Vascular endothelial cell(VEC) is a kind of simple squamous epithelium lined on the inner surface of blood vessels. VEC is an important barrier between the blood and tissue and it also plays a key role in regulating inflammation, thrombosis, endothelial cells mediated vasodilatation and endothelial regeneration. These processes should be controlled by a variety of complex mechanism which requires us to find out. With results of the researches in vascular endothelial cell function, the important roles that microRNA in vascular endothelial cell function draws more and more researchers' attention. MicroRNAs control gene expression in post-transcriptional level and affect the function of endothelial cells. This review focuses on the research progress on regulatory mechanism of microRNA to endothelial cell inflammation, thrombosis, vasodilation and endothelium regeneration.
目的 系统评价白细胞介素1β（IL-1β）与癫痫发作的相关性。 方法 2012年5月－2013年10月检索PubMed数据库（1985年1月－2013年7月）、Medline数据库（1985年1月－2013年7月）、中国知网（1998年1月－2013年7月）和万方数据库（1996年1月－2013年7月），并辅以谷歌学术搜索引擎进行手工检索。由两名研究者按照研究的纳入与排除标准进行病例对照研究的选择，对入选文献的质量参照“非随机对照临床试验质量评价标准与计分表”进行评价和计分，评估纳入研究的方法学质量并对有效的信息进行数据提取。然后采用RevMan 5.0统计软件进行Meta分析，以加权均数差（WMD）为效应指标。 结果 共纳入5个研究，包括82例癫痫发作的患者和471例正常对照。所纳入的研究未描述详细的抽样方法及其检测方法的特异性。Meta分析结果显示：癫痫发作72 h以内的患者与正常对照人群之间血浆IL-1β的浓度差异无统计学意义[WMD=0.04 pg/mL，95%CI（−0.07，0.16）pg/mL，P=0.46]。 结论 IL-1β可能没有直接参与癫痫的发作，而是通过与其他炎性因子之间的相互作用来实现。因此，需要进一步的研究来证明IL-1β在癫痫发作中的作用。
目的：探讨N-乙酰半胱氨酸对烫伤大鼠炎症反应的影响。方法：48只Wistar大鼠随机分为实验组和对照组，制作烫伤休克模型，伤后1小时腹腔注射生理盐水40ml/kg抗休克，实验组于抗休克盐水中加入N-乙酰半胱氨酸160mg/kg，其后足量饮水。分别于烫伤前、烫伤后8小时、16小时及24小时，处死每组各6只大鼠并立即心脏取血，采用ELISA法检测大鼠血清中TNF-a含量，于创周近头侧 0.5cm处取皮肤全层组织，在显微镜下进行中性粒细胞计数。 结果：两组大鼠血清TNF-a含量伤后显著升高，8小时达到高峰，其后逐渐下降，两组各时点比较有显著差异（P＜0.05）；创周组织中性粒细胞计数于伤后随时间延长逐渐增多，两组比较有显著性差异（P＜0.05）。 结论：N-乙酰半胱氨酸有助于降低烫伤大鼠血浆中TNF-a含量及创周组织中的中性粒细胞计数量，减轻烫伤大鼠的全身及局部炎症反应。
Objective To research the effect of ω-3 polyunsaturated fatty acid (PUFA) on inflammatory response and nutritional condition after operation for patients with gastrointestinal malignancies. Methods Forty patients with gastrointestinal malignancies were included in this study from February 1st, 2009 to June 1st, 2009. Forty cases were randomly allocated to experimental group (20 cases) and control group (20 cases). Parenteral nutrition was conducted in continuous 7 days after operation. Comparing with control group, a dose of 10 g of ω-3 PUFA was given to experimental group every day in 7 days after operation in addition. Blood samples were gained before operation, the 2nd and 8th day after operation respectively to measure relative indexes about inflammatory response (WBC, neutrophilic granulocyte and C-reaction protein) and nutrition (total protein, albumin, prealbumin, siderophilin and lymphocyte). Reduction of body mass was also recorded. Results The baseline between experimental group and control group was comparable (Pgt;0.05). The levels of indexes about inflammatory response (WBC, neutrophilic granulocytem and C-reaction protein) and nutrition (total protein, albumin, prealbumin, siderophilin and lymphocyte) between experimental and control group did not reach statistically significant difference in the 2nd day after operation (Pgt;0.05). The levels of neutrophilic granulocyte and C-reaction protein in experimental group were lower than those of control group, and the level of lymphocyte in experimental group was higher than that of control group in the 8th day after operation, and all of them reached statistical significance (Plt;0.05). There was no statistical different in reduction of body mass between experimentalgroupandcontrolgroup.Conclusion ω-3 PUFA can depress the excessively inflammatory reaction and improve the nutritional condition of patients with gastrointestinal malignancies after operation.
ObjectiveTo investigate the changes of diamine oxidase(DAO) and endotoxin(ET) during the treatment of systemic inflammatory response syndrome with human growth hormone and the relationship between human growth hormone and intestinal mucosal barrier injury. MethodsOne hundred and fortysix patients with systemic inflammatory response syndrome were randomly divided into operative group and nonoperative group, which were again randomly divided into the study group and control group.Plasma concentration of DAO and ET were determined before the treatment and 1 week after the treatment.ResultsPlasma concentration of DAO and ET in study group decreased after treatment with significant difference (P＜0.05，P＜0.01).ConclusionHuman growth hormone can protect intestinal mucosa barrier.
To evaluate the process from systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS) and probe the therapeutic strategies for elderly patients, we retrospectively studied the clinical data of SIRS and MODS in 292 elderly patients with surgical abdominal emergency. Results: On admission, the morbidity rate of SIRS was 41.1%. Afterwards the morbidity rate of MODS was 14.2%, and the mortality rate of the elderly patients with SIRS was 11.7%. After 48 hours of therapy, MODS was developed in 40.5% of the cases also with SIRS. Of all the 292 elderly patients, 19 cases (6.5%) developed MODS and 16 patients (84.2%) died. Conclusion: The outcome of the patients with surgical abdominal emergency may be improved if SIRS is early diagnosed, the cause of SIRS after 48 hours therapy is well defined and the body inflammatory response is properly regulated.
Objective To investigate the percentage of CD4+CD25+ Treg in peripheral blood of patients with severe multiple trauma and systemic inflammatory response syndrome（SIRS） and its effects on cellular immunity and secondary infection.Metheds Peripheral blood of 23 patients with severe multiple trauma was collected in 24 h after SIRS was diagnosed，and flow cytometry was used to determine the percentage of CD4+CD25+ Treg and CD4/CD8 ratio.Simultaneously，in order to explore the cell proliferation，silver staining was used to determine Ag-NORs of leukomonocyte in peripheral blood represented by IS%.In order to investigate the infection in patients，sputum and secretion sample were collected for bacteriological examination on 1 and 5 day after SIRS was established.Forty healthy volunteers were enrolled as control.Results Compared with the control，the percentage of CD4+CD25+ Treg was significant higher[（14.21±3.43）% vs（9.53±3.22），Plt;0.01] and the ratio of CD4/CD8 and IS% were significant lower in patients with severe multiple trauma[（5.94±0.66）% vs（6.74±0.95）%，（1.22±0.25）% vs（1.72±0.36）%，respectively，both Plt;0.01].In those patients（n=14） who developed secondary infection，Treg% was significant higher [（18.69±4.21）% vs（12.58±2.49）%，Plt;0.01]，while IS% and CD4/CD8 were significant lower [（5.79±0.68）% vs（6.15±0.57）%，（1.15±0.25）% vs（1.39±0.25）%，both Plt;0.01].compared to the patients without secondary infection Conlusion CD4+CD25+ Treg is valuable to estimate the cellular immunity and predict secondary infection in patients with severe multiple trauma.
Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
【摘要翻译】 一 氧化氮合酶( NOS) -2( NOS-2) 的诱导和一氧化氮产物增加是过敏性气道疾病的共同特征。严重哮喘与气道S-亚硝基硫醇减少相关。S-亚硝基硫醇是NO的生化产物, 可通过促炎症转录因子NF-κB 的S-亚硝基化抑制炎症反应。因此, 重建气道S-亚硝基硫醇对治疗可能有益。我们对此假设在以卵清蛋白诱导的过敏性炎症大鼠模型中进行验证。未使用或使用卵清蛋白致敏的动物均在卵清蛋白激发前于气管内灌注S-亚硝基谷胱甘肽( GSNO;50 μl, 10 mM) , 并在48 h 以后进行分析。GSNO 给药增加了肺组织S-亚硝基硫醇水平。与对照组比, GSNO 降低了卵清蛋白致敏动物NF-κB 的活性, 但对支气管肺泡灌洗细胞总数、分类计数及杯状细胞化生标记物均无显著影响。GSNO给药也改变了HIF-1 的活性, 导致未致敏大鼠HIF-1 活化,但抑制卵清蛋白致敏大鼠的HIF-1 活性。我们使用NOS-2基因敲除小鼠来评价内源性一氧化氮合成酶-2 在调节NF-κB和( 或) HIF-1 活性及气道过敏性炎症的作用。尽管在NOS-2 基因敲除小鼠中卵清蛋白诱导的NF-κB 活力轻度增高, 这与支气管肺泡灌洗中性粒细胞轻度增加有关, 其他的过敏性炎症指标和HIF-1 活性在NOS-2 基因敲除及野生型小鼠之间却无明显相差。总体来说, 我们的研究表明GSNO灌注能抑制气道过敏性炎症中NF-κB 活性, 但是并不能显著地影响大部分炎症及杯状细胞化生指标, 这样可能因为对其他信号通道( 比如HIF-1) 的影响而限制了它的治疗价值。【述评】 GSNO 是近年哮喘治疗研究的热点。既往的研究发现GSNO 在哮喘治疗中有一定前景。本研究却发现GSNO 气管内滴注虽能抑制过敏性气道炎症中NF-κB 活性,但并不能显著抑制气道炎症反应及杯状细胞化生这两个哮喘关键病理改变, 可能与GSNO 同时影响了HIF-1 等其他信号通路有关。该研究表明GSNO 对哮喘气道炎症治疗效果有限, 同时表明哮喘气道炎症调控机制较为复杂, 治疗药物的设计需考虑多种信号通路对哮喘气道炎症的影响。