Background. Lung cancer (LC) is the leading cause of malignancy-related mortalities globally, and the existing treatment interventions are associated with harmful side effects. In the current study, we evaluated the anti-tumor efficiency of nerolidol (NRD) on human non-small cell lung cancer (NSCLC) cells. Objectives. Nerolidol is a sesquiterpene alcohol extracted from the essential oils of aromatic flora with known anti-cancer activities. Materials and methods. The latent action of NRD on antiproliferative and apoptotic effects in A549 cells is uncertain. Thus, our work is designed to explore the antiproliferative and apoptotic actions of NRD (20 and 25 mu M/mL) against A549 cells. The activity of NRD on A549 cell cytotoxicity, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), apoptosis, anti-apoptotic proteins, and MAPK/ TAT3/NF-kappa B and P13K/AKT signaling pathways were assessed using MTT tests, dichlorodihydrofluorescein diacetate (DCFH-DA), dual acridine orange/ethidium bromide (AO/EB), DAPI, Rh-123, reverse transciption polymerase chain reaction (RT-PCR), and western blot analyses. Results. We found that NRD could inhibit NSCLC cell viability through elevated intracellular ROS and MMP loss and elicited apoptosis in a quantity-dependent manner. Similarly, NRD can reduce inflammatory cytokines and anti-apoptotic elements, as well as trigger apoptotic signaling pathways. Conclusions. Our data established that NRD decreases A549 cell proliferation through ROS-mediated apoptosis, triggering the MAPK/STAT3/NF-kappa B and P13K/AKT pathways, suggesting that NRD is a possible protective remedy for NSCLC.

Background: The cigarette smoking epidemic is one of the desperate threats experienced all over the world. Cigarettes cause diseases such as chronic obstructive pulmonary disease (COPD), asthma, lung cancer, stroke, heart diseases, etc. Paclobutrazol is a growth regulator hormone that increases antioxidant enzymes, mineral absorption, carbohydrate synthesis, and flowering and fruit production in plants. Objective: In the current study, we assessed the ameliorative effect of paclobutrazol against chronic cigarette smoke-induced COPD in rats. Methodology: A side-stream cigarette exposure rat model was used for the study, which is a well-accepted model to evaluate cigarette smoke-induced lung damage. The paclobutrazol treatment was given for 12 weeks, and since the reduction in body weight is the primary symptom of COPD, the food efficiency and the weight gain were measured. Muscular strength was analyzed with a grip strength test, and respiratory functions were assessed with a whole-body plethysmograph. Plasma leptin was measured to detect the fat mass index. C-reactive protein was quantified to assess the level of inflammation. Further bronchoaleveolar fluid was collected and analyzed for the total white blood cell count, neutrophils, lymphocytes, and monocytes to evaluate the inflammation. In order to confirm the anti-inflammatory property of paclobutrazol against cigarette smoke-induced lung inflammation, histopathological analysis of lung tissue was done. Results: The paclobutrazol treatment increased the body weight, improved respiratory func-tions, and decreased inflammation in the rats exposed to secondhand cigarette smoke. Our results of histopathological analysis confirm that paclobutrazol has effectively inhibited cigarette smoke -induced lung tissue damage in young Wistrar rats. Conclusion: Hence, it can be used as a supplementary drug to protect smokers from cigarette smoke-induced lung damage. (c) 2023 The Authors. Published by Elsevier B.V. on behalf of King Saud University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

In this study, we have investigated the chemopreventive role of 6-shogaol (6-SGL) on benzopyrene (BaP) exposed lung carcinogenesis by modulating PRDX1-associated oxidative stress, inflammation, and proliferation in Swiss albino mouse models. Mice were exposed to BaP (50 mg/kg b.wt) orally twice a week for four consecutive weeks and maintained for 16 weeks, respectively. 6-SGL (30 mg/kg b.wt) were orally administered to mouse 1 h before BaP exposure for 16 weeks. After the experiment's termination, 6-SGL (30 mg/kg b.wt) prevented the loss in body weight, increased lung weight, and the total number of tumors in the mice. Moreover, we observed that 6-SGL treatment reverted the activity of BaP-induced lipid peroxidation and antioxidants in mice. Also, 6-SGL impeded the phosphorylation of MAPK family proteins such as Erk1, p38, and Jnk1 in BaP-exposed mice. PRDX1 is an essential antioxidant protein that scavenges toxic radicals and enhances several antioxidant proteins. Overexpression of PRDX1 substantially inhibits MAPKs, proliferation, and inflammation signaling axis. Hence, PRDX1 is thought to be a novel targeting protein for preventing BaP-induced lung cancer. In this study, we have obtained the 6-SGL treatment in a mouse model that reverted BaP-induced depletion of PRDX1 expression. Moreover, pretreatment of 6-SGL (30 mg/kg b.wt) significantly inhibited enhanced proinflammatory cytokines (TNF-α, IL-6, IL-β1, IL-10) and proliferative markers (Cyclin-D1, Cyclin-D2, and PCNA) in BaP-exposed mice. The histopathological studies also confirmed that 6-SGL effectively protected the cells with less damage. Thus, the study demonstrated that 6-SGL could be a potential phytochemical and act as a chemopreventive agent in BaP-induced lung cancer by enhancing PRDX1 expression.

Objective: To explore the role of NLRP3 in mucus hypersecretion in asthmatic patients. Methods: From January 2020 to June 2022, 90 patients with asthma and 60 healthy patients under the Department of Pulmonary and Critical Care Medicine of the First Affiliated Hospital of Xi’an Medical University were selected. Immunohistochemistry and enzyme-linked immunosorbent assay were performed. NLRP3 inflammasome and mucins MUC5AC and MUC5B levels in lung tissue and sputum were detected. Results: Compared to the healthy control group, the asthma group had significantly higher sputum MUC5A (20.12 ± 5 .07 versus 36.21 ± 6.13) and NLRP3 (72.31 ± 15.13 versus 119.21 ± 31.21) levels (P < 0.05) but lower MUC5B levels (1.35 ± 0.12 versus 0.53 ± 0.11, P < 0.05). Immunohistochemistry showed that NLRP3, MUC5AC, and MUC5B expressions were consistent with the sputum results. Conclusion: NLRP3 and MUC5AC levels are significantly increased in asthmatic patients, whereas MUC5B levels are reduced in these patients. They can be used as targets for the diagnosis and treatment of asthma.

目的 总结肺炎克雷伯杆菌侵袭性感染(KPII)的临床特点.方法 对29例KPII患者的临床资料作回顾性分析.结果 29例KPII患者中,社区感染16例、医院感染13例,年龄(74.4±14.7)岁,均伴基础疾病.29例KPII患者中,肺炎23例、泌尿道感染19例、血流感染12例、结石性胆囊炎4例、皮肤感染2例、肾脓肿1例、脑膜炎1例、肝脓肿1例、腹膜炎1例.白细胞总数升高14例、中性粒细胞比例升高22例、PCT升高27例、CRP升高升高26例、电解质紊乱21例、肝功能异常28例、肾功能异常16例、凝血功能异常27例.29例KPII患者的分离菌株中25例耐药,其中社区感染的16例KPII患者分离菌株中12例耐药,医院感染的13例KPII患者分离菌株均耐药.所有患者均采用抗菌药物治疗,其中β-内酰胺/β-内酰胺酶抑制剂复方制剂药物治疗者23例、碳青霉烯类治疗者17例、氨基糖苷类药物治疗者6例、替加环素者6例,有13例患者采用联合抗菌药物方案治疗.患者治疗后,24例康复出院,5例死亡.结论 KPII好发于伴基础疾病的中老年人群,常见感染部位为肺部、泌尿道、血液及胆道,常伴白细胞总数升高、降钙素原升高、CRP升高、电解质紊乱、肝肾功能异常、凝血功能异常,耐药率高,治疗需根据药敏结果精准选取抗菌药物.

目的 分析吸烟的慢性阻塞性肺疾病(COPD)患者嗜酸性粒细胞(EOS)、C反应蛋白(CRP)、黏蛋白5AC(MUC5AC)水平变化与肺功能的关系.方法 选取2020年1月—2021年5月西安医学院第一附属医院呼吸与危重症科收治吸烟COPD患者120例(COPD组),按病情严重程度分为轻度亚组40例、中度亚组50例、重度亚组30例;另选取同期健康体检者100例作为健康对照组.比较各组EOS、CRP、MUC5AC水平,COPD各亚组患者第1秒用力呼气容积(FEV1)、用力肺活量(FVC)、FEV1占预计值的百分比(FEV1％)、FEV1/FVC水平,采用Pearson相关系数分析EOS、CRP、MUC5AC水平与FEV1、FVC、FEV1％、FEV1/FVC水平的相关性,Logistic回归分析EOS、CRP、MUC5AC水平对患者预后的影响.结果 COPD组患者EOS、CRP、MUC5AC水平均高于健康对照组(t=15.336、48.020、28.218,P均<0.001),重度亚组>中度亚组>轻度亚组(F=11.157、177.486、72.013,P均<0.001).FEV1、FVC、FEV1％、FEV1/FVC水平比较,重度亚组<中度亚组<轻度亚组(F=8.730、28.376、53.665、38.847,P均<0.001).Pearson相关分析显示,EOS、CRP、MUC5AC水平与FEV1、FVC、FEV1％、FEV1/FVC水平均呈负相关(EOS:r/P=-0.352/0.035、-0.458/0.029、-0.674/0.012、-0.658/0.014;CRP:r/P=-0.725/<0.001、-0.384/0.031、-0.658/0.021、-0.612/0.025;MUC5AC:r/P=-0.674/0.012、-0.721/0.002、-0.584/0.024、-0.624/0.027).EOS、CRP、MUC5AC高水平均是影响COPD患者预后的独立危险因素[HR(95％CI)=1.037(1.002～1.053)、5.403(1.245～9.561)、5.150(3.028～7.272)].结论 吸烟的COPD患者EOS、CRP、MUC5AC水平均升高,其水平随着COPD患者病情程度的加重而升高,且与肺功能呈负相关.

目的 探讨淡豆豉提取物对肺癌细胞增殖、迁移和侵袭的影响及作用机制.方法 设置不同浓度淡豆豉提取物组(100μg/ml、200μg/ml、400μg/ml)、对照组(无淡豆豉提取物)、si-NC组、si-miR155HG组、miR-NC组、miR-409-3p组、淡豆豉提取物+pcDNA组、淡豆豉提取物+pcDNA-miR155HG组.qRT-PCR检测miR-409-3p和miR155HG的表达水平;West-ern印迹检测蛋白表达;四甲基偶氮唑蓝(MTT)比色法检测细胞增殖抑制率;Transwell检测细胞侵袭和迁移;双荧光素酶报告实验检测miR155HG和miR-409-3p的靶向关系.结果 相较于对照组,不同浓度淡豆豉提取物组肺癌细胞A549的增殖抑制率升高,迁移和侵袭数量降低,miR-409-3p表达水平升高,miR155HG表达水平降低(均P<0.05).miR155HG可靶向负调控miR-409-3p的表达.抑制miR155HG表达或miR-409-3p过表达均抑制A549细胞增殖、迁移和侵袭(均P<0.05).miR155HG过表达逆转了淡豆豉提取物对肺癌A549细胞的作用.结论 淡豆豉提取物可抑制A549细胞的增殖、迁移和侵袭,其机制可能与调控miR155HG/miR-409-3p的表达有关.

目的 探究人类白细胞抗原复合体(HCG)11对肺癌细胞增殖、迁移、侵袭的影响和机制.方法 实时荧光定量-聚合酶链反应(qRT-PCR)检测46例肺癌组织样本和与其配对的癌旁组织样本中HCG11和miR-1297的表达.以肺癌细胞A549为研究对象,建立过表达HCG11的细胞株,四甲基偶氮唑蓝(MTT)比色法检测细胞活力,Transwell法检测细胞迁移和侵袭能力,Western印迹检测细胞周期蛋白(Cyclin)D1、P21、E-钙黏附蛋白(E-cadherin)和基质金属蛋白酶(MMP)-2蛋白表达情况.双荧光素酶报告实验和Western印迹验证HCG11和miR-1297的靶向关系.结果 与癌旁组织比较,肺癌组织中HCG11的表达显著下调,miR-1297的表达显著上调(均P<0.05).过表达HCG11可显著抑制CyclinD1和MMP-2蛋白表达,促进P21和E-cadherin表达,抑制A549细胞增殖、迁移和侵袭(均P<0.05).miR-1297是HCG11的靶基因,HCG11可负性调控miR-1297的表达.过表达miR-1297可逆转HCG11对A549细胞增殖、迁移和侵袭的抑制作用.结论 HCG11通过靶向下调miR-1297表达可抑制肺癌细胞增殖、迁移和侵袭.

目的 探讨B7-H1、B7-H4和滤泡辅助性T细胞(Tfh)在小细胞肺癌中的表达及与肺癌预后的关系.方法 选取2014年1月至2017年10月间西安医学院第一附属医院收治的82例小细胞肺癌患者.所有患者均经手术、化疗或放疗等综合疗法,病理资料齐全,检测放化疗前B7-H1、B7-H4和Tfh细胞在小细胞肺癌中的表达水平.单因素分析患者临床病理关系,Logistic回归分析探讨B7-H1、B7-H4和Tfh细胞对肺癌预后的影响.结果 82例小细胞癌患者中,B7-H1阳性表达有68.3％(56/82);B7-H4阳性表达有41.5％(34/82).外周血Tfh细胞与CD4+T细胞占比为(2.94±0.31)％.单因素结果显示,小细胞癌中位生存时间与患者性别、年龄、肿瘤分期、手术、体质量下降、肺炎、症状至治疗时间、低电解质、B7-H1、B7-H4和Tfh细胞等有关,差异均有统计学意义(均P<0.05).Cox回归分析显示,广泛期、男性、B7-H1阳性、B7-H4阳性和Tfh细胞升高等5项参数是小细胞癌患者死亡的独立危险因素,差异均有统计学意义(均P<0.05).结论 性别、肿瘤分期、B7-H1、B7-H4及Tfh细胞等参数是小细胞癌患者死亡的独立危险因素,而B7-H1、B7-H4和Tfh细胞可用于预测和评估小细胞癌预后情况,值得临床进一步研究并推广.

目的 通过回顾性分析肺癌患者的临床、实验室及随访资料,探讨淋巴细胞绝对计数(ALC)与肺癌侵袭性及患者预后的关系.方法 收集98例确诊为肺癌且未接受过任何抗肿瘤治疗患者的临床资料,分析ALC与肺癌侵袭性及患者预后的关系.结果 根据外周血ALC平均值将患者分为对照组(ALC≥1.29×109/L,n=48)及研究组(ALC<1.29×109/L,n=50).与研究组相比,对照组具有较低的TNM临床分期、较少的远处转移及较长的总生存期(OS).结论 与肺癌ALC低者相比,ALC高者肿瘤侵袭性低且生存期较长.ALC可作为肺癌患者预后的一个独立预测指标.

目的 探讨纤维支气管镜肺泡灌洗诊疗术联合振动排痰对呼吸机相关性肺炎(VAP)患者的影响.方法 选取2018年3月-2019年3月西安医学院第一附属医院ICU收治的VAP患者88例,采用随机数字表法分为对照组和观察组,每组44例.在常规治疗基础上,对照组患者给予纤维支气管镜肺泡灌洗诊疗术治疗,观察组患者在对照组治疗基础上给予振动排痰治疗;两组患者均持续治疗1周.比较两组患者临床疗效、机械通气时间、抗菌药物应用时间、ICU入住时间,治疗前后呼吸功能指标〔包括气道峰值吸气压力(PIP)、气道阻力(RAW)、呼吸做功(WOB)、动态肺顺应性(CLdyn)〕、动脉血气分析指标〔包括动脉血氧分压(PaO2)、动脉血氧饱和度(SaO2)、氧合指数(OI)、动脉血二氧化碳分压(PaCO2)〕,并观察两组患者治疗期间不良反应发生情况.结果 (1)观察组患者临床疗效优于对照组(P<0.05).(2)与对照组比较,观察组患者机械通气时间、抗菌药物应用时间、ICU入住时间缩短(P<0.05).(3)观察组患者治疗前PIP、RAW、WOB、CLdyn与对照组相似,差异无统计学意义(P>0.05);与对照组比较,观察组患者治疗后PIP、RAW、WOB降低,CLdyn升高(P<0.05).(4)观察组患者治疗前PaO2、SaO2、OI、PaCO2与对照组相似,差异无统计学意义(P>0.05);与对照组比较,观察组患者治疗后PaO2、SaO2、OI升高,PaCO2降低(P<0.05).(5)治疗期间两组患者不良反应发生率比较,差异无统计学意义(P>0.05).结论 纤维支气管镜肺泡灌洗诊疗术联合振动排痰治疗VAP患者的临床疗效确切,能有效缩短患者机械通气时间、抗菌药物应用时间及ICU入住时间,改善患者呼吸功能及缺氧状态,且安全性较高.

目的 探索基于呼吸治疗团队教学的以问题为基础的教学法(problem based learning,PBL)在全科住院医师规范化培训中的应用.方法 呼吸系统以老年人慢性疾病为主,是全科医学生教育的重要环节.开展PBL教学法的教学探索,以期达到对全科医师的专科疾病培训,使其理解并掌握相关疾病知识,能适应未来医学发展和社会需要,为患者提供更好的社区医疗服务.结果 PBL教学法的精髓是发挥问题对学习过程的指导作用,调动学生学习的积极性和主动性,整体提升学生的综合素质和能力.结论 在全科医学规范化培训教学中运用PBL教学,带教老师以任务为主线、以学员为主体进行引导,可极大的提高学生的学习兴趣、主动性以及自学能力,从而培养学员的分析问题、解决问题的能力.可以更好的帮助学员形成以患者为中心的临床诊断思路、提高解决临床问题的综合能力及团队合作能力.

BackgroundCircular RNAs (circRNAs) participate in the development of human cancers by regulating multiple cell processes. CircRNA antisense to the cerebellar degeneration‐related protein 1 transcript (circCDR1as) expression is dysregulated in many cancers, including non‐small‐cell lung cancer (NSCLC). However, the mechanism by which circCDR1as mediates the development of NSCLC remains unknown.MethodsA total of 30 paired cancer and normal tissues were collected from patients with NSCLC. The expression levels of circCDR1as, microRNA (miR)‐219a‐5p and Sex determining region Y‐box protein 5 (SOX5) were measured in tissues or cells by quantitative real‐time polymerase chain reaction or western blot. Cell viability, apoptosis, migration and invasion were detected by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide, colony formation, flow cytometry and transwell assays, respectively. The target relationship between miR‐219a‐5p and circCDR1as or SOX5 was validated by dual‐luciferase reporter assay.ResultsCircCDR1as expression was elevated in NSCLC tissues and cells in comparison to the matched controls. Interference of circCDR1as led to obvious inhibition of cell viability, migration and invasion and increase of apoptosis in NSCLC cells. MiR‐219a‐5p acted as a target of circCDR1as and miR‐219a‐5p downregulation attenuated the regulatory effect of circCDR1as silencing on NSCLC progression. Moreover, miR‐219a‐5p targeted SOX5 to repress the progression of NSCLC in vitro. Besides, circCDR1as knockdown reduced the expression of SOX5 by increasing miR‐219a‐5p level.ConclusionKnockdown of circCDR1as inhibited the progression of NSCLC by decreasing cell viability, migration and invasion and increasing apoptosis by upregulating miR‐219a‐5p and downregulating SOX5.

Background: Temperature and air pollution has been reported to be associated with respiratory diseases. However, little is known about these effects on healthy people, and the potential interaction between the two factors is still uncertain. This study aims to estimate the effects of air pollution combined with temperature on lung function in healthy people. Methods: The lung function of 428 healthy people was measured in Xi’an, Shaanxi province of Northwest China in summer and winter. Meanwhile, the daily concentrations of air pollution and temperature were obtained from monitoring stations. Statistical analyses were assessed by generalized estimating equations (GEEs). Results: In winter, Every 10μg/m 3 increase of PM 2.5 concentration, PEF change amount is -0.015L/S(-0.028,-0.002), FEV1 is -0.007 L/S(-0.012,-0.001). The change is -0.022(-0.043,-0.001) and -0.010(-0.011,-0.009) after adjusting for SO 2 . In summer, PEF and FEV1 were were negatively correlated with the concontration of O3. We also found that temperature weaken the adverse effect of PM 2.5 on lung PEF in winter but aggravated effect of O3 on FEV1 in summer. Lag effects showed that Lag0 of FEV1, FEV1/FVC and FEF25-75% were more strongly associated with PM 2.5 . Conclusions: Our findings indicate that Lung function was significantly negative correlated with O3 in summer and PM 2.5 in winter, and a higher temperature has a greater impact on lung function in both summer and winter in Xi’an.

Kartagener综合征是一种临床罕见的常染色体隐性遗传性疾病,发病率极低,主要表现为支气管扩张、慢性鼻窦炎、内脏反位三联征,电镜下纤毛超微结构联合光镜下纤毛功能检查是目前临床诊断Kartagener综合征的"金标准".本文报道了两例完全型Kartagener综合征患者并进行了文献复习,为进一步提高临床对该病的诊治水平提供参考.

目的 探讨基于呼吸治疗团队的以案例为基础的教学模式在全科住院医师规范化培训中的实施效果.方法 选择2016年9月-2018年9月在某院呼吸内科进行轮转的全科规培医师共86人为研究对象,随机分为A、B两组.A组43人由呼吸内科医师带教,B组43人由呼吸内科医师和呼吸治疗师共同指导,选用5个案例对两组规培医师进行多批次的以案例为基础的教学法,出科前进行基础理论及呼吸机操作考核,并采用调查问卷方式评价教学效果.结果 规培医师理论及实践考核成绩B组明显高于A组,差异均有统计学意义(t=8.528、5.670,P＜0.05);教学满意度调查结果显示规培医师对以案例为基础教学法的总体满意率为87.2％(675/774),其中满意度最高的是“教学形式”和“提高解决问题能力”,满意率均为97.7％ (84/86),满意率最低的是“增加医学人文知识”和“提高医患沟通能力”,满意率分别为69.8％ (60/86)和70.9％ (61/86).两组规培医师对带教老师的满意率无统计学意义(=0.622,P=0.430).结论 规培医师对呼吸治疗团队以案例为基础的教学法满意度高,学习效果好,积极性高,有助于提高临床思维及提高解决临床问题的能力,教学效果良好.

目的 观察吸烟对慢性阻塞性肺疾病(COPD)稳定期患者外周血及支气管肺泡灌洗液中CD8+T细胞含量的影响.方法 选取自2014年5月至2018年1月在我院收治的COPD缓解期患者,按照吸烟情况将其纳入非吸烟COPD组、吸烟COPD组、戒烟COPD组,每组均为50例,另选取50例健康体检者纳入健康组.4组均于入院首日抽取外周静脉血5 mL,检测其中CD3+、CD4+及CD8+T细胞水平;采血完成后,采用纤维支气管镜行肺泡灌洗术取4组患者的支气管肺泡灌洗液,检测其中CD3+、CD4+及CD8+T细胞水平.结果 非吸烟COPD组、吸烟COPD组及戒烟COPD组的肺功能预测值(FEV1)、病程、疾病程度及合并症均基本一致(P>0.05).与健康组比较,非吸烟COPD组、吸烟COPD组及戒烟COPD组患者血清及支气管肺泡灌洗液中CD3+、CD4+T细胞及CD4+/CD8+比值均明显降低(P<0.05),而CD8+T细胞均明显增高(P<0.05).与吸烟COPD组比较,健康组、非吸烟COPD组及戒烟COPD组患者血清及支气管肺泡灌洗液中CD3+、CD4+T细胞及CD4+/CD8+比值均明显增高(P<0.05),而CD8+T细胞均明显降低(P<0.05).结论 吸烟的COPD缓解期患者肺部及全身均存在CD8+等T淋巴细胞异常变化,而戒烟可有效改善COPD患者肺部及全身CD8+T淋巴细胞功能紊乱.

Objective To investigate the role of Wnt/β-catenin pathway in regulating allergic airway inflammation in asthmatic mice.Methods We induced dendritic cells (DCs) from bone marrow of BALB/c mice,and then treated the cells with LiCl and PKF118-310,separately.We observed the morphological features of DCs under light microscope.Mixed lymphocyte reaction (MLR) was used to observe the functional changes of DCs.Western blot was used to detect the expressions of GSK-3β and β-catenin at the protein level.We established a mouse asthma model by using ovalbumin (OVA),and then treated these mice with LiCl and PKF118-310.The total number of cells and eosinophil percentage in BALF were determined.The lungs of mice were observed by HE staining to evaluate the degree of allergic inflammation.The cytokines in BALF and spleen cells supernatant were assayed by enzyme-linked immunoassay (ELISA),and the total IgE in the serum was also measured by ELISA.The protein expression levels of GSK-3β and β-catenin in lung tissue were assayed by Western blot.Results ① The DCs treated with LiCl promoted the proliferation of allogeneic T lymphocytes in MLR more weakly than those treated with PKF118-310 (P＜0.01).② The GSK-3β protein expression level of DCs treated with LiCl was significantly lower than DCs treated with PKF118-310.In contrast,the β-catenin protein expression of DCs treated with LiCl was higher than that of DCs treated with PKF118-310 (P ＜ 0.01).③ The total number of cells and eosinophil percentage in BALF were significantly increased in the experimental group compared with those in the control group (P＜0.01).There was also a significant difference between LiCl group and PKF118-310 group (P＜0.01).④ In the three experimental groups,the severity of inflammation in the lungs of LiCl group was weaker than that in PKF118-310 group (P＜0.05).⑤ Compared with that in the normal control group,IL-4 in BALF and spleen cell culture supernatant of the experimental group was significantly higher while IFN-γ was the opposite (P＜0.01).LiCl group had the lowest level of IL-4 and the highest level of IFN-γ;PKF groups was the opposite (P＜0.05).⑥ The total IgE in serum was significantly increased in the experimental group compared with the control group (P＜0.01).There was also a significant difference between LiCl group and PKF118-310 group (P＜0.05).⑦ GSK-3β protein expression was significantly lower in LiCl group than in PKF118-310 group (P＜0.05),while β-catenin protein expression was significantly higher in LiCl group than in PKF118-310 group (P＜0.05).Conclusion LiCl and PKF118-310 can affect the severity of asthma by regulating Wnt/β-catenin signal pathway and the expressions of GSK-3β andβ-catenin protein,which provides a new direction for asthma treatment.

Objectives: Asthma is a chronic inflammatory, heterogeneous airway disease affecting millions of people around the world. Curcumin has been found to have anti-inflammatory and antifibrosis effects. Researchers reported that curcumin regulated Wnt/beta-catenin signaling in lots of cells. However, whether curcumin regulates the levels of Wnt/beta-Catenin signaling in lung tissues and DCs (dendritic cells) remains unclear. In this study, we assessed the effects of curcumin on DCs and asthma. Methods: C57BL/6 mice immunized with OVA (ovalbumin) were challenged thrice with an aerosol of OVA every second day for 8 days. Dexamethasone or curcumin was administered intraperitoneally to OVA-immunized C57BL/6 mice on day 24 once a day for 9days. Mice were analyzed for effects of curcumin on asthma, inflammatory cell infiltration and cytokine levels in lung tissue. DCs were isolated from mouse bone morrow. The surface markers CD40, CD86 and CD11c of DCs was detected by FACS (fluorescence activated cell sorting) and the function of DCs was detected by mixed lymphocyte reaction. The expression of GSK-3 beta and beta-catenin was detected by Western Blot. Results: Results showed that OVA increased the number of inflammatory factors in BALF (bronchoalveolar lavage fluid), elevated lung inflammation scores in mice. Curcumin dose-dependently reversed the alterations induced by OVA in the asthmatic mice. Curcumin activated Wnt/beta-catenin signaling pathway in DCs and asthmatic mouse lungs. Conclusions: Curcumin could influence the morphology and function of DCs, ease asthma symptom and inflammatory reaction through the activation of Wnt/beta-catenin signaling. These results provide new evidence new evidence for application of curcumin on asthma.

Objective To investigate the changes of the levels of interleukin 6(IL-6)and interleukin 8(IL-8)in the pathogenetic process of acute respiratory distress syndrome(ARDS). Methods We enrolled 50 ARDS patients who were admitted into the Department of Respiratory and Critical Care Medicine of the First Affiliated Hospital of Xi'an Medical University from December 2010 to February 2013. The patients were divided into cure group(30 patients)and a non - survival group(20 patients). The levels of serum IL-6 and IL-8 were measured on day 1 after admission and right before discharge for cure group and were also measured right before death for non - survival group. We also enrolled 50 healthy subjects as control group,and the levels of serum IL-6 and IL-8 were detected. SPSS 19. 0 statistical software was employed to conduct statistical treatment. Results ARDS group was higher(P ﹤ 0. 01)than control group in the levels of serum IL-6〔(2. 1 ± 1. 8)ng/ L vs. (1. 1 ± 0. 2)ng/L〕and IL-8〔(639. 6 ± 98. 3)ng/ L vs. (415. 9 ± 56. 8) ng/ L〕. Non - survival group was higher(P ﹤ 0. 01)than cure group in the levels of serum IL-6〔(3. 8 ± 0. 2)ng/ L vs. (1. 8 ± 0. 4)ng/ L〕and IL-8〔(687. 8 ± 70. 2)ng/ L vs. (493. 9 ± 71. 7)ng/ L〕,and cure group and non - survival group were all higher(P ﹤ 0. 01) than control group in the two levels. Conclusion The levels of serum IL-6 and IL-8 play an important role in the development of ARDS,and the non - survival group is significantly higher in the level of serum IL-6 and IL-8.