Objective To investigate the protective effects of antitumor necrosis factor-α antibody （TNF-αAb） on lung injury after cardiopulmonary bypass （CPB） and their mechanisms. Methods Forty healthy New Zealand white rabbits，weighting 2.0-2.5 kg，male or female，were randomly divided into 4 groups with 10 rabbits in each group. In groupⅠ，the rabbits received CPB and pulmonary arterial perfusion. In group Ⅱ，the rabbits received CPB and pulmonary arterial perfusion with TNF-αAb. In group Ⅲ，the rabbits received CPB only. In group Ⅳ，the rabbits only received sham surgery. Neutrophils count，TNF-α and malondialdehyde （MDA） concentrations of the blood samples from the left and right atrium as well as oxygenation index were examined before and after CPB in the 4 groups. Pathological and ultrastructural changes of the lung tissues were observed under light and electron microscopes. Lung water content，TNF-α mRNA and apoptoticindex of the lung tissues were measured at different time points. Results Compared with group Ⅳ，after CPB，the rabbitsin group Ⅰ to group Ⅲ showed significantly higher blood levels of neutrophils count，TNF-α and MDA（P＜0.05），higherTNF-α mRNA expression，apoptosis index and water content of the lung tissues （P＜0.05），and significantly lower oxyg-enation index （P＜0.05） as well as considerable pathomorphological changes in the lung tissues. Compared with group Ⅱ，after CPB，the rabbits in groups Ⅰ and Ⅲ had significantly higher blood concentrations of TNF-α （5 minutes after aortic declamping，220.43±16.44 pg/ml vs.185.27±11.78 pg/ml，P＜0.05；249.99±14.09 pg/ml vs.185.27±11.78 pg/ml，P＜0.05），significantly higher apoptosis index （at the time of CPB termination，60.7‰±13.09‰ vs. 37.9‰±7.78‰，P＜0.05；59.6‰±7.74‰ vs. 37.9‰±7.78‰，P＜0.05），significantly higher blood levels of neutrophils count and MDA （P＜0.05），significantly higher TNF-α mRNA expression and water content of the lung tissues （P＜0.05），and significantly loweroxygenation index （P＜0.05） as well as considerable pathomorphological changes in the lung tissues. Compared with groupⅠ，rabbits in group Ⅲ had significantly higher above parameters （P＜0.05） but lower oxygenation index （P＜0.05） only at 30 minutes after the start of CPB. Conclusion Pulmonary artery perfusion with TNF-αAb can significantly attenuate inflammatory lung injury and apoptosis of the lung tissues during CPB.
目的研究依達拉奉影響肝臟缺血再灌注過程中TNF-α的表達情況，探討依達拉奉對肝臟缺血再灌注損傷的逆轉作用。 方法將80只Wistar大鼠編號，根據計算機產生隨機數字，前40為一組，后40為一組，分為實驗組和對照組2組，建立常溫下部分肝缺血再灌注損傷動物模型。 在肝臟缺血再灌注損傷開始前1 h和開始時對實驗組大鼠給予依達拉奉注射液10 ml，對照組則給予同等容量的生理鹽水。分別于再灌注后0、1、2及4 h測定肝臟脂質過氧化物酶（LPO）和肝臟谷草轉氨酶(AST) 濃度； 應用RT-PCR法檢測肝組織TNF-α mRNA含量，并測定肝組織和血清中TNF-α水平； 應用TUNEL染色法檢測缺血肝組織的細胞凋亡情況。結果再灌注后1、2及4 h，實驗組大鼠肝臟LPO及AST濃度均明顯低于對照組（Plt;0.001）； 實驗組再灌注后1 h時肝組織TNF-α mRNA表達量、肝組織和血清TNF-α含量均明顯升高且達峰值，但均明顯低于對照組（Plt;0.05）； 再灌注后各時相實驗組肝細胞凋亡率明顯升高，但均明顯低于對照組（Plt;0.05）。 結論依達拉奉能抑制氧化應激反應，從而降低肝缺血再灌注損傷； 并顯著減少炎性細胞因子TNF-α的產生，抑制炎性反應的發生，減少肝細胞的凋亡。
Objective To analyze the outcome of patients with Blunt Abdominal Injury (BAI) in the Deyang People’s Hospital after the Wenchuan Earthquake, in order to provide evidence for future improvement in emergency response after earthquakes and in the treatment of BAI patients. Methods Data on the BAI patients within 1 week after the earthquake were collected from the Information Department of the Hospital. Microsoft EXCEL was used for data input. Results A total of 23 BAI inpatients were treated, of whom 15 were from Mianzhu City and sent to hospital within 12 hours of the earthquake. This was 1.9% of the total inpatients. The BAI inpatients suffered severe and complex injuries, and 5 of them died (mortality rate: 22%). Linenectomy was conducted for patients with spleen injuries and two inpatients developed incision infection due to lack of antibiotics during the perioperative period. Conclusions It is important to establish an emergency response mechanism for medical rescue for patients with the viscera injury, including BAI, after an earthquake. This would help to guarantee rational allocation of the rescue workers, triage of the wounded, optimization of operation, as well as a reduction in mortality from BAI.
Objective To explore the expression of tumor necrosis factor (TNF) mRNA, TNF and TNFR in the gallbladder mucosa which developed from hyperplasia, dysplasia to carcinoma, and to further discuss the relationship between TNF and pathogenesis of gallbladder carcinoma. Methods In situ hybridization and immunohistochemistry were used to determine TNF mRNA, TNF protein and TNFR protein expression in hyperplasia, dysplasia and carcinoma of gallbladder. Results ①No one of 20 cases of gallbladder hyperplasia was found to express TNF mRNA, while 4 of 20 (20%) cases of dysplasia and 18 of 20 (90%) cases of carcinoma were found to express TNF mRNA (P＜0.05). ②For the expression of TNF mRNA in mononuclear cells (MNC), positive staining was found in 15% of gallbladder hyperplasia, 85% of dysplasia and 90% of carcinoma, respectively (P＜0.05). The cell numbers of positive staining MNC were 4.85±1.50, 6.00±2.71 and 9.33±3.07, respectively (P＜0.05). ③In gallbladder carcinoma, the cell number of carcinoma and MNC with positive TNF mRNA expression was correlated with clinical stage (P＜0.05). The higher the clinical stage, the more the positive staining cell numbers. The positive staining cell numbers of carcinoma in stage Ⅰ-Ⅲ and Ⅳ-Ⅴ were 9.13±4.39 and 14.80±4.02, respectively (P＜0.01), and the positive staining cell numbers of MNC were 7.13±2.53 and 11.10±2.23, respectively (P＜0.05). ④The cell numbers of carcinoma and MNC with TNF mRNA expression increased with tumor size. In tumors with diameter over 2 cm and less than 2 cm, the positive staining cell numbers of carcinoma were 14.00±4.20 and 8.83±4.96, respectively (P＜0.05), and that of MNC were 10.50±2.54 and 7.00±2.83, respectively (P＜0.05). ⑤The region of TNF protein expression was similar to that of TNF mRNA, but TNF protein expression was more frequent and wider than that of TNF mRNA. ⑥The tumor necrosis factor receptor was expressed in tumoral vascular endothelial cells and MNC in all cases of carcinoma, but was negatively stained in mucosa epithelial cells and tumor cells of all cases. ⑦There was positive linear correlation in TNF mRNA between tumor cell and MNC (r=0.687, P＜0.01), same as that in TNF protein expression (r=0.742, P＜0.01); and there was positive linear correlation in tumor cell between TNF mRNA and TNF protein expression (r=0.847, P＜0.01), same as that in MNC (r=0.643, P＜0.01). Conclusion The TNF mRNA and TNF protein expression are increasing during the development of gallbladder mucosa epithelial from hyperplasia, dysplasia to carcinoma, and increasing with tumor stage. It suggests that TNF may contribute to carcinogenesis of gallbladder carcinoma induced by gallstone, and related to the progression of gallbladder carcinoma.
Objective To investigate the changes and significance of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-α (TNF-α) in intestinal mucosa in rats with obstructive jaundice. MethodsTwenty-four SD rats were randomly divided into sham operation (SO) group and bile duct ligation (BDL) group, and each group were randomly divided into the day 7 and day 14 subgroup. The expression of ICAM-1 was assayed by immunohistochemistry. The level of TNF-α was determined by ELISA. The activity of myeloperoxidase (MPO) and diamine oxidase (DAO) was determined as well.ResultsOn the day 7 and 14, in the bile duct ligation group, the ICAM-1 protein was mainly expressed in the intestinal epithelia and increased with the time on (P＜0.05); the level of TNFα increased from （14.25±1.01） ng/g to （23.83±1.43） ng/g （P＜0.01）； the intestinal DAO activity decreased from （1.70±0.36） U/mg to （1.22±0.41） U/mg （P＜0.01），and plasma DAO activity increased from （6.44±1.74）U/ml to （8.93±1.29） U/ml （P＜0.01）; the MPO activity increased from （2.85±1.22 ） U/mg to （4.93±1.37） U/mg （P＜0.01）. ConclusionThe ICAM-1 expression is significantly upregulated and the level of TNFα significantly increases after bile duct ligation, which may be involved in the PMNmediated injury to intestinal mucosa.
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.
【Abstract】Objective To study the influence of early hemofiltration on plasma concentrations of proinflammatory cytokines TNF-α and IL-1β and their transcription levels in severe acute pancreatitis (SAP) pigs. Methods The model of SAP was induced by retrograde injection of artificial bile into pancreatic duct in pigs. Animals were divided randomly into two groups: SAP hemofiltration treatment group (HF group, n=8) and SAP no hemofiltration treatment group (NHF group, n=8). TNF-α and IL-1β plasma concentrations were measured by ELISA. Their transcription levels in the tissues of pancreas, liver and lung were assayed by semi-quantitative reverse transcription polymerase chain reaction. Results After hemofiltration treatment, the plasma concentrations of TNF-α and IL-1β increased gradually but were lower than those of NHF group at the same time spot 〔at 6 h after hemofiltration treatment, (618±276) pg/ml vs (1 375±334) pg/ml and (445±141) pg/ml vs (965±265) pg/ml, P＜0.01〕. At 6 h after hemofiltration treatment, the transcription levels of TNF-α and IL-1β in tissues of pancreas, liver and lung were lower than in NHF group (57.8±8.9 vs 85.7±17.4, 48.0±8.1 vs 78.1±10.2, 46.2±9.6 vs 82.4±10.5; 55.9±9.0 vs 82.2±15.7, 40.6±9.2 vs 60.0±10.6, 35.7±9.8 vs 58.1±9.3, P＜0.01). Conclusion Early hemofiltration can reduce TNF-α and IL-1β plasma concentrations and transcription levels in SAP pigs.