pars plana before cryotherapy ,vitrectomy and gas injection and stored in liquid nitrogen at －70℃ within 30 minites for ELISA. Results ①The levels of IL-12,IL-2，and TNF in the vitreous of PVR were positively correlated with the degree of severity of disease.②The levels of IL-12, IL-2,and TNF in the PVR were higher than those in simple retinal detachment caused by macular hole and those in control group(Plt;0.01 ).③The levels of IL-12,IL-2，and TNF in retinal detachment caused by macular hole were also higher than those in the control group(Plt;0.01). Conclusion IL-12,IL-2，and TNF may play a role at lease to some extent in the pathogenesis of PVR. (Chin J Ocul Fundus Dis,1999,15:75-77)
63 normal human gallbladders (non-stone group) and 47 inflammed cholesterol stone gallbladders(stone group) were assayed for the amount of macrophages(ΜΦ),the levels of tumor necro-sis factor (TNF) and interleukin 1(1L-1).It was found that in stone group,the amount of ΜΦ was significantly higher than in non-stone group(ΜΦ4101.90±295.72 vs 572.13±30.07AU,Plt;0.01).The levels of TNF and 1L-1 released mainly from the MΦ in stone group were also significantly increased in comparison with those in non-stone group(TNF 18.12±2.03 vs 4.45±0.39ng/mg,Plt;0.001;1L-1 102.42±7.84 vs 66.75±9.50u/mg protein,Plt;0.05).These results suggest that the activited ΜΦ and increases of TNF,1L-1 may be closely related to the inflammatory reaction in gallbladders and the formation of cholesterol gallstones.
Objective To explore the mechanism of Liuhedan in promoting wound healing through applying Liuhedan to the infective wounds of New Zealand white rabbits. Methods A total of forty New Zealand white rabbit models of infective wounds were established after anesthesia. Five circular infective incisions were generated on the back of each rabbit, with a diameter of 2 cm. Five wounds of each rabbit were assigned respectively to the control group, model group, traditional Chinese medicine (TCM) group (Oleum Lithospermum), Western medicine group (calcium alginat), and treatment group (Liuhedan). Wound dressings were performed every day since postoperative day 1. Ten rabbits were selected randomly to be euthanized on postoperative day 3, 7, 14 and 21, respectively. Each specimen was divided into two parts. One was used for detecting interleukin-1β (IL-1β) by enzyme-linked immunosorbent assay, and the other was used for detecting tumor necrosis factor-α (TNF-α) by immunocytochemistry. Results On postoperative day 3 and 7, groups with the expression of IL-1β from low to high were respectively the control group, the treatment group, the Western medicine group, the TCM group, and the model group [postoperative day 3: (680.81±185.53), (1 028.67±205.57), (1 278.67±251.15), (1 449.86±230.74), (1 544.62±371.77) pg/mL; postoperative day 7: (1 024.43±239.94), (1 333.57±257.31), (1 635.14±222.40), (1 784.71±323.85), (1 953.29±324.78) pg/mL], and all the differences among the groups were significant (P<0.05); On postoperative day 14, groups with the expression of IL-1β from low to high were respectively the treatment group, the control group, the Western medicine group, the TCM group, and the model group [(908.71±108.61), (978.57±161.75), (1 120.43±265.39), (1 129.71±298.06), (1 191.14±234.92) pg/mL], and all the differences among groups were significant (P<0.05) except the difference between the Western medicine group and the TCM group (P>0.05); On postoperative day 21, the expression of IL-1β in the control group, the model group, the TCM group, and the Western medicine group was (487.19±121.80), (496.35±102.15), (500.31±139.34), (499.08±120.67) pg/mL, respectively, with no significant differences among the groups (P>0.05), which were all higher than that in the treatment group [(398.62±102.93) pg/mL] with significant difference (P<0.05). The expression of TNF-α in the model group was significantly greater than those in the other groups. The expression of TNF-α in the treatment group and Western medicine group was significantly lower compared with the model group. The expression of TNF-α in the TCM group was stronger compared with those in the treatment group and the Western medicine group. Conclusion Liuhedan can specifically suppress the expressions of IL-1β and TNF-α in the treatment of infective wounds, decrease the release of inflammatory factor and promote the healing.