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| 1 | Effect of hepatocyte apoptosis induced by TNF-α on acute severe hepatitis in mouse models显示文摘AIM To study the effect of hepatocyteapoptosis and necrosis induced by TNF-α on thepathogenesis of acute severe hepatitis(ASH).METHODS The model of ASH was prepared inD-galactosamine(GAIN)sensitized BALB/c miceby injection of either endotoxin(ET)or tumornecrosis factor-α(TNF-α).Morphologicalchanges of apoptotic hepatocytes were studiedby both light and electron microscope and in siteend labeling method(ISEL).Molecular biologicalchanges of DNA ladder were observed byelectrophoresis of extract from liver tissues.Biochemical changes were measured by alanineaminotransferase(ALT),asparticaminotransferase(AST)and TNF-α.The relationbetween apoptosis and necrosis was evaluatedsimultaneously.RESULTS The sequence of hepatocyteapoptosis,necrosis,and final death from ASHwas observed both in GAIN/ET and GAIN/TNF-agroup.Apoptosis was prominent at 3.5 h and 5 hafter injection of inducer,while necrosis becamedominant at 9 h after challenge.The appearanceof apoptosis was earlier in GAIN/TNF-α groupthan that in GAIN/ ET group.Pretreatment ofmice with antiTNF IgG1 may completely preventthe liver injury induced by GalN/ET.CONCLUSION TNF-α can cause liver damageby inducing hepatic apoptosis and necrosis inmice with endotoxemia. | Guo Qing Zang Xia Qiu Zhou Hong Yu Qing Xie Guo Ming Zhao Bin Wang Qing Guo Yue Qin Xiang Dan Liao Department of Infectious Diseases,Rujin Hospital,Shanghai Second Medical University,Shanghai 200025,China | 2000 | World Journal of Gastroenterology2000，6，5： | 30 |
| 2 | Possible relationship between intestinal barrier function and formation of pigment gallstones in hamsters显示文摘BACKGROUND:The presence of bacteria in bile is an important factor in the formation of pigment gallstones The bile of healthy people is sterile and bacteria in the biliary system come from endogenous infection from the gut.Yet,the route of bacterial translocation into the bile duct is still unclear.Theoretically,two routes exist: one is through the intestinal barrier and the other is by direct reflux from the sphincter of Oddi.This study was undertaken to explore the relationship between the effectiveness of intestinal barrier and the formation of pigment gallstones in hamsters. METHODS:Thirty-two hamsters were divided into an experimental and a control group,with 16 hamsters in each group.A low protein and high cellulose diet was given for 6 weeks to induce the formation of pigment gallstones in the experimental group(PS)and a normal diet was given to the control group(CON).Morphological changes,changes in the levels of serum endotoxin and diamine oxidase,and changes in the numbers of B lymphocytes,plasma cells and secretory immunoglobin A(sIgA)in the intestinal mucosa were assessed after 6 weeks. RESULTS:Four hamsters died during lithogenesis and body weight decreased in the PS group.Pigment gallstones were found in 11 hamsters at the end of the experiment giving a lithogenesis rate of 91.67%.The serum endotoxin level before and after gallstone formation in the PS group was 0.2960±0.1734 U/ml and 8.2964±4.6268 U/ml respectively(P<0.05).The blood diamine oxidase level before and after gallstone formation in the PS group was 2.6333±0.8037 U/ml and 3.3642±0.9545 U/ml,respectively (P<0.05).The numbers of B lymphocytes,plasma cells and sIgA in the intestinal mucosa in the PS group were 71.56±2.89,68.65±2.09 and 27.56±1.07,respectively,and were significantly decreased compared with the corresponding values in the CON group(94.25±3.69,93.47±3.98 and 42.57±1.96,respectively,P<0.05). CONCLUSIONS:A low protein and high cellulose diet can markedly reduce intestinal barrier function and facilitate the formation of pigment gallstones.The decrease of intestinal barrier function may take part in the formation of pigment gallstones. | Fan, Ying Wu, Shuo-Dong Sun, Lei Fu, Bei-Bei Su, Yang | 2008 | Hepatobiliary & Pancreatic Diseases International2008，7，5： | 8 |
| 3 | Expression of TNF mRNA in the internal organs after severe burn injury in rats显示文摘Tumor necrosis factor(TNF) mRNA was determined with dot blotting in various viscera 24 h after severe burn injury in rats. It was found that TNF mRNA was detected in the liver, kidneys, spleen,lungs and small intestines in normal conditions. After burn in | 袁建成 肖光夏 周立新 秦孝建 黎鳌 | 1995 | Journal of Medical Colleges of PLA(China)1995，10，1： | 4 |
| 4 | Lack of new antiinfective agents: Passing into the pre-antibiotic age?显示文摘The lack of newly developed antibiotics, together with the increase in multi-resistance of relevant pathogenic bacteria in the last decades, represents an alarming signal for human health care worldwide. The number of severely infected persons increases not only in developing but also in highly industrialized countries. This relates in first line to the most severe form of a bacterial infection, sepsis and the septic shock syndrome, with high mortality on critical care units. No particular anti-sepsis drug is available, and the therapy with conventional antibiotics more and more fails to provide a survival benefit. Due to the fact that the pharmaceutical industry has withdrawn to a high degree from the development of anti-infectious agents, a huge challenge for health care is approaching in the 21 st century. In this article, these problems are outlined and possible alternatives are presented which may be helpful to solve the problem. | Klaus Brandenburg Tobias Schürholz | 2015 | World Journal of Biological Chemistry2015，6，3： | 2 |
| 5 | Potential roles of functional bacterial amyloid proteins,bacterial biosurfactants and other putative gut microbiota products in the etiopathogeny of Parkinson’s Disease显示文摘An increasing number of studies provide evidence for the existence of a microbiota-gut-brain axis and its potential involvement in the development of sporadic Parkinson’s disease and other neurodegenerative conditions.The neuropathologic hallmark of Parkinson’s disease is the presence of brain intraneuronal aggregates of misfolded alpha-synuclein,known as Lewy bodies.Some gut microbiota products may trigger alpha-synuclein conformational changes in the neurons of the enteric nervous system,which can then spread to the brain in a prion-like fashion through the vagus nerve.Others may interfere with neuroinflammatory pathways and susceptibility to neurodegeneration.In this review,we assess the potential role of putative gut microbiota products in the etiopathogeny of Parkinson’s disease,with a special emphasis on functional bacterial amyloid proteins,bacterial biosurfactants,endotoxins and short-chain fatty acids.The possible roles of molecular hydrogen,a common byproduct of bacterial fermentation,are also addressed. | EMILIA MANOLE LAURA DUMITRESCU CRISTINA NICULIȚE BOGDAN OVIDIU POPESCU LAURA CRISTINA CEAFALAN | 2021 | BIOCELL2021，45，1： | 2 |
| 6 | Changes of mucosal permeability to lipopolysaccharide in the colon of chronic alcoholic rats显示文摘ChangesofmucosalpermeabilitytolipopolysaccharideinthecolonofchronicalcoholicratsCHENXianMing,XURuiLing,MAXueHui,ZHAOYuanC... | CHEN Xian Ming, XU Rui Ling, MA Xue Hui, ZHAO Yuan Chang and HAN De Wu Department of Pathophysiology, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China | 1997 | World Journal of Gastroenterology1997，3，3： | 1 |
| 7 | Changes of pulmonary α_1-and β-adrenergic receptors after endotoxininduced acute lung injury in rats显示文摘Changes of pulmonary α1-and βadrenergic receptors (α1- ARs and β-ARs) after endotoxin-induced lung injury were dynamically observed with radioligand binding assay and the pulmonary rnicrovascular permeability and histopathology were also studied in rats to investigate the relationship between changes of pu1monary ARs and acute lung injury. It was found that the contents of both α1-ARs and β-ARs were significantly decreased after endotoxin-induced acute lung injury. On the basis of these findings, the authors inferred that the down regulation of β-ARs might be one of the factors to increase pulmonary microvascular permeability and that of α1-ARs seems to be a protective reaction. This inference might serve as the theoretical basis to treat pulmonary edema with α1-antagonists and β-agonists clinically. | 孙耕耘 毛宝龄 吕宝璋 | 1997 | Journal of Medical Colleges of PLA(China)1997，12，1： | 0 |
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