|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Dysfunction of peripheral blood dendritic cells from patients with chronic hepatitis B virus infection显示文摘AIM To identify the property of dendritic cella (DCs) of peripheral blood monocytes (PBMC) in patlents with chronic HBV infection.METHODS Twenty patients with persistent HBV infectlon were included in this study, 10 healthy subjects being used as a control group. The peripheral blood mononuclear cells (PBMC) of T cell-depleted populations were incubated and induced into mature dendritic cells in the RPMI-1640 medium in the presence of cytokines GMCSF, IL-4, FLt-3, TNF-α and 100 mL@ L-1 of fetal calf serum for a total of 10 - 12 days. The expressions of surface markers on DCs were evaluated using flow cytometric analysis. ELISA method was used to determine the cytokine levels of interleukin-12 (IL-12) and IL-10 in the supernatant produced by DCs. For detection of the stimulatory capacity of DCs to T cell proliferation,mytomycin C-treated DC were incubated with allogenic T cells.RESULTS A typical morphology of mature DCs from healthy subjects and HBV-infected patients was induced in in vitro incubation, but the proliferation ability and cellular number of DCs from HBV-infected patients significantly decreased compared with healthy individuals. In particular, the expression levels of HLADR, CD80 (B7-1) and CD86 (B7-2) on DC surface from patients were also lower than that from healthy individuals (0.46 vs 0.92 for HLA-DR, 0.44 vs 0.88 for CD80 and 0.44 vs 0. 84 for CD86, P< 0.05). The stimulatory capacity and production of IL-12 of DCs from patients in allogenic mixed lymphocyte reaction (AMLR) significantly decreased, but the production level of nitric oxide (NO) by DCa simultaneously increased compared with healthy subjects (86± 15 vs 170±22 μmoI@L 1, P<0.05).CONCLUSION The patients with chronic HBV infection have the defective function and immature phenotype of dendritic cells, which may be associated with the inability of efficient presentation of HBV antigens to host immune system for the clearance of HBV. | Fu-Sheng Wang Li-He Xing Ming-Xu Liu Chuan-Lin Zhu Hui-Gang Liu Hui-Fen Wang Zhou-Yun Lei Division of Biological Engineering,~2 Fourth Department of Liver Diseases,Beijing Institute of Infectious Diseases,Beijing Hospital of Infectious Diseases,Beijing 100039,China | 2001 | World Journal of Gastroenterology2001，7，4： | 131 |
| 2 | Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide显示文摘Hepatic ischemia-reperfusion injury(IRI) is a patho-physiological event post liver surgery or transplantation and significantly influences the prognosis of liver func-tion. The mechanisms of IRI remain unclear, and effec-tive methods are lacking for the prevention and therapy of IRI. Several factors/pathways have been implicated in the hepatic IRI process, including anaerobic metabo-lism, mitochondria, oxidative stress, intracellular cal-cium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines. The role of nitric oxide(NO)in protecting against liver IRI has recently been report-ed. NO has been found to attenuate liver IRI through various mechanisms including reducing hepatocellular apoptosis, decreasing oxidative stress and leukocyte adhesion, increasing microcirculatory flow, and enhanc-ing mitochondrial function. The purpose of this review is to provide insights into the mechanisms of liver IRI, indicating the potential protective factors/pathways that may help to improve therapeutic regimens for control-ling hepatic IRI during liver surgery, and the potential therapeutic role of NO in liver IRI. | Lian-Yue Guan Pei-Yao Fu Pei-Dong Li Zhuo-Nan Li Hong-Yu Liu Min-Gang Xin Wei Li | 2014 | World Journal of Gastrointestinal Surgery2014，6，7： | 44 |
| 3 | Molecular mechanisms of liver ischemia reperfusion injury:Insights from transgenic knockout models显示文摘Ischemia reperfusion injury is a major obstacle in liver resection and liver transplantation surgery.Understanding the mechanisms of liver ischemia reperfusion injury(IRI) and developing strategies to counteract this injury will therefore reduce acute complications in hepatic resection and transplantation,as well as expanding the potential pool of usable donor grafts.The initial liver injury is initiated by reactive oxygen species which cause direct cellular injury and also activate a cascade of molecular mediators leading to microvascular changes,increased apoptosis and acute inflammatory changes with increased hepatocyte necrosis.Some adaptive pathways are activated during reperfusion that reduce the reperfusion injury.IRI involves a complex interplay between neutrophils,natural killer T-cells cells,CD4+ T cell subtypes,cytokines,nitric oxide synthases,haem oxygenase-1,survival kinases such as the signal transducer and activator of transcription,Phosphatidylinositol 3-kinases/Akt and nuclear factor κβ pathways.Transgenic animals,particularly genetic knockout models,have become a powerful tool at elucidating mechanisms of liver ischaemia reperfusion injury and are complementary to pharmacological studies.Targeted disruption of the protein at the genetic level is more specific and maintained than pharmacological inhibitors or stimulants of the same protein.This article reviews the evidence from knockout models of liver IRI about the cellular and molecular mechanisms underlying liver IRI. | Gourab Datta Barry J Fuller Brian R Davidson | 2013 | World Journal of Gastroenterology2013，19，11： | 50 |
| 4 | Protective effects of nitric oxide on salt stress-induced oxidative damage to wheat (Triticum aestivum L.)leaves显示文摘The changes of chlorophyll and malondialde-hyde (MDA) contents, plasma membrane permeability confirmed that 0.1 and 1 mmol/L sodium nitroprusside (SNP), a donor of nitric oxide (NO) in vivo, could markedly alleviate the oxidative damage to wheat (Triticum aestivum L.) leaves induced by 150 and 300 mmol/L NaCl treatments, respectively. Further results proved that NO significantly enhanced the activities of superoxide dismutase (SOD) and catalase (CAT), both of which separately contributed to the delay of O2- and H2O2 accumulation in wheat leaves under saltstress. Meanwhile, the accumulation of proline was apparently accelerated. Therefore, these results suggested that NO could strongly protect wheat leaves from oxidative damage caused by salt stress. | Haihua Ruan Wenbiao Shen Maobing Ye Langlai Xu | 2002 | Chinese Science Bulletin2002，47，8： | 37 |
| 5 | A study on relationship of nitric oxide,oxidation,peroxidation,lipoperoxidation with chronic cholecystitis显示文摘AIM To study relationship of injury induced bynitric oxide,oxidation,peroxidation,lipoperoxidation with chronic cholecystitis.METHODS The values of plasma nitric oxide(P-NO),plasma vitamin C(P-VC),plasma vitamin E(P-VE),plasma β-carotene(P-β-CAR),plasmalipoperoxides(P-LPO),erythrocyte superoxidedismutase(E-SOD),erythrocyte catalase(E-CAT),erythrocyte glutathione peroxidase(E-GSH-Px)activities and erythrocyte lipoperoxides(E-LPO)level in 77 patients with chronic cholecystitisand 80 healthy control subjects were determined,differences of the above average values betweenthe patient group and the control group anddifferences of the average values betweenpreoperative and postoperative patients wereanalyzed and compared,linear regression andcorrelation of the disease course with the abovedetermination values as well as the stepwiseregression and correlation of the course with thevalues were analyzed.RESULTS Compared with the control group,theaverage values of P-NO,P-LPO,E-LPO weresignificantly increased(P<0.01),and of P-VC, P-VE,P-β-CAR,E-SOD,E-CAT and E-GSH-Pxdecreased(P<0.01)in the patient group.Theanalysis of the linear regression and correlationshowed that with prolonging of the course,thevalues of P-NO,P-LPO and E-LPO in the patientswere gradually ascended and the values of P-VC,P-VE,P-β-CAR,E-SOD,E-CAT and E-GSH-Pxdescended(P<0.01).The analysis of thestepwise regression and correlation indicated thatthe correlation of the course with P-NO,P-VE andP-β-CAR values was the closest.Compared withthe preoperative patients,the average values of P-NO,P-LPO and E-LPO were significantlydecreased(P<0.01)and the average values of P-VC,E-SOD,E-CAT and E-GSH-Px in postoperativepatients increased(P<0.01)in postoperativepatients.But there was no significant difference inthe average values of P-VE,P-β-CAR preoperativeand postoperative patients.CONCLUSION Chronic cholecystitis could inducethe increase of nitric oxide,oxidation,peroxidation and lipoperoxidation. | Jun Fu Zhou Dong Cai You Gen Zhu Jin Lu Yang Cheng Hong Peng Yang Hai Yu | 2000 | World Journal of Gastroenterology2000，6，4： | 36 |
| 6 | A meta-analysis of oxidative stress markers in schizophrenia显示文摘Oxidative stress has been identified as a possible element in the neuropathological processes of schizophrenia(SCZ).Alteration of oxidative stress markers has been reported in SCZ studies,but with inconsistent results.To evaluate the risk of oxidative stress to schizophrenia,a meta-analysis was conducted,including five markers of oxidative stress [thiobarbituric reactive substances(TBARS),nitric oxide(NO),catalase(CAT),glutathione peroxidase(GP) and superoxide dismutase(SOD)] in SCZ patients versus healthy controls.This study showed that TBARS and NO significantly increased in SCZ,while SOD activity significantly decreased in the disorganized type of SCZ patients.No significant effect size was found for the activities of GP and CAT in SCZ patients(P>0.05).Egger’s regression test observed no significant publication bias across the oxidative stress markers,but found high heterogeneities in all the 5 markers.The subgroup analysis suggested that the ethnicity,sample size of patients and sample sources may contribute to the heterogeneity of the results for TBARS,NO and SOD.The result further demonstrated the involvement of oxidative stress in the pathophysiology of schizophrenia. | ZHANG Ming1,2,ZHAO ZhongMing3,HE Lin1,2,4 & WAN ChunLing1,2 1 Bio-X Center,Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders(Ministry of Education),Shanghai Jiao Tong University,Shanghai 200030,China 2 Institutes for Nutritional Sciences,Shanghai Institute of Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China 3 Departments of Biomedical Informatics,Psychiatry,and Cancer Biology,Vanderbilt University Medical Center,Nashville,TN 37232,USA 4 Institutes of Biomedical Sciences,Fudan University,Shanghai 200032,China | 2010 | Science China(Life Sciences)2010，53，1： | 32 |
| 7 | Overview of cytokines and nitric oxide involvement in immuno-pathogenesis of inflammatory bowel diseases显示文摘Inflammatory bowel diseases(IBDs), including Crohn's disease and ulcerative colitis are complex disorders with undetermined etiology. Several hypotheses suggest that IBDs result from an abnormal immune response against endogenous flora and luminal antigens in genetically susceptible individuals. The dysfunction of the mucosal immune response is implicated in the pathogenesis of IBD. The balance between pro-inflammatory cytokines [tumor necrosis factor(TNF)-α, interleukin(IL)-1b, IL-8, and IL-17A], anti-inflammatory cytokines(IL-4 and IL-13), and immunoregulatory cytokines(IL-10 and transforming growth factors b) is disturbed. Moreover, evidence from animal and clinical studies demonstrate a positive correlation between an increased concentration of nitric oxide(NO) and the severity of the disease. Interestingly, proinflammatory cytokines are involved in the up-regulation of inducible oxide synthase(iN OS) expression in IBD. However, anti-inflammatory and immunoregulatory cytokines are responsible for the negative regulation of iN OS. A positive correlation between NO production and increased pro-inflammatory cytokine levels(TNF-α, IL-6, IL-17, IL-12, and interferon-γ) were reported in patients with IBD. This review focuses on the role of cytokines in intestinal inflammation and their relationship with NO in IBD. | Imene Soufli Ryma Toumi Hayet Rafa Chafia Touil-Boukoffa | 2016 | World Journal of Gastrointestinal Pharmacology and Therapeutics2016，7，3： | 30 |
| 8 | Coronary microvascular dysfunction in diabetes mellitus:A review显示文摘The exploration of coronary microcirculatory dysfunction in diabetes has accelerated in recent years.Cardiac function is compromised in diabetes.Diabetic patients manifest accelerated atherosclerosis in coronary arteries.These data are confirmed in diabetic animal mod-els,where lesions of small coronary arteries have been described.These concepts are epitomized in the classic microvascular complications of diabetes,i.e.blindness,kidney failure and distal dry gangrene.Most importantly,accumulating data indicate that insights gained from the link between inflammation and diabetes can yield predictive and prognostic information of considerable clinical utility.This review summarizes the evidence for the predisposing factors and the mechanisms involved in diabetes,and assesses the current state of knowledge regarding the triggers for inflammation in this disease.We evaluate the roles of hyperglycemia,oxidative stress,polyol pathway,protein kinase C,advanced glycation end products,insulin resistance,peroxisome proliferator-activated receptor-γ,inflammation,and diabetic cardiomyopathy as a 'stem cell disease'.Furthermore,we discuss the mechanisms responsible for impaired coronary arteriole function.Finally,we consider how new insights in diabetes may provide innovative therapeutic strategies. | Andrea Picchi Stefano Capobianco Marta Focardi | 2010 | World Journal of Cardiology2010，2，11： | 24 |
| 9 | Sevoflurane postconditioning protects against myocardial ischemia/reperfusion injury by restoring autophagic flux via an NO-dependent mechanism显示文摘Volatile anesthetics improve postischemic cardiac function and reduce infarction even when administered for only a brief-time at the onset of reperfusion.A recent study showed that sevoflurane postconditioning (SPC)attenuated myocardial reperfusion injury, but the underlying mechanisms remain unclear,in this study,we examined the effects of sevoflurane on nitric oxide (NO)release and autophagic flux during the myocardial ischemia/reperfusion (I/R)injury in rats in vivo and ex vivo.Male rats were subjected to 30 min ischemia and 2 h reperfusion in the presence or absence of sevoflurane (1.0 minimum alveolar concentration)during the first 15 min of reperfusion.We found that SPC significantly improved hemodynamic performance after reperfusion,alleviated postischemic myocardial infarction,reduced nicotinamide adenine dinucleotide content loss,and cytochrome c.release in heart tissues.Furthermore,SPC significantly increased the phosphorylation of endothelial nitric oxide synthase (NOS)and neuronal nitric oxide synthase,and elevated myocardial NOS activity and NO production.All these effects were abolished by treatment with an NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME,10 mg/kg,i.v.).We also observed myocardial I/R-induced accumulation of autophagosomes in heart tissues,as evidenced by increased ratios of microtubule:associated protein 1 light chain 3 Ⅱ/Ⅰ,upregulation of Beclin 1 and P62,and reduced lysosome-assciated membrane protein-2 expression.SPC significantly attenuated I/R- impaired autophagic flux,which were blocked by L-NAME.Moreover,pretreatment with the autophagic flUX blocker chloroquine (10 mg/kg,i.p.)increased autophagosome accumulation in SPC-treated heart following I/R and blocked SPC-induced cardioprotection.The same results were also observed in a rat model of myocardial I/R injury ex vivo,suggesting that SPC protects rat hearts against myocardial reperfusion injury by restoring I/R-impaired autophagic flux yia an NO-dependent mechanism. | Shi-gang Qiao Ying Sun Bo Sun An Wang Jia Qiu Lei Hong Jian-zhong An Chen Wang Hui-ling Zhang | 2019 | Acta Pharmacologica Sinica2019，40，1： | 21 |
| 10 | Effects of aminoguanidine on nitric oxide production induced by inflammatory cytokines and endotoxin in cultured rat hepatocytes显示文摘AIM To study the effects of aminoguanidine(AG) and two L-arginine analogues Nω-nitro-L-arginine methyl ester (L-NAME) and Nω-nitro-L-arginine (L-NNA) on nitric oxide (NO) productioninduced by cytokines (TNF-α, IL-11β, and IFN-γ)and bacterial lipopolysaccharide (LPS) mixture(CM) in the cultured rat hepatocytes, andexamine their mechanisms action.METHODS Rat hepatocytes were incubatedwith AG, L-NAME, L-NNA, Actinomycin D (ActD)and dexamethasene in a medium containing CM(LPS plus TNF-α, IL-1β, and IFN-γ) for 24 h. NOproduction in the cultured supernatant wasmeasured with the Griese reaction. IntracellularcGMP level was detected with radioimmunoasey.RESULTS NO production was markedlyblocked by AG and L-NAME in a dose-dependentmanner under inflammatory stimuli conditiontriggered by CM in vitro. The rate of themaximum inhibitory effects of L-NAME (38.9%)was less potent than that obtained with AG(53.7%, P<0.05). There was no significantdifference between the inhibitory effects of AGand two L-arginine analogues on intracellularcGMP accumulation in rat cultured hepatocytes.Non-specific NOS expression inhibitordexamethasone ( DEX ) and iNOS mRNAtranscriptional inhibitor ActD also significantlyinhibited CM-induced NO production. AG(0.1mmol.L-1) and ActD (0.2ng@Lt) wereequipotent in decreasing NO production inducedby inflammatory stimuli in vitro, and botheffects were more potent than that induced bynon-selectivity NOS activity inhibitor L-NAME(0. 1 mmol@ L- 1) under similar stimuli conditions(P | Guo Liang Zhang Ye Hong Wang Hui Ling Teng Zhi Bin Lin Department of Pharmacology,School of Basic Medical Sciences,Beijing University,Beijiog 100083,ChinaDr.Guo Liang Zhang graduated from Xinxiang Medical College in 1982,got Ph.D.at Nagoya City University Medical School,Japan in 1994,finished postdoctoral research at Beijing Medical Univcrsity in 1996,now an associate professor of pharmacology,specialized in hepatic pharmacology,having 15 papers published. | 2001 | World Journal of Gastroenterology2001，7，3： | 20 |
| 11 | Plasma endothelin and nitric oxide levels in patients with acute pancreatitis显示文摘Objective: To explore the changes of plasma endothelin(ET) and nitric oxide (NO) levels in patients with a-cute pancreatitis.Methods: The level of plasma ET was measured by ra-dioactive-immunoassay, and NO by spectrophotometry.Results: The levels of ET, NO and the ET/NO ratioin patients with severe acute pancreatitis(SAP) within24 hours in hospital were all significantly higher thanthose in other groups of patients [(176±8)pg/ml,(97±11) μmol/L, and 1.83±0.12, P<0.01]. Com-pared to healthy controls(N), the levels of ET and NOin patients without pancreatitis acute abdomen (NAP)and patients with mild acute pancreatitis (MAP) in-creased significantly (P<0.01). After appropriate treat-ment, the levels of ET and NO in the MAP groupwere lower (P<0.01). Compared with those beforetreatment, the levels of ET and NO in the SAP groupon the 3rd and 7th day in hospital dropped signifi-cantly(P<0.01).The ET/NO ratio on the 7th daywas also lower than that on admission (P<0.01).Conclusions: The malfunction of endothelial cells andthe increased ET/NO ratio may be related to the mecha-nism of pancreatic microcirculatory disturbance in pa-tients with SAP; early dynamic determination of theseparameters may help predict the prognosis of SAP. | Xiao-Hua Zeng Shi-Qin Zhu Xing-Ming Zhang Wen-Jun Luo Sheng-Wei Li From the Department of General Surgery, Second Clinical College, Chongqing University of Medical Sciences, Chongqing 400010, China | 2002 | Hepatobiliary & Pancreatic Diseases International2002，1，1： | 19 |
| 12 | Current concepts on the role of nitric oxide in portal hypertension显示文摘Portal hypertension(PHT) is defined as a pathological increase in portal venous pressure and frequently accompanies cirrhosis.Portal pressure can be increased by a rise in portal blood flow,an increase in vascular resistance,or the combination.In cirrhosis,the primary factor leading to PHT is an increase in intra-hepatic resistance to blood flow.Although much of this increase is a mechanical consequence of architectural disturbances,there is a dynamic and reversible component that represents up to a third of the increased vascular resistance in cirrhosis.Many vasoactive substances contribute to the development of PHT.Among these,nitric oxide(NO) is the key mediator that paradoxically regulates the sinusoidal(intra-hepatic) and systemic/splanchnic circulations.NO deficiency in the liver leads to increased intra-hepatic resistance while increased NO in the circulation contributes to the hyperdynamic systemic/splanchnic circulation.NO mediated-angiogenesis also plays a role in splanchnic vasodilation and collateral circulation formation.NO donors reduce PHT in animals models but the key clinical challenge is the development of an NO donor or drug delivery system that selectively targets the liver. | Liang Shuo Hu Jacob George Jian Hua Wang | 2013 | World Journal of Gastroenterology2013，19，11： | 18 |
| 13 | Progress in investigating the pathogenesis of hepatopulmonary syndrome显示文摘BACKGROUND: The pathogenesis of hepatopulmonary syndrome is complicated and remains unknown. This review aims to provide an updated knowledge about the pathogenesis of the syndrome. DATA SOURCES: Five medical databases, MEDLINE, Science-Direct, OVID, Springer Link, and Wiley InterScience were searched for articles on 'hepatopulmonary syndrome', 'cirrhosis', 'angiogenesis', 'intestinal endotoxemia', 'nitric oxide', 'carbon monoxide', and other related subjects. RESULTS: Currently, imbalance between vasodilation and vasoconstriction, intestinal bacterial translocation, intestinal endotoxemia, and activation of the lung monocyte/macrophage system may play important roles in the pathogenesis of hepatopulmonary syndrome. Recent studies found that angiogenesis is also an important factor in the pathogenesis of experimental hepatopulmonary syndrome. CONCLUSION: Angiogenesis inhibition may be a potential approach for the treatment of hepatopulmonary syndrome in the future. | Zhang, Zhao-Jie Yang, Chang-Qing | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，4： | 16 |
| 14 | Role of nitric oxide in hepatic ischemia-reperfusion injury显示文摘Hepatic ischemia-reperfusion injury (IRI) occurs upon restoration of hepatic blood flow after a period of ischemia. Decreased endogenous nitric oxide (NO) production resulting in capillary luminal narrowing is central in the pathogenesis of IRI. Exogenous NO has emerged as a potential therapy for IRI based on its role in decreasing oxidative stress,cytokine release,leukocyte endothelial-adhesion and hepatic apoptosis. This review will highlight the influence of endogenous NO on hepatic IRI,role of inhaled NO in ameliorating IRI,modes of delivery,donor drugs and potential side effects of exogenous NO. | Arunotai Siriussawakul Ahmed Zaky John D Lang | 2010 | World Journal of Gastroenterology2010，16，48： | 14 |
| 15 | Effect of nitric oxide on toll-like receptor 2 and 4 gene expression in rats with acute lung injury complicated by acute hemorrhage necrotizing pancreatitis显示文摘BACKGROUND: Toll-like receptor (TLR) 2/4 might play important roles in mediating proinflammatory cytokine synthesis and release. And nitric oxide (NO) has been used to treat acute respiratory distress syndrome (ARDS). This study aimed to investigate the changes in TLR2/4 gene expression in the lungs of rats with acute lung injury (ALI) complicated by acute hemorrhage necrotizing pancreatitis (AHNP) and the effect of NO on the TLR2/4 gene expression. METHODS: One hundred and ten SD male rats were randomly divided into sham-operated group ( n = 10) , AHNP group (n = 30) , chloroquine-treated group ( n = 30) , and L-Arg-treated group (n =40). The lungs were dissected for lung histological scoring, and bronchoalveolar lavages were harvested for lung injury indexing. TLR2/4 mRNA expression in the lungs was measured by RT-PCR. RESULTS: TLR2/4mRNA was detected in the lungs with low values in the sham-operated group (0.016±0. 210E-2, 0.112 ±0.750E-2) , but it was markedly increased at 3 hours in the AHNP group (0.787±0.751E-2, 1.512 ±1.794E-2) , peaking at 12 hours (1.113 ±6.141E-2, 2.957±2.620E-2; P <0.05 or P <0.01). When lung injuries were aggravated, TNF-α concentrations in the lungs were increased, but NO concentrations were decreased ( P < 0.05 or P < 0.01 ) . When TLR2/4mRNA was inhibited by CQ (3h: 0.313 ± 5.491E-2, 0.005 ±1.419E-3 ; 6h: 0.488 ±7.442E-2, 0.010 ± 1.518E-3; 12h: 0.883 ± 8.911E-2, 0.024 ± 2.760E-3; P< 0.05 or P <0.01) , lung injuries were relieved. NO concentrations in the lungs were increased but TNF-α concentrations were decreased (P <0. 05 or P <0.01). When the rats with AHNP were treated with L-Arg, TLR2/4mRNA expression in the lungs could be effectively inhibited (50mg-T: 0.656 ±3. 977E-2, 1. 501 ±6.111E-2; 100mg-T: 0.260± 0.891E-2, 0.732 ±5.135E-2; 200mg-T: 0.126 ±0.914E-2, 0.414 ± 1.678E-2; 400mg-T: 0.091 ±0.399E-2, 0.287 ± 0.176E-2; P <0.05 or P <0. 01) and lung injuries were relieved. At the same time, NO concentrations in the lungs were markedly increased, but TNF-α concentrations were decreased (P <0.05 or P <0.01). CONCLUSIONS: The expression of TLR2/4mRNA is increased in the lungs in rats with AHNP and lung injuries are aggravated. TLR2/4mRNA gene expression of the lungs of rats with AHNP could be markedly inhibited by NO, leading to the relief of lung injuries. | He-Shui Wu, Lei Zhang, Yan Chen, Xing-Jun Guo, Lin Wang, Jian-Bo Xu, Chun-You Wang and Jing-Hui Zhang Center of Pancreatic Surgery Laboratory of General Surgery Affiliated Union Hospital of Tongji Medical College, Hua-zhong University of Science and Technology, Wuhan 430022, China Pe-diatric Department, Affiliated Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. | 2005 | Hepatobiliary & Pancreatic Diseases International2005，4，4： | 12 |
| 16 | Enzymohistochemical study on burn effect on rat intestinal NOS显示文摘INTRODUCTION The blood irrigate flow obstruction,especially thegastrointestinal(GI)ischemia,is the main factorof the damage to the digestive tract caused byserious burns.The effect of GI ischemia on thewhole body is extensive and profound,which notonly causes the increase of intestinal permeabilityand the movement of bacteria and toxin in theintestinal cavity,but releases a large quantity ofinflammatory media.Neuroendocrine element | Wang QG He LY Chen YW Hu SL | 2000 | World Journal of Gastroenterology2000，6，3： | 12 |
| 17 | Effect of Korean red ginseng on blood pressure and nitric oxide production显示文摘AIM: To investigate the effect of crude saponin and non-saponin fraction of Korean red ginseng (KRG) on the blood pressure and nitric oxide (NO) production in the conscious rats and cultured endothelial cell line, ECV 304 cells. METHODS: Systolic blood pressure and heart rate were monitored in the conscious rats. Nitric oxide levels and the expression of nitric oxide synthase were measured by a spectrophotometric assay using Griess reagents and Western blotting, respectively. Nitric-oxide synthase activity was measured based on the conversion rate of [3H]arginine to [3H]citrulline. RESULTS: Systolic blood pressure was decreased by crude saponin (100 mg/kg, iv) of KRG in the conscious control and one-kidney, one-clip Goldblatt hypertensive (IK, 1C-GBH) rats. The hypotensive effect induced by crude saponin of KRG reached maximum at 2 - 4 min and slowly recovered after 20 min to the initial level in both groups. Crude saponin of KRG induced tachycardia in the conscious rats but induced bradycardia in the | JEON Byeong Hwa KIM Cuk Seong KIM Hoe-Suk PARK Jin-Bong NAM Ki Yeul CHANG Seok Jong | 2000 | Acta Pharmacologica Sinica2000，21，12： | 12 |
| 18 | Acute respiratory distress syndrome and lung injury: Pathogenetic mechanism and therapeutic implication显示文摘To review possible mechanisms and therapeutics for acute lung injury(ALI) and acute respiratory distress syndrome(ARDS). ALI/ARDS causes high mortality. The risk factors include head injury, intracranial disorders, sepsis, infections and others. Investigations have indicated the detrimental role of nitric oxide(NO) through the inducible NO synthase(i NOS). The possible therapeutic regimen includes extracorporeal membrane oxygenation, prone position, fluid and hemodynamic management and permissive hypercapnic acidosis etc. Other pharmacological treatments are anti-inflammatory and/or antimicrobial agents, inhalation of NO, glucocorticoids, surfactant therapy and agents facilitating lung water resolution and ion transports. β-adrenergic agonists are able to accelerate lung fluid and ion removal and to stimulate surfactant secretion. In con-scious rats, regular exercise training alleviates the endotoxin-induced ALI. Propofol and N-acetylcysteine exert protective effect on the ALI induced by endotoxin. Insulin possesses anti-inflammatory effect. Pentobarbital is capable of reducing the endotoxin-induced ALI. In addition, nicotinamide or niacinamide abrogates the ALI caused by ischemia/reperfusion or endotoxemia. This review includes historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS. | Chain-Fa Su Shang Jyh Kao Hsing I Chen | 2012 | World Journal of Critical Care Medicine2012，1，2： | 12 |
| 19 | Abnormal metabolism of nitric oxide, oxidative stress and lipoperoxidative stress in patients with acute viral myocarditis显示文摘Objective To investigate metabolic status of nitric oxide (NO) as well as oxidative and lipoperoxidative stress, pathological chain reactions of a series of free radicals, and oxidative and lipoperoxidative damages in patients with acute viral myocarditis (AVM)、 Methods Using a random paired control design, plasma levels of NO, lipoperoxides (LPO), vitamin C (VC), vitamin E (VE) and β-carotene (β-CAR), erythrocytic level of LPO as well as activities of erythrocytic superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were investigated by spectrophotometric assays in 60 AVM patients and 60 healthy adult volunteers (HAV)、 Results Compared with the HAV group, plasma NO, and LPO in plasma and in erythrocyte of the AVM group significantly increased (P=0、0001), while VC, VE, β-CAR, SOD, CAT and GSH-Px of the AVM group significantly decreased (P=0、0001)、 Compared with the AVM group before treatment, plasma NO, and LPO in plasma and in erythrocyte of the AVM group post treatment significantly decreased (P<0、05), whereas plasma VC, VE and β-CAR as well as erythrocytic SOD, CAT and GSH-Px of the AVM group post treatment significantly increased (P<0、05)、Conclusion The findings in this study suggested that in the AVM patients the metabolism of NO was disturbed, and the pathological chain reactions of a series of free radicals were severely aggravated, thus produced the oxidative damage and lipoperoxidative damages、 Therefore, we recommend that antioxidants at suitable dosage, such as VC, VE, β-CAR and others, should be given to AVM patients daily to alleviate potential oxidative and lipoperoxidative damages in their | 陈鹏 周君富 | 2001 | Chinese Medical Journal2001，，11： | 11 |
| 20 | Distribution of nitric oxide synthase in stomach myenteric plexus of rats显示文摘AIM: To study the distribution of nitric oxide synthase (NOS) in rat stomach myenteric plexus.METHODS: The distribution of NOS in gastric wall was studied in quantity and location by the NADPH-diaphorase (NDP) histochemical staining method and whole mount preparation technique.RESULTS: NOS was distributed in whole stomach wall, most of them were located in myenteric plexus, and distributed in submucosal plexus. The shape of NOS positive neurons was basically similar, most of them being round and oval in shape. But their density, size and staining intensity varied greatly in the different parts of stomach. The density was 62 -± 38 cells/mm2(antrum), 43 ± 32 cells/mm2(body), and 32 ± 28 cells/mm2 (fundus), respectively. The size and staining intensity of NOS positive neurons in the fundus were basically the same, the neurons being large and dark stained, while they were obviously different in antrum. In the body of the stomach, the NOS positive neurons were in an intermediate state from fundus to antrum. There were some beadlike structures which were strung together by NOS positive varicosities in nerve fibers, some were closely adherent to the outer walls of blood vessels.CONCLUSION: Nitric oxide might he involved in the modulation of motility, secretion and blood ciroulation of the stomach, and the significant difference of NOS positive neurons in different parts of stomach myenteric plexus may be related to the physiologic function of stomach. | Xi Peng Jin-Bin Feng Hong Yan Yun Zhao Shi-Liang Wang Institute of Burn Research,Southwest Hospital,Third Military Medical University,Chongqing 400038,China | 2001 | World Journal of Gastroenterology2001，7，6： | 11 |
您所在的机构暂未开通此部分的功能，请联系管理员