目的 研究核因子-κB激活剂1（Act1）对高糖诱导肾小管上皮细胞炎症反应及细胞外基质表达的调控作用。方法 培养肾小管上皮细胞MK2,设置对照组和高糖组,处理12 h、24 h、48 h、72 h后检测细胞中Act1的mRNA和蛋白表达水平;设置si-NC组（5.5 mmol/L葡萄糖培养基中转染NC siRNA）、si-NC+高糖组（30 mmol/L葡萄糖培养基中转染NC siRNA）、si-Act1+高糖组（30 mmol/L葡萄糖培养基中转染Act1 siRNA）,48 h后检测细胞中Act1、E-钙黏蛋白（E-cadherin）、N-钙黏蛋白（N-cadherin）、I型胶原（Col-I）、III型胶原（Col-III）的mRNA和蛋白表达水平以及培养基中肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）、干扰素-γ（IFN-γ）的含量。结果 高糖组处理12 h、24 h、48 h、72 h时细胞中Act1的mRNA和蛋白表达水平均高于对照组（P<0.05）;si-NC+高糖组处理48h时细胞中Act1、N-cadherin、Col-I、Col-III的mRNA和蛋白表达水平以及培养基中TNF-α、IL-1β、IFN-γ的含量均高于si-NC组,细胞中E-cadherin的mRNA和蛋白表达水平均低于si-NC组（P<0.05）;si-Act1+高糖组处理48h时细胞中Act1、N-cadherin、Col-I、Col-III的mRNA和蛋白表达水平以及培养基中TNF-α、IL-1β、IFN-γ的含量均低于si-NC+高糖组,细胞中E-cadherin的mRNA和蛋白表达水平均高于si-NC+高糖组（P<0.05）。结论 Act1表达增加对高糖诱导肾小管上皮细胞炎症反应激活和细胞外基质增多具有促进作用。

Objective To study the regulation effect of nuclear factors-κB activator 1（NF-κB activator 1,Act1）on high glucose induced inflammatory response and extracellular matrix expression in renal tubular epithelial cells．Methods Renal tubular epithelial cells MK2 were cultured and control group and high glucose group were set．The mRNA and protein expression of Act1 were detected after treatment for 12,24,48 and 72 hours．MK2 were divided into si-NC group（transfected with NC siRNA in 5.5 mmol/L glucose medium）,si-NC+high glucose group（transfected with NC siRNA in 30 mmol/L glucose medium）and si-Act1+high glucose group（transfected with Act1 siRNA in 30 mmol/L glucose medium）．The mRNA and protein expression of Act1,E-cadherin,N-cadherin,type I collagen（Col-I）,and type III collagen（Col-III）and the contents of tumor necrosis factor-α（TNF-α）,interleukin-1β（IL-1β）,interferon-γ（IFN-γ）in culture medium were detected．Results The mRNA and protein expression levels of Act1 in cells of high glucose group were higher than those of control group at 12 h,24 h,48 h and 72 h（P<0.05）．The mRNA and protein expression levels of Act1,N-cadherin,CoL-I,Col-III in cells and the contents of TNF-α,IL-1β,IFN-γ in culture medium of si-NC+high glucose group were higher than those of si-NC group,the mRNA and protein expression levels of E-cadherin in cells were lower than those of si-NC group at 48 h（P<0.05）．The mRNA and protein expression levels of Act1,N-cadherin,CoL-I,Col-III in cells and the contents of TNF-α,IL-1β,IFN-γ in culture medium of si-Act1+high glucose group were lower than those of si-NC+high glucose group,the mRNA and protein expression levels of E-cadherin in cells were higher than those of si-NC+high glucose group at 48 h（P<0.05）．Conclusions The increased expression of Act1 promotes the activation of inflammatory response and the increase of extracellular matrix in renal tubular epithelial cells induced by high glucose．

严重烧伤后患者免疫功能的失调,易导致创面感染、全身炎症反应综合征、脓毒症、感染性休克等并发症,增加患者病死率。免疫细胞功能适度的活化将有助于烧伤患者抵御外界病原体的侵袭、促进创面的愈合,但功能过度激活或者功能低下,则会引发一系列严重的后果。本文旨在归纳严重烧伤后中性粒细胞、单核/巨噬细胞、肥大细胞、NK细胞及T淋巴细胞等免疫细胞的功能变化与炎症反应之间的关系,为完善烧伤患者诊疗、减少并发症、改善预后提供新的思路。

The imbalance of immune function in severely burned patients can easily lead to wound infection,systemic inflammatory response syndrome,sepsis,septic shock and other complications,which increase the mortality of patients. Moderate activation of immune cell function will help burned patients to resist the invasion of external pathogens and promote wound healing,but excessive activation or low function can lead to a series of serious consequences. The purpose of this paper is to summarize the relationship between the functional changes of immune cells such as neutrophils,monocytes/macrophages,mast cells,NK cells,T lymphocytes and inflammatory reaction after severe burns,and to provide new ideas for improving the diagnosis and treatment of burned patients,reducing complications and improving the prognosis.

目的 探讨吸烟对稳定期COPD患者炎症反应和肺功能的影响。方法 选取2013年8月—2016年9月我院门诊收治的稳定期COPD患者70例为研究对象,其中吸烟35例(X1组)、不吸烟35例(X2组),另选取同期入院的不吸烟健康志愿者35例纳入健康组,采用酶联免疫吸附试验(ELISA)测定血清白介素-6(IL-6)、白细胞介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)水平,以肺功能检测仪测定三组一秒用力呼气容积(FEV1)、一秒用力呼气容积/用力肺活量比值(FEV1/FVC)、FEV1占预计值百分比(FEV1％),并采用自拟症状评分表及简明健康调查简表(SF-36)评价呼吸困难程度及生活质量。结果 X1组IL-6、IL-8及TNF-α依次为(135.27±1.24)pg/mL、(189.45±1.14)pg/mL、(39.39±1.14)pg/mL,明显高于X2组、健康组(P均<0.05);X1组FEV1(0.75±0.14)L、FEV1/FVC(3.65±1.87)％、FEV1％(3.45±0.12)％低于X2组、健康组(P均<0.05);X1组症状积分(10.17±1.02)分较X2组、健康对照组高(P<0.05),而其SF-36评分(54.27±1.46)分明显低于X2及健康组(P<0.05);X2组上述指标与健康组比较亦有统计学意义(P均<0.05)。结论 吸烟可明显增加稳定期COPD患者IL-6、IL-8、TNF-α等炎症因子水平,同时降低肺功能,临床应采取措施进行有效干预,防止患者病情恶化。

目的 探讨ε-3多不饱和脂肪酸在胃肠道肿瘤患者化疗后的胃肠道毒性及生活质量的作用。方法 在研究前经过化疗筛选,按照WHO化疗副反应在2级或者以上的50名住院的胃癌或者直结肠癌患者,随机分为对照组(单纯化疗)(n=25)和研究组(化疗加ε-3多不饱和脂肪酸)(n=25),两组的化疗方案均为化疗筛选的方案。预防性每天静脉使用ε-3多不饱和脂肪酸 200 mg,连续5天,记录评估胃肠道并发症,如恶心、呕吐和腹泻,以及KPS评分、血清白蛋白、IL-2、IFN-γ和CRP。结果 与对照组比较,恶心、呕吐和腹泻评分、IL-2、IFN-γ和CRP低于于对照组,相反,生活质量评分研究组高于对照组,差异有统计学意义(P<0.05)。结论 预防性使用ε-3多不饱和脂肪酸能够减轻胃肠道肿瘤患者化疗后的胃肠道毒性症状、降低全身炎症因子反应并改善生活质量。

Objective To explore the effect omega-3polyunsaturated fatty acid omega-3 FA on clinical manifestations of gastrointestinal toxicity and quality of life (QOL) induced by chemotherapy for patients with gastric or colorectal cancer. Methods After screening chemotherapy, Fifty patients with gastric or colorectal cancer, according to developing WHO side-effect grading system of grade 2 or higher were randomly divided into either control group (n=25) or omega-3 FAs group (n=25) during next cycle of chemotherapy. In the control group, the patients received the same chemotherapy regimens as screening cycle and in the omega-3 FA group, received chemotherapy and omega-3 FAs. Prophylactic intravenous 200 mL /d was given for 5 days. The gastrointestinal complications such as nausea,vomiting or diarrhoea and Karnofsky performance status(KPS ),IL-2,IFN-γandCRP,ect, were evaluated respectively. Results Compared with the control group, the scores of nausea vomiting and diarrhea and IL-2,IFN-γor CRP levels decreased , significantly,on the contrary, the score of QOL increased. There was significantly statistical difference (P<0.05). Conclusion Prophylactic intravenous omega-3 FA can ameliorate clinical manifestations of gastrointestinal toxicity and systemic inflammatory response syndrome(SIRS) induced by chemotherapy and improve QOL for patients with gastric or colorectal cancer.