丙丁酚对载脂蛋白E~(-/-)小鼠主动脉粥样硬化病变及病变处凝集素样氧化型低密度脂蛋白受体1表达的影响

目的观察丙丁酚对载脂蛋白E-/-小鼠主动脉粥样硬化斑块形成及主动脉凝集素样氧化型低密度脂蛋白受体1表达的影响,以探讨丙丁酚调节血脂以外的可能的抗动脉粥样硬化作用机制。方法将21只4周龄的雄性载脂蛋白E-/-小鼠随机分成基础饮食对照组、高脂饮食对照组和高脂饮食加丙丁酚组     

猪心脏移植缺血再灌注损伤中NO和NOS的表达

①目的　了解猪同种原位心脏移植术后早期一氧化氮 (NO)、一氧化氮合酶 (NOS)含量的变化 ,及其与早期缺血再灌注损伤的关系。②方法　建立猪同种原位心脏移植模型。供心在移植前低温保存 (Thomas液 ,4℃ ) 4h ,移植成功心脏复搏后 2h取材。应用组织化学方法测定心肌组织中NO、NOS的含量 ,应用核酸原位末端标记法 (TUNEL)测定心肌细胞凋亡指数 ,作为评价心肌缺血再灌注损伤的指标。以正常心肌及单纯缺血心肌组织作为对照。③结果　移植后心肌组织NO、NOS的含量较缺血组与正常组低 ,差异有显著意义 (F =2 7.2 2 9、16 .2 0 3,q =5 .716～ 6 .4 12 ,P <0 .0 1)。移植组心肌细胞凋亡指数与正常组及缺血组比较明显升高 ,差异有显著性(F =16 3.884 ,q =7.4 82、6 .975 ,P <0 .0 1)。心肌组织NO、NOS含量与心肌细胞凋亡指数呈负相关关系 (r =- 0 .886、- 0 .795 ,P <0 .0 1)。④结论　猪心脏移植后早期心肌缺血再灌注损伤所致的细胞死亡主要表现为心肌细胞凋亡 ;再灌注期间内源性NO、NOS的减少参与了心脏移植后早期缺血再灌注损伤的发生     

肠缺血/再灌注致肺损伤时肺内HO-1/CO与iNOS/NO相互作用的研究

目的观察肠缺血/再灌注(I/R)致肺损伤时肺内HO-1/CO与iNOS/NO的相互作用。方法采用肠缺血/再灌注模型。32只Wistar大鼠随机分为假手术组(Sham组)、肠缺血1 h再灌注6 h组(I/R组)、氨基胍组(AG组)和血晶素组(hemin组)。检测肺组织中HO-1和iNOS的表达,观察肺组织丙二醛(MDA)、血清一氧化氮(NO)及动脉血中氧血红蛋白(Hb-CO)的含量,同时观察肺组织病理形态学改变。结果与Sham组比较,I/R组HO-1和iNOS表达显著增强(均P<0.01);AG组HO-1和iNOS表达较I/R组明显降低(均P<0.05);Hemin组iNOS表达较I/R组明显降低而HO-1表达明显升高(均P<0.05);I/R组肺组织MDA、血清NO、血中HbCO较Sham组显著增加(P<0.05或P<0.01);与I/R组比较,AG组、Hemin组肺组织MDA、血清NO显著降低(P<0.05或P<0.01)。AG组的HbCO明显降低而Hemin组的HbCO明显升高(P<0.05)。病理学检查显示,AG组与Hemin组肺组织损伤程度较I/R组明显减轻。结论NO及CO对肠I/R肺组织具有保护作用,两者之间存在着相互作用,肺内HO-1/CO的大量生成具有使NO产生减少的作用,同时iNOS/NO的过量生成具有上调HO-1表达使CO产生增多的作用。     

Expression of inducible nitric oxide synthase induced by lipid-associated membrane proteins of Ureaplasma urealyticum is regulated by nuclear factor κB-mediated mechanism in murine macrophages

U.urealyticumisthesmallestprokaryoticorgan ismcapableofself replication.Thetinymicroor ganismcouldbeisolatedfromurogenital,placen tasandtherespiratorytractsofpreterminfants.Moreover,U.urealyticuminfectionmaybein volvedinnon specificurethritis(NSU),prostati tis,postpartumfever,infertility,pelvicinflamma torydisease,neonatalpneumoniaandevenchronic lungdisease(CLD)[1].ItisknownthatU.urealyticumlackscellwallstructureandcontains abundantmembraneproteins,butitspathogenicity isstillunknownclearly.…     

Allergic conversion of protective mucosal immunity against nasal bacteria in patients with chronic rhinosinusitis with nasal polyposis

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Blood endotyping distinguishes the profile of vitiligo from that of other inflammatory and autoimmune skin diseases

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Chromogranin A activates diverse pathways mediating inducible nitric oxide expression and apoptosis in primary microglia

Chromogranin A (CgA) is associated with microglial activation cascades implicated in neurodegeneration in Alzheimer's, Pick's and Parkinson's diseases. In primary rat microglia, CgA-mediated inducible nitric oxide (iNOS) expression, nitric oxide (NO) production, mitochondrial depolarisation and apoptosis were inhibited by PP2 (Src kinase inhibitor). CgA-mediated iNOS expression and NO production were also inhibited by U0126 (MEK inhibitor), but mitochondrial depolarisation and apoptosis were not. PP2 inhibited ERK phosphorylation; therefore, Src mediates CgA-induced ERK phosphorylation leading to iNOS expression and NO production. Glutamate release induced by CgA was independent of both pathways. These findings provide insights into the way microglia are activated by CgA and the microglial signalling mechanisms associated with neurological disorders such as Alzheimer's disease.     

Protective effect of retinoic acid on interleukin-1 beta-induced cytotoxicity of pancreatic beta-cells

Cytokines produced by immune cells in pancreatic islets infiltrating are important mediators of beta-cell destruction in insulin-dependent diabetes mellitus. In this study, the effects of retinoic acid (RA) on cytokine-induced beta-cell dysfunction were examined. RA significantly protected interleukin-1 beta (IL-1) and interferon-gamma (IFN-gamma)-mediated cytotoxicity of rat insulinoma cell (RINm5F), and also reduced in IL-1 and IFN-gamma-induced nitric oxide (NO) production, which correlated well with reduced levels of the inducible form of NO synthase (iNOS) mRNA and protein. The molecular mechanism, by which RA inhibited iNOS gene expression, appeared to involve the inhibition of NF-kappa B activation. Our results suggest possible therapeutic value of RA for the prevention of diabetes mellitus progression.