简介：Objective:Tostudytheanti-inflammatoryactivityandtissuedistributionpatternsofintravenousemulsionofdexamethasoneacetateinmice.Methods:Theanti-inflammatorysolutionforinjectionandLimethasone(Jepaneseproduct)givenintravenouslywereevaluatedbyusingthepreformedcarrageenangranulomapouchmethodinrats.Results:Theanti-inflammatoryactivityofdexamethasoneacetateemulsionatlowdoseof0.05mg.kg1wasaspotentasdexamethasonesodiumphosphatesolutionathighdoseof0.3mg.kg1.Thedistributionpatternsinmicetissuesof[^3H]dexamethasoneacetateemulsionand[^3H]dexamethasonesodiumphosphatesolutioninmiceweremarkedlydifferent.Dexamethasoneacetateemulsionshowedamuchhigherconcentrationintheliver,spleen,lung,andinflamedtissues,whereasdexamethasonesodiumphosphatehadahighconcenti,moninthemusclesofvastuslateralis.Theseresultsmayindicatethatdexamethasoneincoporatedinlipidemulsionwastakenupbythereticuloendothelialsystemandinflammatorycellsmuchmorethandexamethasonesodiumphosphatesolution.Conclusion:Whendexamethasoneacetatewasincorporatedinemulsion,thedistributionpatternsintissueswerechangedandtheyhadastrongeranti-inflammatoryactivity.

简介：Thepresentstudywasdesignedtoexaminetheanti-hyperuricemicandanti-inflammatoryeffectsandpossiblemechanismsofvaticaffinol,aresveratroltetramerisolatedfromethanolextractsofDipterocarpusalatus,inoxonate-inducedhyperuricemicmice.At1hafter250mg·kg~(-1)potassiumoxonatewasgiven,vaticaffinolat20,40,and60mg·kg~(-1)wasintragastricallyadministeredtohyperuricemicmiceoncedailyforsevenconsecutivedays.Vaticaffinolsignificantlydecreasedserumuricacidlevelsandimprovedkidneyfunctioninhyperuricemicmice.Itinhibitedhepaticactivityofxanthinedehydrogenase(XDH)andxanthineoxidase(XOD),regulatedrenalmRNAandproteinlevelsofuratetransporter1(URAT1),glucosetransporter9(GLUT9),organicaniontransporter1(OAT1),organiccationtransporter1(OCT1),OCT2,organiccation/carnitinetransporter1(OCTN1),andOCTN2inhyperuricemicmice.Moreover,vaticaffinolmarkedlydown-regulatedrenalproteinlevelsofNOD-likereceptor3(NLRP3),apoptosis-associatedspeck-like(ASC),andCaspase-1,resultinginthereductionofinterleukin(IL)-1β,IL-18,IL-6andtumornecrosisfactor-α(TNF-α)levelsinthisanimalmodel.Additionally,HPLCandLC-MSanalysesclearlytestifiedthepresenceofvaticaffinolinthecrudeextract.Theseresultssuggestthatvaticaffinolmaybeusefulforthepreventionandtreatmentofhyperuricemiawithkidneyinflammation.

简介：Notopterygiumincisum(QH)hasbeenusedforthetreatmentofrheumatoidarthritis(RA),andvolatileoilsmaybeitsmainlybioactiveconstituents.ThepresentstudywasdesignedtoanalyzethevolatilecompoundsinQHandtodeterminetheanti-arthriticcapacityofNotopterygiumvolatileoilsandthepotentialmechanismofaction.ThevolatilecompoundsanalysiswasconductedbyGC-MS.Theanti-arthriticcapacitytestofthevolatileoilswasconductedonadjuvant-inducedarthritis(AIA)rats.Theanti-inflammatorypropertywastestedinNOreleasemodelinRAW264.7cells.Endothelialcellswereusedtoevaluatetheanti-proliferativeandanti-tubeformativeeffects.70compoundswereanalyzedbyGC-MSinthevolatileoils.NotopterygiumvolatileoilsweakenedtheratAIAinadose-dependentmanner(2,4,and8gcrudedrug/kg).TheNOproductionbyRAW264.7wasdecreasedbymorethan50%inNotopterygiumvolatileoils(5,15,and45μg·mL-1)pretreatedgroups.NotopterygiumvolatileoilsalsoinhibitedEAhy926cellproliferationandfurtherdelayedEAhy926cellcapillarytubeformationinaconcentration-dependentmanner.Theanti-NOproductive,anti-proliferative,andanti-tubeformativeeffectsofNotopterygiumvolatileoilsstronglysuggestedthatthetherapeuticeffectofQHinAIAmightberelatedtothepotentanti-inflammatoryandanti-angiogeniccapacitiesofthevolatileoils.

简介：Directionalmigrationofleukocytesisindispensabletoinnateimmunityforhostdefense.However,recruitmentofleukocytestoasiteoftissueinjuryalsoconstitutesaleadingcauseforinflammatoryresponses.Mechanistically,itinvolvesacascadeofcellulareventspreciselyregulatedbytemporalandspatialpresentationofarepertoireofmoleculesinthemigratingleukocytesandtheirsurroundings(microenvironments).HereIwillsummarizetheemergingevidencethathasshedlightsontheunderlyingmolecularmechanismfordirectionalmigrationofleukocytes,whichhasguidedthetherapeuticaldevelopmentforinnovativeanti-inflammatorymedicines.

简介：试图学习在里面vivo男白化体老鼠上的Tabernaemontanadivaricata叶摘录的反煽动性的活动。方法水的煎和甲醇叶摘录为他们减少巴豆的能力被测试在在热门申请以后的鼠标耳朵的导致油的浮肿。甲醇叶摘录dose-dependently禁止了巴豆在老鼠的导致油的耳朵浮肿(ID50<500?g

简介：Hypertonicsaline(HS)hasbeenappliedinseveralmedicalareassuchaspneumology(asthma,cysticfibrosisandbronchiolytis),endocrinology(hyponatremia)andespeciallyinemergencymedicine,intraumaticandinflammatory/infectiousdisorders.Itmaybecomposedof

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简介：Themostimportantriskfactorforstrokeandneurodegenerationisaging.Infact,survivalafterstrokediminisheslargelywithaging.Infact,recoveryafterbrainarteryocclusionisdramaticallyworsenedbyaging,evennormalagingisassociatedwithneurondamageandcognitivedecline.Mechanismsinvolvedinaging-related,cognitivedeclineandsusceptibilitytoneurondamageinstrokeandneurodegenerationarelargelyunknown.Oneofthemostimportant

简介：AIMTo在导致的lipopolysaccharide(LPS)上调查asiatic酸(AA)的反煽动性的效果在人的角膜的上皮的房间(HCEC)的煽动性的反应.METHODSCell生存能力用数kit-8(CCK-8)的一个房间被测量试金。量的即时聚合酶链反应(qRT-PCR)被用来决定mRNAinterleukin-8(IL-8)的表示，interleukin-6(IL-6)，interleukin-1(IL-1)，肿瘤坏死factor-alpha(TNF-)，和转变生长因素--(TGF-)在HCEC。细胞内部的反应的氧种类(ROS)用ROS试金工具包被测量。谷胱甘肽(GSH)集中用全部的GSH试金工具包被测量。Akt1和Aktphosphorylation(p-Akt1)层次被西方的弄污测量，immunofluorescence.RESULTSAA在高集中导致了毒性并且显著地在20的集中刺激了HCEC的增长

简介：作为一个内部应用的反煽动性的代理人，Escin广泛地在从损伤或操作导致诊所的发炎和浮肿的治疗被使用了。然而，它皮肤的发炎和浮肿上的外部使用的效果仍然保持未经勘探。在现在的学习，反煽动性并且escin的外部使用的anti-edematous效果在老鼠，在老鼠胀大的导致paraxylene的耳朵，和棉花在导致carrageenan的爪浮肿和导致组织安的毛状的渗透被学习在老鼠的导致小团的granuloma。前列腺素E2(PGE2)上的escin胶化的外部使用的效果，肿瘤坏死因素--(TNF-)，并且interleukin-1(IL-1)被ELISA决定。反煽动性的机制被与西方的弄污和实时PCR分析检测glucocorticoid受体(GR)的表示探索，与原子factor-B(NF-B)的进一步的探索，p38激活mitogen的蛋白质kinase(P38MAPK)和使活跃之物protein-1(AP-1)表情。我们证明escin的外部使用证明在不同动物模型的尖锐、长期的发炎上的重要反煽动性的效果和它的反煽动性的效果可能与PGE2，TNF-，和IL-1的下面规定有关。结果也证明escin由支持GR的表示施加了它的反煽动性的效果，与是的可能的机制象NF-B和AP-1那样的GR相关的发信号的分子的表情的抑制。

简介：AIMTo评估热门non-steroidal的预防管理的功效在糖尿病的病人的有斑点的浮肿追随者奔流外科上的反煽动性的药(NSAID)，并且在NSAID的类型之间比较(ketorolactromethamine0.4%并且nepafenac0.1%).METHODSGroup(控制)1作为一个安慰剂组接待了人工的眼泪代用品，(nepafenac)组2收到了热门nepafenac(ketorolac)0.1%，和组3收到了热门ketorolactromethamine0.4%。病人们在完成一个以后手术后地被检查为评估似胞的有斑点的浮肿(CME)的星期，一个月，二个月和三月间隔开发。主要学习结果在与光连贯地形学(10月)测量的中央有斑点的厚度(CMT)正在完成最好改正的视觉尖酸(BCVA)和变化76个病人的.RESULTSEighty眼睛在这研究被包括。BCVA在第三个月显示出统计上重要的差别手术后列在后面在上面在控制组和NSAID组(P=0.04)之间。在开始从的所有情况中的CMT有增加手术后第一个星期直到第三个月。CMT显示出控制组和NSAID组之间的统计上重要的差别从手术后第一个月直到第三个月(P=0.008，0.027，0.004)。在BCVA和外科手术前的10月CMT.CONCLUSIONProphylacticnepafenac和ketorolac组之间没有统计上重要的差别，手术后的NSAID可以在在跟随奔流外科的糖尿病的眼睛减少CME的频率和严厉有一个角色。

简介：ScutellariaeRadix(SR),therootofScutellariabaicalensisGeorgi,isusedasanantipyreticdrugandhasbeendemonstratedtohaveanti-inflammatoryactivity.SRisdividedintotwospecifications,'KuQin'(KQ)and'ZiQin'(ZQ),foruseagainstdifferentsymptoms(upperenergizerheatorlowerportionofthetripleenergizer),accordingtothetheoryoftraditionalChinesemedicine(TCM).However,differencesintheefficaciesofthesetwospecificationshavenotbeendetermined.Inthepresentstudy,weaimedtocharacterizethedifferencesintheanti-inflammatoryactivitiesbetweenKQandZQandtoexplorehowtheirdifferencesaremanifestedinlipopolysaccharide(LPS)-inducedmacrophages.Ourresultsshowedthat,inRAW264.7cells(amousemacrophagecelllinederivedfromascites),KQandZQdisplayedanti-inflammatoryeffectsbyinhibitingthereleaseofnitricoxide(NO),inducibleNOS(iNOS),andnuclearfactor-κB(NF-κB)inadose-dependentmannerwithoutdistinction.InNR8383cells(aratalveolarmacrophagecellline),KQandZQdisplayedsimilareffectsonNO,iNOS,andNF-κBasseeninRAW264.7cells,butKQshowedahigherinhibitionrateforNOandiNOSthanthatshownbyZQatthesameconcentration.TheseresultsindicatedthatthereweredifferencesinefficacybetweenKQandZQintreatinglunginflammation.OurfindingsprovidedanexperimentalevidencesupportingthedifferentusesofKQandZQinclinic,asnotedinancientherbalrecords.

简介：AbstractBackground:Excessive inflammatory responses play a critical role in the development of severe acute pancreatitis (SAP), and controlling such inflammation is vital for managing this often fatal disease. Dexmedetomidine has been reported to possess protective properties in inflammatory diseases. Therefore, this study aimed to investigate whether dexmedetomidine pre-treatment exerts an anti-inflammatory effect in rats with SAP induced by sodium taurocholate, and if so, to determine the potential mechanism.Methods:SAP was induced with sodium taurocholate. Rats received an intraperitoneal injection of dexmedetomidine 30 min before sodium taurocholate administration. α-bungarotoxin, a selective alpha-7 nicotinic acetylcholine receptor (α7nAchR) antagonist, was injected intra-peritoneally 30 min before dexmedetomidine administration. The role of the vagus nerve was evaluated by performing unilateral cervical vagotomy before the administration of dexmedetomidine. Efferent discharge of the vagal nerve was recorded by the BL-420F Data Acquisition & Analysis System. Six hours after onset, serum pro-inflammatory cytokine (tumor necrosis factor α [TNF-α] and interleukin 6 [IL-6]) levels and amylase levels were determined using an enzyme-linked immunosorbent assay and an automated biochemical analyzer, respectively. Histopathological changes in the pancreas were observed after hematoxylin and eosin staining and scored according to Schmidt criteria.Results:Pre-treatment with dexmedetomidine significantly decreased serum levels of TNF-α, IL-6, and amylase, strongly alleviating pathological pancreatic injury in the rat model of SAP (TNF-α: 174.2 ± 30.2 vs. 256.1±42.4 pg/ml; IL-6: 293.3 ± 46.8 vs. 421.7 ± 48.3 pg/ml; amylase: 2102.3 ± 165.3 vs. 3186.4 ± 245.2 U/L). However, the anti-inflammatory and pancreatic protective effects were abolished after vagotomy or pre-administration of α-bungarotoxin. Dexmedetomidine also significantly increased the discharge frequency and amplitude of the cervical vagus nerve in the SAP rat model (discharge frequency: 456.8 ± 50.3 vs. 332.4 ± 25.1 Hz; discharge amplitude: 33.4 ± 5.3 vs. 20.5 ± 2.9 μV).Conclusions:Dexmedetomidine administration attenuated the systemic inflammatory response and local pancreatic injury caused by SAP in rats through the cholinergic anti-inflammatory pathway involving vagus-and α7nAChR-dependent mechanisms.

简介：AIMTo比较fluorometholone的联合0.1%并且0.5%在控制发炎并且与intraocular透镜implantation.METHODSSixty在phacoemulsification以后阻止感染掉到tobramycin/dexamethasone眼睛的levofloxacin从60看经历奔流phacoemulsification的病人被使随机化进二个组；病人的一半与与levofloxacin(4times/d)相结合的fluorometholone(6times/d)被对待，当另外的一半与眼睛掉一个星期的tobramycin/dexamethasone(4times/d)被对待时。在操作和1wk追随者treatments.RESULTSThere不是在角膜的厚度(P0.629)的二个组之间的统计上重要的差别以前，外科手术前、手术后的intraocular压力，水的闪光，角膜的厚度，和症状被记录，水的闪光(P0.398)，并且症状分数(P0.350)在每次指。眼睛的高血压仅仅在与levofloxacin治疗表演相结合的tobramycin/dexamethasonegroup.CONCLUSIONFluorometholone在二只眼睛被观察可比较的功效但是没有增加intraocular压力的趋势；因此，它可能是为手术后的使用的更好的政体。

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简介：Thepresentstudywasdesignedtosynthesize2-Cyano-3,12-dioxooleana-1,9(11)-en-28-oate-13β,28-olide(1),alactonederivativeofoleanolicacid(OA)andevaluateitsanti-inflammatoryactivity.Compound1significantlydiminishednitricoxide(NO)productionanddown-regulatedthemRNAexpressionofiNOS,COX-2,IL-6,IL-1β,andTNF-αinlipopolysaccharide(LPS)-stimulatedRAW264.7cells.FurtherinvivostudiesinmurinemodelofLPS-inducedacutelunginjury(ALI)showedthat1possessedmorepotentprotectiveeffectsthanthewell-knownanti-inflammatorydrugdexamethasonebyinhibitingmyeloperoxidase(MPO)activity,reducingtotalcellsandneutrophils,andsuppressinginflammatorycytokinesexpression,andthusamelioratingthehistopathologicalconditionsoftheinjuredlungtissue.Inconclusion,compound1couldbedevelopedasapromisinganti-inflammatoryagentforinterventionofLPS-inducedALI.

简介：Thirty-ninewomenofreproductiveagesufferingfromchronicpelvicinflammatorydisease(PID)foratleasttwoyears,previouslytreatedpharmacologicallywithnoeffect,wereenrolledinafour-weektherapeuticprotocolconsistingof12acupuncturetreatmentsperformedwiththefrequencyofthreeperweek.Ineachfemalepatientatbaselineandafterthestudy,painscoreandthefollowingparametersinbloodserumwereevaluated:concentrationofimmunoglobulinM(IgM),albumins,alphal-globulins,alpha2-globulinsandgamma-globulins,erythrocytesedimentationrate(ESR)andwhitebloodcell(WBC)count.Duringthestudy,weobtainedasignificantdropinESRandIgMlevelstogetherwithariseingamma-globulinconcentrations.Asignificantdecrease(from4.89±0.82to0.63±1.05)inpainscorewas

简介：Salmeterol是长行动的β；激活adenylatecyclase的2收缩筋，引起长持续的bronchodilation并且被用于许多年到控制气喘。然而，很少信息都不关于salmeterol的immunoregulatory效果是可得到的。我们发现salmeterol减少在表示了肿瘤坏死factor-alpha，interleukin-1和interleukin-6的质问变应原的老鼠的一个模型的支持inflammatorycytokines的生产。树枝状的房间(DC)是介绍抗原的房间并且在航线充当哨兵。我们发现了那salmeterol(10−5mol/l)减少了lipopolysaccharide引起的发炎(0.1µ；g/ml)在激活的鼠科的骨头导出髓的DC。而且，西方的污点证明这保护的效果被禁止通过原子factor-kappaB发信号部分调停(NF-κ；B)，激活mitogen的蛋白质kinase(MAPK)小径和津贴的戏剧性地减少的层次。我们建议salmeterol由modulatingDC调整导致变应原的气喘的发炎。在结论，我们提供DC是为对气喘的salmeterol的行动负责的目标免疫者房间的证据。

简介：Airwaydiseasesarethemostcommonlydescribedlungmanifestationsofinflammatoryboweldisease(IBD).However,thesimilaritiesindiseasepathogenesisandthesharingofimportantenvironmentalriskfactorsandgeneticsusceptibilitysuggestthatthereisacomplexinterplaybetweenIBDandairwaydiseases.RecentevidenceofIBDoccurrenceamongpatientswithairwaydiseasesandthehigherthanestimatedprevalenceofsubclinicalairwayinjuriesamongIBDpatientssupportthehypothesisofatwo-wayassociation.Futureresearcheffortsshouldbedirectedtowardfurtherexplorationofthisassociation,asairwaydiseasesarehighlyprevalentconditionswithasubstantialpublichealthimpact.