目的 观察不同剂量卡介苗核酸(Bacille Calmette-guerin DNA , BCG-DNA)在不同干预时间对哮喘小鼠气道高反应性及气道炎症的干预作用。方法 1.将Balb/c雌鼠随机分为哮喘模型组、NS对照组、BCG- DNA干预组。干预组根据干预的时间和干预制剂剂量的不同分为-7DNA1 μg、-7DNA10 μg、-7DNA100 μg、10DNA1 μg、10DNA10 μg、10DNA100 μg、17DNA1 μg、17DNA10 μg、17DNA100 μg组。2.在末次激发48小时后,测定各浓度级乙酰甲胆碱激发下的增强的呼气间歇 (Enhanced Pause, Penh)值,将其与小鼠激发前吸入NS后的Penh的百分比(Penh%NS),作为其气道反应性评价指标;其次对肺泡灌洗液进行细胞学分析。结果 1.气道反应性:①-7DNA1 μg组从Mch为3.12～50 mg/mL之间的Penh%NS显著低于哮喘组(P<0.05);②-7DNA10 μg组和-7DNA 100 μg组从Mch为6.25～25 mg/mL之间的Penh%NS显著低于哮喘组(P<0.05);③10DNA10 μg组从Mch为12.5～25 mg/mL之间的Penh%NS显著低于哮喘组(P<0.05);④10DNA100 μg组从Mch为3.12、12.5～50 mg/mL之间的Penh%NS显著低于哮喘组(P<0.05);⑤17DNA1 μg组在Mch为3.12、12.5 mg/mL的Penh%NS显著低于哮喘组(P<0.05);⑥17DNA10 μg组在Mch为12.5 mg/mL之间的Penh%NS显著低于哮喘组(P<0.05) 2.气道炎症:10DNA1 μg、-7DNA10 μg、10DNA10 μg和17DNA10 μg组的BALF细胞分类Eos%分别为:35.34±3.81、27.30±6.91、38.20±6.56、42.17±5.17;显著低于哮喘组的Eos%(48.8±6.12)(P<0.05);10DNA1 μg组的Eos%显著低于-7DNA1 μg组的Eos%(P<0.05);-7DNA10 μg组的Eos%显著低于10DNA10 μg、17DNA10 μg、-7DNA1 μg和-7DNA100 μg组的Eos%(P<0.05)。结论 BCG-DNA能降低哮喘小鼠的气道高反应性,减轻哮喘小鼠的气道炎症,早期(－7 d)中小剂量的干预效果较佳。

Objective To investigate the effect of Bacille Calmette-Guerin BCG-DNA on airway hyperresponsiveness and airway inflammation in asthmatic mouse model. Methods 1.According to different intervention, mouse were divided into asthma groups, NS control group, BCG-DNA group. According to different time and dosage intervened with asthma model, the BCG-DNA group were subdivided into -7DNA1 μg、-7DNA10 μg、-7DNA100 μg、10DNA1 μg、10DNA10 μg、10DNA100 μg、17DNA1 μg、17DNA10 μg and 17DNA100 μg group. 2.48 hours after the final incitation, the mice were stimulated with increasing concentrations of methacholine, and the airway resistance was measured. Enhance pause (Penh) was taken for each group. Bronchoalveolar lavage cytology was performed to evaluate the airway inflammation. Results 1.Airway hyperresponsiveness: ① Penh%NS of-7DNA1 μg group was significantly lower than the asthma group when Mch was 3.12~50 mg/mL (P<0.05); ② Penh%NS of -7DNA10 μg group and -7DNA100 μg group were significantly lower than the asthma group when Mch was 6.25~50 mg/mL (P<0.05);③ Penh%NS of 10DNA10 μg group was significantly lower than the asthma group when Mch was 12.5~25 mg/mL (P<0.05); ④ Penh%NS of 10DNA100 μg group was significantly lower than the asthma group when Mch was 3.12,12.5~50 mg/mL (P<0.05); ⑤ Penh%NS of 17DNA1 μg group was significantly lower than the asthma group when Mch was 3.12 or 12.5 mg/mL (P<0.05);⑥Penh%NS of 17DNA10 μg group was significantly lower than the asthma group when Mch was 12.5 mg/mL(P<0.05). 2.Airway inflammation: The Eos% of 10DNA1 μg, -7DNA10 μg,10DNA10 μg and 17DNA10 μg group (35.34±3.81、27.30±6.91、38.20±6.56、42.17±5.17) were lower than the asthma group (P<0.05); The Eos% of 10DNA1 μg group was lower than the -7DNA1 μg group (P<0.05); The Eos% of -7DNA10 μg group was lower than the 10DNA10μg, 17DNA10 μg,-7DNA1 μg and -7DNA100 μg group (P<0.05). Conclusion BCG-DNA can inhibit the airway inflammation and hyperresponsiveness in asthmatic mouse model. Early interventions with middle dose bring better results.

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 探究曲美他嗪对慢性心力衰竭患者血清炎症因子水平及心功能的影响。方法 选择2015年4月—2016年3月我院收治的慢性心力衰竭患者94例,根据随机数表法分为两组,每组47例。对照组实施阿托伐他汀治疗,观察组在此基础上予以曲美他嗪治疗。比较两组患者治疗6个月后血清炎症因子和脑利钠肽(BNP)、心功能以及临床疗效。结果 观察组血清C-反应蛋白(CRP)、BNP、肿瘤坏死因子-α(TNF-α)水平均低于对照组,差异有统计学意义(P＜0.05);观察组左收缩末期内径(LVESD)、左室舒张末期内径(LVEDd)水平较对照组明显降低,而左室射血分数(LVEF)高于对照组,差异有统计学意义(P＜0.05);观察组患者治疗有效率与对照组相比明显提高,差异有统计学意义(P＜0.05)。结论 对慢性心力衰竭患者实施曲美他嗪治疗,能有效提高患者临床疗效,降低患者血清炎症因子,改善心功能,值得临床推广与应用。

Objective To investigate the effect of Trimetazidine on serum inflammatory factors levels and cardiac function in patients with chronic heart failure (CHF). Methods 94 CHF patients admitted into our hospital from April 2015 to March 2016 were divided into two groups randomly, 47 cases in each. Control group took Atorvastatin, and on this basis observation group was given Trimetazidine. The serum inflammatory factors levels, brain natriuretic peptide (BNP), cardiac function and clinical efficacy of two groups after treatment for 6 months were compared. Results The serum C-reactive protein (CRP), BNP, Tumor necrosis factor-α (TNF-α) levels of observation group were lower than control group (P<0.05); The left ventricular end-systolic diameter (LVESD), Left ventricular end-diastolic diameter (LVEDd) levels of observation group significantly decreased compared with control group, but left ventricular ejection fraction (LVEF) was higher than control group (P<0.05); The curative effective rate of observation group significantly increased compared with control group (P<0.05). Conclusion Trimetazidine for treating CHF patients may effectively increase clinical efficacy, decrease serum inflammatory factors and improve cardiac function, which is worthy of clinical promotion and application.

目的 了解异鼠李素对LPS刺激下THP-1细胞炎症因子IL-6、MCP-1、TNF-α释放的影响及其抗炎特征。方法 用PI单染色法检测其细胞存活率;用ELISA法检测THP-1细胞炎症因子IL-6、MCP-1、TNF-α释放。结果 不同浓度的LPS均能使炎症因子IL-6释放增高,且24 h及48 h间水平无差异,但随着LPS刺激浓度的增高,细胞的坏死数量也会随之升高;不同浓度的异鼠李素能在不同时间点不同程度地抑制炎症因子MCP-1、TNF-α、IL-6的释放。结论 异鼠李素能抑制LPS刺激下THP-1细胞炎症因子IL-6、TNF-α、MCP-1的释放,并呈浓度依赖性。

Objectives Our study is aim to investigate the influence of the isorhamnetin on the releasing of inflammatory factor cytokines of the THP-1 cells. Methods PI single staining method was used to detect the cell survival rate. ELISA was used to detecte the concentrations of inflammatory cytokines(MCP-1、IL-6、TNF-α). Results The concentration of IL-6 in THP-1 cells were increased after stimulated with LPS and there no difference between the 24 h group and 48 h group. The survival rate of THP-1 cells decreased as the concentration of LPS increased.The isorhamnetin in different concentration could inhibit the secretion of inflammatory cytokines in different time. Conclusion It is found in our study that isorhamnetin may inhibit the secretion of MCP-1, IL-6, TNF-α in THP-1 cells stimulated by LPS in a concentration dependent way.

目的 研究孟鲁斯特治疗哮喘的临床疗效及其对患者Th1/Th2细胞免疫平衡和相关炎症因子水平的影响。方法 选取哮喘患者68例随机分为对照组31例及观察组37例,对照组予以常规糖皮质激素吸入治疗,观察组在此基础上加服孟鲁斯特。用药3个月后流式细胞仪检测两组患者外周血Th1、Th2数量变化,ELISA定量外周血IL-4及IFN-γ含量变化并作临床效果评定。结果 两组患者经治疗后,外周血Th1/Th2比例均升高,IL-4/IFN-γ细胞因子水平下降,但观察组较对照组变化更为明显,差异有统计学意义(P＜0.01)。疗效方面,观察组总有效率94.59%,高于对照组的74.19%,差异具有统计学意义(P＜0.01),同时两组均未见明显不良反应。结论 哮喘患者加用孟鲁斯特具有明显免疫调节功能,使Th1/Th2水平趋于平衡,作为哮喘辅助治疗药物疗效确切。

目的 对晚期非小细胞肺癌(NSCLC)患者进行回顾性分析,探讨参一胶囊维持治疗对患者炎症因子的影响。方法 经参一胶囊联合化疗一线治疗后取得缓解或稳定的37名晚期NSCLC患者意向性分为治疗组(A组,21人)和对照组(B组,16人)。A组继续服用参一胶囊每天2次,每次20 mg,服药至疾病进展或无法耐受;B组未予特殊治疗。分别于第1 d、90 d采血,检测白细胞计数、中性粒细胞计数、C反应蛋白、肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、白细胞介素1α(IL-1α)、白细胞介素6(IL-6)和白细胞介素10(IL-10)。结果 治疗前后比较,治疗组各项炎症指标均未发生明显变化(P>0.05);而对照组的TNF-α、IL-1β、IL-6上升(P值分别为<0.001、0.032、0.001),IL-10下降(P=0.035);治疗后两组间比较,对照组TNF-α、IL-1β、IL-6上升(P值分别为<0.001、0.001、0.004),IL-10则下降(P=0.002)。两组间IL-1α及白细胞计数、中性粒细胞计数、C反应蛋白无变化(P>0.05)。结论 参一胶囊维持治疗可使晚期NSCLC患者TNF-α、IL-1β及IL-6的低表达,提示调节炎症反应可能是参一胶囊维持治疗抑制NSCLC进展的机制之一。

Objective To retrospectively investigate the influence of Shenyi Capsule maintenance therapy on inflammatory factors in patients with advanced NSCLC. Methods Thirty seven patients with advanced NSCLC, who had become palliative or stable after first-line treatment with combined Shenyi capsule chemotherapy, were intentionally assigned to treatment group (group A, 21 patients) and control group (group B, 16 patients). Shenyi capsule was given to group A (20mg p.o., bid) until appearance of deterioration or intolerance, while no special treatment was given to group B. Leukocytes, neutrophils, C-reactive protein, tumor necrosis factor α (TNF-α), interleukin-1β(IL-1β), interleukin-1α (IL-1α),interleukin-6(IL-6) and interleukin-10(IL-10) were tested by blood specimens taken respectively on 1st day and 90th day. Results There were no statistical differences (P>0.05) between the level of inflammatory factors on 1th day and 90th day in treatment group. In control group, however, TNF-α、IL-1β and IL-6 increased (P<0.001, P=0.032、P=0.001 respectively) and IL-10 decreased significantly (P=0.035). Furthermore, the level of TNF-α、IL-1β and IL-6 in treatment group were also higher (P<0.001, P=0.001, P=0.004 respectively), while IL-10 was lower (P=0.002)than control group on 90th day. There were no statistical differences(P>0.05)between the two groups in the level of IL-1α, leukocyte, neutrophils or C reactive protein on 1th day and 90th day. Conclusion Shenyicapsule maintenance therapy could lower the expression of TNF-α、IL-1β and IL-6 in patients with advanced NSCLC, which indicates that the regulation of inflammatory reaction may be one of the mechanisms of inhibition from NSCLC progression in Shenyi capsule maintenance therapy.

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.

目的 观察并评估内毒素性急性肺损伤大鼠吸入一氧化氮后外周血中内皮祖细胞和炎症介质的变化情况。方法 90只SPF级健康大鼠分为3组,A组为正常对照组(n=30),B组为急性肺损伤组(ALI)(n=30), C组为一氧化氮(NO)组(n=30)。分别计算各组外周血内皮祖细胞(Endothelial progenitor cells,EPCs) 数量,同时监测肺组织中白细胞介素-10(Interleukin-10,IL-10)水平和髓过氧化物酶(Myeloperoxidase,MPO)活性。结果 我们成功建立了大鼠的ALI肺损伤模型, C组EPCs数量、MPO活性上升幅度均小于B组、而IL-10上升水平均高于B组,差异有统计学意义(P<0.05)。结论 大鼠吸入一氧化氮可减轻内毒素所致急性肺损伤程度,其机制可能与外周血中内皮祖细胞数量及MPO水平下降和IL-10水平上升有关。

Objective To investigate the effect of nitric oxide(NO) inhalation in endotoxin-induced acute lung injury mice. Methods Ninety SPF mice were randomly assigned to the normal group(group A), ALI group(group B)and ALI+NO group(group C). The number of endothelial progenitor cells was counted and the level of Interleukin-10(IL-10) and myeloperoxidase (MPO) were measured. Results Endotoxin administration resulted in pulmonary edema. The pulmonedema was lightened and the level of MPO were decreased by the inhalation of nitric oxide while the level of IL-10 increased. Conclusion NO inhalation can mitigate acute lung injure. The decline of EPCs and MPO and the increase of IL-10 may be one of the mechanism.

目的 水解乳清蛋白对炎症性肠病大鼠的抗炎作用及机制。方法 将40只雄性大鼠随机分为实验组和对照组,并建立炎症性肠病动物模型,分别喂食添加了水解乳清蛋白及普通蛋白的饲料,喂养4周后处死大鼠,每周检测体重,血清ALB、TNF-α、IL-2、IL-6等。结果 二组间体重及血清白蛋白无区别(P>0.05),实验组与对照组的TNF-α、IL-2及IL-6无区别(P>0.05),从第二周到第四周,实验组的炎症因子水平低于对照组(P<0.05)。结论 水解乳清蛋白具有抗炎作用,能够减少炎症性肠病大鼠动物模型的炎症因子的释放,并改善其营养状况。

Objective To evaluate the anti-inflammatory effects of whey protein on SD rats model of inflammatory bowel disease. Methods 40 SD rats model of inflammatory bowel disease were established and randomly divided into experimental and control groups equally. Experimental and control groups were fed whey protein and ordinary protein respectively. After 4 weeks, TNF-α, IL-2 and IL-6 were detected. Results There were no significant difference between the two groups of weights and the level of ALB. The level of TNF-α, IL-2 and IL-6 between groups were not significantly different in the first week(P>0.05). However, thelevels of TNF-α, IL-2 and IL-6 in experimental group were significantly lower than those of the control group in the follow weeks. Conclusion The whey protein could reduce the production of inflammatory cytokines.

       目的   研究SOCS6/STAT6通路在前列腺细胞炎性增殖作用中的调控作用。方法  使用人前列腺细胞株RWPE-1建立炎症模型，将细胞分为对照（CON）组和炎症刺激（INF）组，后者通过添加脂多糖（LPS）模拟炎症环境。采用ELISA检测白细胞介素-1β（IL-1β）-1β、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）表达水平，蛋白免疫印迹法检测细胞因子信号抑制物-6（SOCS6）、信号转导和转录激活因子-6（STAT6）及磷酸化STAT6蛋白的表达水平。结果  经过LPS处理后，RWPE-1细胞中的SOCS6蛋白表达水平显著下降（P＜0.01），而磷酸化STAT6表达水平上升（P＜0.01）。结论  SOCS6/STAT6通路可能通过调节炎症环境下STAT6的磷酸化水平，参与调节前列腺细胞的炎性增殖作用。

       Objective   To explore the  regulatory  role of  SOCS6/STAT6  pathway in the inflammatory  proliferation of 

prostate cells．Methods  The human prostate cell line RWPE-1 was used to establish an inflammation model．Cells were divided into a control（CON）group and an inflammation-stimulated（INF）group，with the latter subjected to lipopolysaccharide（LPS）treatment to simulate an inflammatory environment．The expression levels of interleukin（IL）-1β、IL-6 and  IL-8 were detected by ELISA，and the expression levels of suppressor of cytokine signaling 6（SOCS6），signal transducer and activator oftranscription-6，（STAT6），and phosphorylated STAT6 proteins were detected by Western blot．Results  The  results showed that after LPS treatment，the expression of SOCS6 protein in RWPE-1 cells significantly decreased，while the expression of phosphorylated STAT6 increased．Conclusions  The SOCS6/STAT6 pathway may be involved in  regulating the inflammatory proliferation of prostate cells by modulating the phosphorylation level of STAT6 under inflammatory conditions．