简介：Kappa是1916年在意大利西北部成立的意大利运动休闲服装公司,它的前身是一家叫m.c.t.的小型公司,m.c.t.一直默默耕耘,成绩并不突出。直至60年代,m.c.t.推出＂robedikappa＂等全新品牌,并重新定位,再配合创新宣传,才迅速取得空前的成功。

简介：从2005年底只有1．47亿元的销售收入，到2009年很有可能突破40亿元的市场规模，Kappa究竟做了什么？

简介：向来擅长与不同领域Artists合作的意大利知名时尚运动品牌Kappa此次再度与华语乐坛摇滚实力唱将“信”和国内著名影视明星苗圃携手。激情诠释Kappa的运动、时尚、性感和品位。

简介：欧洲杯战罢，夏日中充斥着足球场上飞扬的热情。7月16日下午5点．FEIGEGAMES桌上足球联赛在北京工体南门美高美俱乐部正式开幕。FEIGEGAMES将后欧洲杯的热情带进酒吧．倡导互动娱乐的“戒独”精神．让你在桌面足球台上叱咤风云。

简介：NuclearfactorkappaB(NF-κB)isoneofthebest-characterizedtranscriptionfactorsplayingimportantrolesinmanycellularresponsestoalargevarietyofstimuli,includinginflammatorycytokines,phorbolesters,growthfactors,andbacterialandviralproducts.TheaimofthisstudyistodemonstrateNF-κBexpressioninthemousecochleaanditsenhancementinresponsetolipopolysaccharides(LPS)andkanamycin(KA)treatment.MethodsKAtreatmentconsistedofsubcutaneousKAinjectionsat700mg/kgtwiceadaywithaneight-hourintervalbetweenthetwoinjectionsfor3or7days.ForanimalsintheLPStreatmentgroup,asingledoseof0.3mgLPSdissolvedin0.2mlsterilesalinewereinjectedintobothbullaethroughthetympanicmembraneandkepttherefor3hours.Animalsinthecontrolgroupreceivedsubcutaneoussalineinjectionfor7days.Followingimmmunohistochemichalprocessingwithrabbitpolyclonalanti-NF-κBp65antibodies,cryosectionsofthecochleawereexaminedforexpressionofNF-κBp65invariousstructuresinthecochlea.ResultsNF-κBp65expression,identifiedbypresenceofbrownreactionproductscharacteristicofDABimmunohistochemistry,wasvisibleinthespiralligament,spiralprominence,tectorialmembrane(TM),spiralganglionandnervefibers.RelativelyweakNF-κBp65expressionwasalsovisualizedintheorganofCorti.WithintheorganofCorti,theinnerhaircells(IHC),outerhaircells(OHC),innerpillarcells(IP),outerpillarcells(OP),Deiter'scells(DC),andBoettcher'scellsexhibitedstrongerstainingthantheinnersulcuscells,Hensen'scells(HC)andClaudius'cells.NoNF-κBp65expressionwasseeninthenucleusoftheIHCandOHC.NF-κBp65expressionwasincreasedinanimalsexposedtoLPSorKA,demonstratingsignificantdifferencesinthestainingbetweencontrolanimalsandLPS/KA-treatedanimals.NF-κBp65expressionwasnotsignificantlydifferentbetweenLPStreatedandKAtreatedanimalsorbetween3and7daysinKA-treatedanimals.Conclusio

简介：KAPPA通过这一波传播活动，宣称要领导一个新的“混搭”潮流，这可能就是一厢情愿了，一则所有的传播并没有太多的新东西，二来，这种什么都要的欲望，很可能让它陷入什么都不是的境地。

简介：摘要目的：研究近视患者双眼暗视至明视状态下Kappa角水平偏移量及垂直偏移量的变化规律。方法：横断面研究。选取2020年11月至2021年12月在宁夏医科大学总医院门诊近视中心明确诊断为近视的患者，并采用单纯随机抽样的方法抽取120例（240眼），采用博士伦Orbscan II角膜地形图仪分别于暗视及明视条件下进行检查，记录明暗视下瞳孔直径大小、Kappa角的大小及水平偏移量和垂直偏移量。采用配对t检验比较左右眼在暗视和明视下的瞳孔直径和Kappa角大小；采用散点分布图分析双眼在明暗视下Kappa角的象限分布。结果：左右眼在暗视状态下的瞳孔直径均明显大于明视状态下的瞳孔直径，差异有统计学意义（t=13.67，P<0.001；t=13.48，P<0.001）。暗视与明视状态下左眼的Kappa角均大于右眼的Kappa角，差异有统计学意义（t=4.15，P=0.021；t=5.27，P=0.008）。由暗视转向明视状态时，双眼Kappa角的分布呈现镜像对称，水平方向主要向鼻侧位移，垂直方向主要向上方位移。右眼矢量位移（0.168±0.100）mm，左眼矢量位移（0.171±0.069）mm；87.5%右眼矢量位移小于0.3 mm，92.5%左眼矢量位移小于0.3 mm，绝大多数近视患者的矢量位移在0.3 mm以内。结论：从暗视至明视状态下，随着瞳孔缩小，近视患者的Kappa角分布主要向鼻上方位移。

简介：2月24日,Kappa-华谊兄弟2009年战略联盟发布会在北京千禧大酒店举行。在此次发布会上,世界知名运动时尚品牌Kappa和顶级娱乐传媒集团华谊兄弟宣布强强联手,2009年,双方将在影视歌等多个领域进行广泛合作。此外,华谊兄弟还正式宣布了其对中乾龙德进行并购的消息,当天的发布会同时也举行了原中乾龙德旗下艺人集体加盟

简介：考试抄袭是最常见，也是最难识别的作弊方式。本文介绍了Kappa统计的原理。并以具体数据对如何识别考试抄袭进行了实证模拟。结果显示，通过运用Kappa统计量能够有效地识别考试抄袭，为“雷同卷”的判断提供了统计学证据。

简介：Kappa在延续以往绚丽多彩风格的夏天推出的系列网球服更突出了清爽透亮的颜色及渐变条纹感觉.

简介：10月8日,国家网球中心外围球场。天蓝色的挡板上,中网巨型LOGO闪耀其上,来自全国六大赛区的128名选手挥汗激战,场边的拉拉队高声欢呼。这项与中网有着千丝万缕关联的业余赛事,从2009年扬帆起航,经历短短两年的时间,开始显示其超强的生命力,正与中网这项亚洲顶级赛事一起,共同构建中国网球的繁华图景。

简介：摘要目的探讨Kappa角大小对飞秒激光小切口角膜基质透镜取出术(SMILE)前后全眼高阶像差(HOA)的影响。方法采用系列病例观察研究方法，纳入2015年4月至2016年5月在天津市眼科医院屈光手术中心行SMILE手术的近视及近视散光患者98例98眼，均选取右眼进行研究。测量患者术前及术后1个月、3个月的裸眼视力(UCVA)、球镜度及柱镜度；采用Pentacam眼前节分析系统测量术前Kappa角大小；采用WaveScan波阵面像差仪测量术前及术后各时间点的全眼像差。比较手术前后UCVA、屈光度及各项HOA；采用Pearson线性相关分析评估Kappa角大小与各项HOA之间的关系。根据Kappa角的范围及分布情况，将Kappa角位移距离≥0.20 mm的34眼作为较大Kappa角组，在位移距离<0.20 mm的64眼中随机选取34眼作为较小Kappa角组，比较不同Kappa角组手术前后各项HOA的差异。结果术前、术后1个月及3个月，患者UCVA(LogMAR视力)分别为0.06±0.23、-0.03±0.07和-0.05±0.07，总体比较差异有统计学意义(F＝779.330，P<0.001)，其中术后1个月及3个月UCVA均优于术前，差异均有统计学意义(均P<0.001)。术眼手术前后球镜度、柱镜度和等效球镜度(SE)总体比较差异均有统计学意义(F＝1 107.811、127.786、1 191.266，均P<0.001)，其中术眼术后各时间点球镜度、柱镜度和SE较术前均明显降低，差异均有统计学意义(均P<0.001)。手术前后总HOA、球差、彗差、第3阶像差(S3)、第4阶像差(S4)、第5阶像差(S5)、第6阶像差(S6)总体比较差异均有统计学意义(F＝75.915、78.231、66.186、64.521、97.161、36.623、28.852，均P<0.001)，其中术后各时间点总HOA、球差、彗差、S3、S4、S5和S6均较术前明显增大，差异均有统计学意义(均P<0.05)。术后1个月及3个月Kappa角大小与总HOA、彗差、S3均呈正相关(总HOA：r＝0.357、0.363，均P<0.001；彗差：r＝0.310、0.341，均P<0.01；S3：r＝0.343、0.371，均P<0.01)。手术前后不同大小Kappa角组患者总HOA、彗差、S3总体比较，差异均有统计学意义(F分组＝3.363、4.277、4.029，均P<0.05)，其中术后1个月及3个月，较大Kappa角组总HOA、彗差及S3均大于较小Kappa角组，差异均有统计学意义(均P<0.05)。结论较大的Kappa角在SMILE术中可能会引入更多的高阶像差。

简介：从纯carrageenans获得的Oligo-carrageenans(OC)从海洋的红水藻提取了由在烟草植物和桉树类树提高光合作用和基础新陈代谢刺激生长。另外，OC刺激第二等的新陈代谢，增加涉及对病原体的防卫的代谢物的水平。在这个工作，我们在高度的增加以后分析了OCkappa的效果，在涉及碳，氮和硫吸收的基础新陈代谢酶的活动，ribulose1,5biphosphatecarboxylase/oxygenase(rubisco)，glutamate脱氢酶(GDH)和O-acetylserinethiol-lyase(OASTL)，并且在支持生长的荷尔蒙，植物生长素吲哚醋酸(IAA)和在松(Pinusradiata)的赤霉素GA3,的水平，树在1和5的集中与OC对待kappa?mg?mL在1点与OCkappa对待的松?mg?mL1在高度显示出类似的增加，但是显示一更高比在5点与OCkappa对待的那些在IAA和GA3的全部的叶绿素，rubisco的活动，GDH和OASTL和水平增加了?mg?mL1。因此，OCkappa刺激生长和基础新陈代谢并且在松树上增加支持生长的荷尔蒙的水平，主要在1点?mg?mL1。

简介：鲜明的活动主题、运动时尚的品牌文化，强大的明星阵容、新颖的对抗方式、构成了2010Kappa杯文体明星对抗赛的丰富内涵。2010年8月11日，在北京奥园高尔夫俱乐部进行的这场对抗赛以尊崇礼仪、分享友谊、品味时尚为主题，采用4人2球赛的比赛方式，让文体大腕们不再“单打独斗”，不仅比拼球技，还要比拼对高尔夫礼仪和规则的理解与运用，同时更是考验了团队的团结与食作精神和作风。

简介：摘要目的：通过术前对高度近视并发白内障患者行Kappa角测定，从而评估Kappa角对高度近视并发白内障患者行区域折射多焦点人工晶状体（MIOL）植入术后视觉质量的影响。方法：回顾性系列病例研究。收集2018年10月至2019年10月因高度近视并发白内障于潍坊市眼科医院行白内障超声乳化抽吸联合区域折射MIOL植入术的患者53例（53眼），年龄42~66（52.2±6.3）岁。根据患者术前测量的Kappa角，即视轴与瞳孔中心的距离（r），将患者分为A组（0<r≤0.182 mm）27例（27眼）和B组（0.182 mm<r≤0.5 mm）26例（26眼）。术后随访3个月并记录2组患者视力，通过客观视觉质量分析仪（OQASII）评估患者客观视觉质量，同时以问卷调查方式记录患者术后脱镜率以及光晕、眩光等视觉不良症状。组间数据比较采用独立样本t检验或t'检验、χ2检验或Fisher确切概率法。结果：术后3个月，2组间患者的裸眼远视力（UCDVA）、裸眼中视力（UCIVA）、裸眼近视力（UCNVA）及最佳矫正远视力（BCDVA）、最佳矫正中视力（BCIVA）、最佳矫正近视力（BCNVA）差异均无统计学意义。A组客观散射指数值为2.11±1.05，B组为2.89±1.24，组间差异有统计学意义（t=-2.48，P=0.016）。A、B组患者的调制传递函数截止频率分别为（32.2±13.3）c/deg和（26.4±11.2）c/deg，2组差异无统计学意义。2组患者在100%、20%、9%对比度下的模拟对比度视力（OV）差异均无统计学意义。此外，2组患者术后的脱镜率和眩光发生率差异亦无统计学意义，但B组光晕发生率高于A组（x2=4.44，P=0.047）。结论：Kappa角对高度近视并发白内障患者行区域折射MIOL植入术后的远、中、近视力无影响，但Kappa角较大的患者术后的客观视觉质量较低，同时Kappa角增大可能引起光晕等视觉不良症状。

简介：AbstractBackground:Vascular endothelial dysfunction is considered a key pathophysiologic process for the development of acute lung injury. In this study, we aimed at investigating the effects of unfractionated heparin (UFH) on the lipopolysaccharide (LPS)-induced changes of vascular endothelial-cadherin (VE-cadherin) and the potential underlying mechanisms.Methods:Male C57BL/6 J mice were randomized into three groups: vehicle, LPS, and LPS + UFH groups. Intraperitoneal injection of 30 mg/kg LPS was used to induce sepsis. Mice in the LPS + UFH group received subcutaneous injection of 8 U UFH 0.5 h before LPS injection. The lung tissue of the mice was collected for assessing lung injury by measuring the lung wet/dry (W/D) weight ratio and observing histological changes. Human pulmonary microvascular endothelial cells (HPMECs) were cultured and used to analyze the effects of UFH on LPS- or tumor necrosis factor-alpha (TNF-α)-induced vascular hyperpermeability, membrane expression of VE-cadherin, p120-catenin, and phosphorylated myosin light chain (p-MLC), and F-actin remodeling, and on the LPS-induced activation of the phosphatidylinositol-3 kinase (PI3K)/serine/threonine kinase (Akt)/nuclear factor kappa-B (NF-κB) signaling pathway.Results:In vivo, UFH pretreatment significantly attenuated LPS-induced pulmonary histopathological changes (neutrophil infiltration and erythrocyte effusion, alveolus pulmonis collapse, and thicker septum), decreased the lung W/D, and increased protein concentration (LPS vs. LPS + UFH: 0.57 ± 0.04 vs. 0.32 ± 0.04 mg/mL, P = 0.0092), total cell count (LPS vs. LPS + UFH: 9.57 ± 1.23 vs. 3.65 ± 0.78 × 105/mL, P= 0.0155), polymorphonuclear neutrophil percentage (LPS vs. LPS+ UFH: 88.05% ± 2.88% vs. 22.20% ± 3.92%, P = 0.0002), and TNF-α (460.33 ± 23.48 vs. 189.33 ± 14.19 pg/mL, P = 0.0006) in the bronchoalveolar lavage fluid. In vitro, UFH pre-treatment prevented the LPS-induced decrease in the membrane expression of VE-cadherin (LPS vs. LPS + UFH: 0.368 ± 0.044 vs. 0.716 ± 0.064, P = 0.0114) and p120-catenin (LPS vs. LPS + UFH: 0.208 ± 0.018 vs. 0.924 ± 0.092, P = 0.0016), and the LPS-induced increase in the expression of p-MLC (LPS vs. LPS + UFH: 0.972 ± 0.092 vs. 0.293 ± 0.025, P = 0.0021). Furthermore, UFH attenuated LPS- and TNF-α-induced hyperpermeability of HPMECs (LPS vs. LPS + UFH: 8.90 ± 0.66 vs. 15.84 ± 1.09 Ω·cm2, P = 0.0056; TNF-α vs. TNF-α + UFH: 11.28 ± 0.64 vs. 18.15 ± 0.98 Ω·cm2, P = 0.0042) and F-actin remodeling (LPS vs. LPS + UFH: 56.25 ± 1.51 vs. 39.70 ± 1.98, P = 0.0027; TNF-α vs. TNF-α + UFH: 55.42 ± 1.42 vs. 36.51 ± 1.20, P = 0.0005) in vitro. Additionally, UFH decreased the phosphorylation of Akt (LPS vs. LPS + UFH: 0.977 ± 0.081 vs. 0.466 ± 0.035, P = 0.0045) and I kappa B Kinase (IKK) (LPS vs. LPS + UFH: 1.023 ± 0.070 vs. 0.578 ± 0.044, P = 0.0060), and the nuclear translocation of NF-κB (LPS vs. LPS + UFH: 1.003 ± 0.077 vs. 0.503 ± 0.065, P = 0.0078) in HPMECs, which was similar to the effect of the PI3K inhibitor, wortmannin.Conclusions:The protective effect of UFH against LPS-induced pulmonary endothelial barrier dysfunction involves VE-cadherin stabilization and PI3K/Akt/NF-κB signaling.

简介：AbstractBackground:Head and neck cancers (HNCs) are a heterogeneous group of tumors that progress owing to varied enviromental and genetic risk factors. Viral infections are threatening and adept at altering the expression of cellular transcription factors such as nuclear factor kappa B (NF-κB) and deregulation of other cellular proteins like NF kappa B inhibitor alpha (IκBα). The present study was conducted to detect high-risk genotypes of human papillomavirus (HPV) and protein expression of NF-κB signaling pathway in HNC patients with HPV infection.Methods:For HPV detection, genomic DNA from 152 HNC tumors was extracted formalin-fixed paraffin-embedded tissue DNA kit. For genotyping, polymerase chain reaction (PCR) using a general primer, HPV type-specific primers and agarose gel electrophoresis were performed. Immunohistochemistry (IHC) was also performed on 4-μm thick tissue sections using HPV E6 monoclonal antibody. Protein expression analysis of NF-κB signaling pathway including p50, p65, and IκBα was performed using IHC.Results:PCR analysis showed that 24.3% (37/152) of HNC cases were HPV positive. Among HPV positive, 86.5% (32/37) were tobacco users, while among HPV negative, 66.9% (77/115) were tobacco users. A significant association of HPV positivity and tobacco user was observed by univariate analysis [P < 0.01; odds ratio (OR): 0.310, 95% confidence interval (CI): 0.110 to 0.870]. More HPV positive patients were with poor oral hygiene (78.3%) when compared with patients with good oral hygiene (21.6%) [P < 0.03, OR: 2.440, 95% CI: 1.650 to 3.600]. The results of the logistic regression analysis showed that age, tobacco use and oral hygiene are significant predictors (P < 0.02). PCR and IHC staining results confirmed that HPV16 was predominant among HNC cases (64.8%) when compared with HPV18 (35.2%). Expression of NF-κB proteins (p50, p65, and IκBα inhibitor) were also observed in HPV and non-HPV infected HNC tissues. IHC expression of p50, and p65 showed nuclear staining, while IκBα inhibitor showed cytoplasmic staining. Protein expression in HPV cases was higher as compared to HPV naive cases (P < 0.05).Conclusions:From the study, it can be established that the use of tobacco, oral hygiene, and HPV infection may be synergistically involved in modulating the expression of NF-κB signaling pathway for the development and progression of HNC in the Pakistani population.

简介：摘要目的：评价视觉功能分析仪和扫频光学生物测量仪测量白内障患者Kappa角和Alpha角的差异性、相关性、一致性和重复性。方法：系列病例研究。纳入2018年10月至2019年10月于武汉大学附属爱尔眼科医院拟进行白内障手术的164例患者，所有患者均选取其右眼数据进行分析。采用iTrace视觉功能分析仪和IOLMaster 700扫频光学生物测量仪采集患者的Kappa角、Alpha角、对应的瞳孔直径及角膜直径，每位患者均进行3次重复测量。采用配对t检验和Wilcoxon符号秩检验分析2种仪器测量结果的差异性。采用Pearson相关分析和Spearmen相关分析对2种仪器Kappa角和Alpha角的相关性进行分析。采用Bland-Altman法计算2种仪器测量Kappa角和Alpha角的一致性界限（95%LoA）。采用组内相关系数（ICC）分析2种仪器3次重复测量Kappa角和Alpha角的重复性。结果：iTrace测得的Kappa角、Alpha角、瞳孔直径及角膜直径分别为0.26（0.18，0.38）mm、（0.35±0.14）mm、4.70（4.22，5.42）mm、（10.85±0.36）mm。IOLMaster 700测得的Kappa角、Alpha角、瞳孔直径及角膜直径分别为0.23（0.15，0.34）mm、（0.42±0.19）mm、4.43（3.74，4.87）mm、（11.73±0.43）mm。2种仪器测得Alpha角、瞳孔直径及角膜直径比较差异有统计学意义（t=-5.541，P<0.001；Z=-9.117，P<0.001；t=-49.463，P<0.001），二者的Kappa角比较差异无统计学意义。iTrace、IOLMaster 700测得的Kappa角大于0.5 mm的比例都为5.4%，测得的Alpha角大于0.5 mm的比例分别为14.0%、32.9%。iTrace和IOLMaster 700测得的Kappa角、Alpha角均呈中等相关（ρ=0.607、r=0.553，均P<0.001）。2种仪器Kappa角、Alpha角的95%LoA分别为0.0164（-0.3032～0.3361）mm、-0.0718（-0.3970～0.2534）mm。iTrace测量Kappa角和Alpha角的ICC（95%CI）分别为0.771（0.689～0.832）、0.771（0.688～0.832），IOLMaster 700测量Kappa角和Alpha角的ICC（95%CI）分别为0.823（0.759～0.870）、0.863（0.814～0.899）。结论：iTrace视觉功能分析仪和IOLMaster 700扫频光学生物测量仪测量的Kappa角差异无统计学意义，但二者测量的瞳孔直径差异存在统计学意义，不可直接替代。二者测量的Alpha角存在显著差异，IOLMaster 700测得的Alpha角更大，2种仪器测得的Alpha角不能代替使用。

简介：AbstractBackground:MicroRNAs are closely associated with the progression and outcomes of multiple human diseases, including sepsis. In this study, we examined the role of miR-23a in septic injury.MethodsLipopolysaccharide (LPS) was used to induce sepsis in a rat model and H9C2 and HK-2 cells. miR-23a expression was evaluated in rat myocardial and kidney tissues, as well as H9C2 and HK-2 cells. A miR-23a mimic was introduced into cells to identify the role of miR-23a in cell viability, apoptosis, and the secretion of inflammatory cytokines. Furthermore, the effect of Rho-associated kinase 1 (ROCK1), a miR-23a target, on cell damage was evaluated, and molecules involved in the underlying mechanism were identified.Results:In the rat model, miR-23a was poorly expressed in myocardial (sham vs. sepsis 1.00 ± 0.06 vs. 0.27 ± 0.03, P < 0.01) and kidney tissues (sham vs. sepsis 0.27 ± 0.03 vs. 1.00 ± 0.06, P < 0.01). Artificial overexpression of miR-23a resulted in increased proliferative activity (DNA replication rate: Control vs. LPS vs. LPS + Mock vs. LPS + miR-23a: H9C2 cells: 34.13 ± 3.12 vs. 12.94 ± 1.21 vs. 13.31 ± 1.43 vs. 22.94 ± 2.26, P < 0.05; HK-2 cells: 15.17 ± 1.43 vs. 34.52 ± 3.46 vs. 35.19 ± 3.12 vs. 19.87 ± 1.52, P < 0.05), decreased cell apoptosis (Control vs. LPS vs. LPS + Mock vs. LPS + miR-23a: H9C2 cells: 11.39 ± 1.04 vs. 32.57 ± 2.29 vs. 33.08 ± 3.12 vs. 21.63 ± 2.35, P < 0.05; HK-2 cells: 15.17 ± 1.43 vs. 34.52 ± 3.46 vs. 35.19 ± 3.12 vs. 19.87 ± 1.52, P < 0.05), and decreased production of inflammatory cytokines, including interleukin-6 (Control vs. LPS vs. LPS + Mock vs. LPS + miR-23a: H9C2 cells: 59.61 ± 5.14 vs. 113.54 ± 12.30 vs. 116.51 ± 10.69 vs. 87.69 ± 2.97 ng/mL; P < 0.05, F = 12.67, HK-2 cells: 68.12 ± 6.44 vs. 139.65 ± 16.62 vs. 143.51 ± 13.64 vs. 100.82 ± 9.74 ng/mL, P < 0.05, F = 9.83) and tumor necrosis factor-α (Control vs. LPS vs. LPS + Mock vs. LPS + miR-23a: H9C2 cells: 103.20 ± 10.31 vs. 169.67 ± 18.84 vs. 173.61 ± 15.91 vs. 133.36 ± 12.32 ng/mL, P < 0.05, F = 12.67, HK-2 cells: 132.51 ± 13.37 vs. 187.47 ± 16.74 vs. 143.51 ± 13.64 vs. 155.79 ± 15.31 ng/mL, P < 0.05, F = 9.83) in cells. However, ROCK1 was identified as a miR-23a target, and further up-regulation of ROCK1 mitigated the protective function of miR-23a in LPS-treated H9C2 and HK-2 cells. Moreover, ROCK1 suppressed sirtuin-1 (SIRT1) expression to promote the phosphorylation of nuclear factor-kappa B (NF-κB) p65, indicating the possible involvement of this signaling pathway in miR-23a-mediated events.Conclusion:Our results indicate that miR-23a could suppress LPS-induced cell damage and inflammatory cytokine secretion by binding to ROCK1, mediated through the potential participation of the SIRT1/NF-κB signaling pathway.

简介：AbstractObjective:This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods:Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group (n= 6), EE-sham group (n = 6), control-IR group (n= 6) and control-sham group (n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test.Results:Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats.Conclusion:Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.