多穗柯三叶苷对脂多糖诱导小鼠炎症反应的保护作用

探讨多穗柯三叶苷对脂多糖（lipopolysaccharide,LPS）诱导的小鼠炎症反应的抗炎症作用。以3、30、300 mg/（kg·d）3 个剂量组的多穗柯三叶苷灌胃小鼠3 d后,腹腔注射0.1 mg/kg LPS,观察三叶苷预处理对LPS诱导的炎症因子表达的影响。酶联免疫反应测定小鼠血清中炎症因子肿瘤坏死因子（tumor necrosis factor-α,TNF-α）和白细胞介素-6（interleukin-6,IL-6）的含量,实时定量聚合酶链式反应法检测肝组织中TNF-α和IL-6的mRNA水平,免疫组织化学染色检测小鼠肝组织中TNF-α和IL-6蛋白水平。结果表明,3 mg/（kg·d）三叶苷剂量组可显著抑制LPS诱导的小鼠血清中TNF-α和IL-6的分泌,降低肝组织中TNF-α和IL-6的表达水平。多穗柯三叶苷对小鼠的炎症反应具有一定的保护作用。     

基于设计结构矩阵的最后计划者体系流程运行评估

最后计划者体系（Last Planner System,LPS）是一种实现精益建造的有力工具,其功能的实现依赖于流程中各活动和交互关系的良好表现,但计算计划完成百分率（the Percent Plan Complete,PPC）的方式不能满足项目管理者对整体流程的掌握。引入一种结构化建模工具——设计结构矩阵（Design Structure Matrix,DSM）帮助管理者表示、理解、管理 LPS流程。基于文件、访谈、实地调查获得的数据,结合两种 DSM 展示了 LPS 流程中活动和交互的情况并选择应用 LPS 的工程建设实例验证 DSM 对 LPS 流程运行评估的有效性。单双值 DSM 共同展示了 LPS 流程中活动和交互情况,双值 DSM 进一步求解出交互活动链,流程评估研究将为 LPS 的高效运行和精益建造管理工作提供依据     

竞争抑制ELISA法检测霍乱灭活疫苗中脂多糖的含量

目的采用竞争抑制ELISA法检测霍乱灭活疫苗中脂多糖(Lipopolysaccharide,LPS)的含量,以替代小鼠免疫力试验方法。方法用竞争抑制ELISA法检测霍乱灭活疫苗中LPS的含量,并分析与小鼠免疫力试验检测结果的一致性。结果霍乱灭活疫苗中LPS的含量与疫苗保护力呈正相关。结论采用竞争抑制ELISA法检测霍乱灭活疫苗中LPS的含量,能够反映疫苗的保护力,为进一步替代小鼠免疫力试验方法奠定了基础。     

布鲁氏菌S-2与S-19株提取的脂多糖在人布鲁氏菌病诊断抗原中的应用

目的使用脂多糖(lipopolysaccharide,LPS)提取试剂盒提取布鲁氏菌S-19与S-2菌株中的脂多糖,检测这2种脂多糖的抗原性与诊断价值。方法用工业化生产的布鲁氏菌S-19与S-2菌株菌液用LPS纯化试剂盒通过裂解、纯化、洗涤的方法提取LPS,用提取的LPS进行斑点酶联免疫吸附实验(enzyme-linked immunosorbent assay,ELISA)与布鲁氏菌病阳性、正常阴性、疱疹病、血吸虫病患者血清反应,观察反应结果并判断诊断价值。结果斑点ELISA实验结果显示从S-19与S-2株中提取的LPS与布鲁氏菌病阳性血清能作出反应,反应颜色明显,诊断价值高。结论S-19与S-2菌株中提取的LPS能与布鲁氏菌病阳性血清反应,有较好的诊断价值。     

核桃蛋白多肽对脂多糖诱导的小鼠急性肝损伤的保护作用

构建脂多糖（LPS）诱导小鼠急性肝损伤模型,研究核桃蛋白多肽（WPP）对肝损伤的保护作用。实验小鼠随机分为5组（空白对照组,LPS模型组,LPS+WPP低、中、高剂量组）,连续灌胃WPP 5周后,采用尾静脉注射LPS诱导肝损伤,检测各处理组小鼠肝脏指数、血清中谷丙转氨酶（ALT）和谷草转氨酶（AST）活性、肝组织中超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）活性、组织病理学变化以及血清中炎症因子白细胞介素IL-1β和IL-6水平。结果表明：与LPS模型组相比,WPP高剂量组肝脏指数显著降低（P<0.05）,WPP中、高剂量组小鼠血清中ALT和AST活性极显著下降（P＜0.01）,WPP低、中、高剂量组小鼠血清中IL-1β和IL-6含量极显著下降（P＜0.01）,WPP中、高剂量组小鼠肝组织中SOD活性显著升高（P<0.05）,WPP低、中、高剂量组小鼠肝组织中GSH-Px活性极显著升高（P＜0.01）;组织病理学观察发现,WPP低、中、高剂量组小鼠肝组织病理损伤明显减轻。WPP对LPS造成的小鼠急性肝损伤具有明显的保护作用。     

抗内毒素多肽对内毒素休克模型家兔的治疗作用

目的: 研究杀菌性通透性增加蛋白模拟肽(BNEP)对内毒素休克家兔重要器官功能的影响。方法: 家兔在静脉注射内毒素(LPS)500μg·kg^-1后,立即注射BNEP5mg·kg^-1,测定、分析不同时相点平均动脉压(MABP)、脉压差、血浆LPS、谷丙转氨酶(ALT)、肌酐(Cr)、肌酸磷酸激酶同工酶(CK-MB)的变化,观察8h死亡率。结果: BNEP组MABP下降速率减慢,并均在攻毒6h后恢复到攻毒前的80%以上。而LPS对照组平均动脉压、脉压差在攻毒后维持在低水平。BNEP组攻毒后各时相点血浆LPS浓度均显著低于单纯攻毒组,脉压差在2、4、6h时相点、CK-MB在4、6h时相点、Cr在6h时相点显著低于LPS组,且8h死亡率显著低于单纯攻毒组。但两组间ALT差别不显著。结论: BNEP具有较强的中和LPS能力,对内毒素休克家兔心血管系统、肾功能改善和恢复具有一定的效果。作为严重感染的辅助治疗手段可能具备较好的应用前景。     

Anti-Inflammatory Characteristics of Local Anesthetics: Inhibition of TNF-α Secretion of Lipopolysaccharide-Stimulated Leucocytes in Human Blood Samples

Background. Local anesthetics (LAs) have potent anti-inflammatory properties. Inflammatory down-regulation is crucial in diseases with overactive immune reactions, such as acute respiratory distress syndrome (ARDS) and chronic inflammation. We investigated the influence of four LAs, procaine, lidocaine, mepivacaine, and bupivacaine, on the reduction of tumor necrosis factor-alpha (TNF-α) secretion in lipopolysaccharide (LPS)-activated human leucocytes. Methods. Blood samples of 28 individuals were stimulated with LPS. The reduction of TNF-α production by each of the four LAs added (0.5 mg/mL) was measured and correlated with biometric variables. A response was defined as reduction to <85% of initial levels. Results. All four LAs down-regulated the TNF-α secretion in 44–61%: Bupivacaine (44.4%), lidocaine (61.5%), mepivacaine (44.4%), and procaine (50% of the individuals, “responders”). The TNF-α secretion was reduced to 67.4, 68.0, 63.6, and 67.1% of the initial values in responders. The effects in both patients and healthy persons were the same. Interindividual responses to LAs were not correlated with the duration or type of complaints, basal TNF-α serum level, sex, BMI, or age of responders. Conclusions. Four clinically relevant LAs (amid-LA and ester-LA) attenuate the inflammatory response provoked by LPS. They are potential candidates for drug repositioning in treating overactive immune reactions and chronic inflammation.     

Chromatin Regulator SRG3 Overexpression Protects against LPS/D-GalN-Induced Sepsis by Increasing IL10-Producing Macrophages and Decreasing IFNγ-Producing NK Cells in the Liver

We previously showed that ubiquitous overexpression of the chromatin remodeling factor SWItch3-related gene (SRG3) promotes M2 macrophage differentiation, resulting in anti-inflammatory responses in the experimental autoimmune encephalomyelitis model of multiple sclerosis. Since hepatic macrophages are responsible for sepsis-induced liver injury, we investigated herein the capacity of transgenic SRG3 overexpression (SRG3^β-actin mice) to modulate sepsis in mice exposed to lipopolysaccharide (LPS) plus d-galactosamine (d-GalN). Our results demonstrated that ubiquitous SRG3 overexpression significantly protects mice from LPS/d-GalN-induced lethality mediated by hepatic M1 macrophages. These protective effects of SRG3 overexpression correlated with the phenotypic conversion of hepatic macrophages from an M1 toward an M2 phenotype. Furthermore, SRG3^β-actin mice had decreased numbers and activation of natural killer (NK) cells but not natural killer T (NKT) cells in the liver during sepsis, indicating that SRG3 overexpression might contribute to cross-talk between NK cells and macrophages in the liver. Finally, we demonstrated that NKT cell-deficient CD1d KO/SRG3^β-actin mice are protected from LPS/d-GalN-induced sepsis, indicating that NKT cells are dispensable for SRG3-mediated sepsis suppression. Taken together, our findings provide strong evidence that SRG3 overexpression may serve as a therapeutic approach to control overwhelming inflammatory diseases such as sepsis.     

低剂量X射线照射对小鼠脾淋巴细胞丝裂原反应的影响

本实验观察了低剂量 X 射线整体和离体照射后对小鼠脾淋巴细胞丝裂原反应的影响。结果表明,X 射线全身照射后小鼠脾脏 T、B 淋巴细胞对刀豆蛋白-A(Con A)和细菌脂多糖(LPS)的反应较对照组增强,尤以75 mGy 组最为明显。在离体照射后,脾淋巴细胞对 Con A 的反应未见明显改变,而对 LPS 反应则低于对照组。提示低剂量 X 射线照射可刺激 T 细胞反应增强。