简介:AIM:ToInvestigatethegeneticfindingsandphenotypiccharacteristicsofaChinesefamilywithNorriedisease(ND).METHODS:MoleculargeneticanalysisandclinicalexaminationswereperformedonaChinesefamilywithND.MutationsintheNorriediseasepseudoglioma(NDP)geneweredetectedbydirectsequencing.Haplotypeswereconstructedandcomparedwiththephenotypesinthefamily.Evolutionarycomparisonsandmutantopenreadingframe(ORF)predictionwerealsoundertaken.RESULTS:TwofamilymemberswithocularmanifestationswerediagnosedwithND.Nosignsofsensorineuralhearinglosswereobservedineitherpatient,whileoneofthemshowedsignsofmildmentalretardation.AnovelheterozygousmutationintheNDPgene,c.-12delAAT,wasdetectedinbothpatients.ThemutationandthemutationbearinghapiotypecosegregatedwiththeNDphenotypeinmalesandwastransmittedfromtheirmothersand/orgrandmothers(Ⅱ:2).ThemalewithoutNDdidnotharborthemutation.Themutationoccurredatthehighlyconservednucleotides.DRFfinderpredictedthatthemutationwouldleadtotheproductionofatruncatedproteinthatlacksthefirst11N-terminalaminoacids.CONCLUSION:Anovelmutation,c.-12delAATintheNDPgene,wasidentifiedinaChinesefamilywithND.ThismutationcausedNDwithoutobvioussensorineuralhearingloss.Mentaldisorderwasfoundinonebutnottheotherpatients.Theclinicalheterogeneityinthefamilyindicatedthatothergeneticvariantsandepigeneticfactorsmayalsoplayaroleinthediseasepresentation.
简介:AIM:Tostudytheassociationsbetweenlysyloxidaselike1(LOXL1)polymorphismsandprimaryopenangleglaucoma(POAG)remaininconsistent.Inthisstudy,wehaveperformedameta-analysistoinvestigatetheassociationofLOXL1polymorphismswithPOAGrisk.METHODS:PublishedliteraturefromPubMedandotherdatabaseswereretrieved.AllstudiesevaluatingtheassociationbetweenLOXL1polymorphisms(rs2165241,rs1048661,rs3825942)andPOAGriskwereincluded.Pooledoddsratio(OR)and95%confidenceinterval(CI)werecalculatedusingrandom-orfixed-effectsmodel.RESULTS:Twelvestudieswereidentifiedaseligiblearticles,withthirteen(2098casesand16473controls),thirteen(1795casesand2916controls)andsixteenpopulationcohorts(2456casesand2846controls)fortheassociationofrs2165241,rs1048661andrs3825942withPOAGriskrespectively.OverallanalysesshowednoassociationbetweeneachLOXL1polymorphismandPOAGrisk,andthenegativeassociationswereremainedwhenthesubjectswerestratifiedasCaucasianandAsian.Theheterozygoteofrs2165241wasassociatedwithreducedPOAGriskinhospital-basedpopulations(TCvsCC:OR,0.79,95%CI:0.63-0.99),andrs1048661wasassociatedwithincreasedPOAGriskinhospitalbasedpopulationsinadominantmodel(TTvsCC+CT:OR,1.23,95%CI:1.01-1.50);however,theseassociationswerenotfoundinpopulation-basedsubjects.CONCLUSION:Thismeta-analysissuggeststhatLOXL1polymorphismsarenotassociatedwithPOAGrisk.Giventhelimitedsamplesize,theassociationsofLOXL1polymorphismswithPOAGriskinhospital-basedpopulationsawaitfurtherinvestigation.
简介:目的:观察色素上皮衍生因子(pigmentepithelium-derivedfactor,PEDF)在氧诱导视网膜病变(oxygen-inducedretinopathy,OIR)中对小鼠视网膜新生血管(retinalneovascularization,RNV)和单核细胞趋化因子-1(monocytechemoattractantprotein-1,MCP-1)表达的影响,探讨PEDF对缺血缺氧性视网膜病变的保护作用和机制。方法:取7日龄C57BL/6J新生小鼠160只,将120只7日龄小鼠与哺乳母鼠共同置于氧浓度为(75±2)%的氧环境内饲养5d,然后返回正常氧环境中饲养5d,建立OIR模型;40只小鼠始终置于正常氧环境饲养。分别于12日龄和14日龄给予PEDF药物治疗组小鼠右眼玻璃体腔注射PEDF(2μg/μL)各1μL,给予PBS治疗对照组和正常对照组小鼠右眼玻璃体腔注射等量的磷酸盐缓冲液(phosphatebufferedsaline,PBS)。所有小鼠于17日龄麻醉处死后取视网膜,采用视网膜铺片和Lectin染色法观察各组小鼠病理性新生血管的生成情况;Western-blot检测PEDF和MCP-1蛋白在各组小鼠视网膜的表达;实时荧光定量逆转录多聚酶链反应(RT-PCR)检测各组小鼠视网膜PEDF和MCP-1mRNA的表达。结果:视网膜铺片和Lectin染色结果显示OIR模型组RNV面积较正常组显著增大,差异有统计意义(P<0.01),PEDF药物治疗组RNV面积较PBS治疗对照组明显减小,差异有统计意义(P<0.01)。Western-blot和RTPCR结果显示,OIR模型组MCP-1蛋白和mRNA的表达水平均明显高于正常组,差异有统计意义(均P<0.05);OIR模型组PEDF蛋白和mRNA的表达水平均明显低于正常组,差异有统计意义(均P<0.01);PEDF药物治疗组MCP-1蛋白和mRNA的表达量较PBS治疗对照组均显著减少,差异有统计意义(均P<0.05);PEDF药物治疗组MCP-1蛋白和mRNA的表达量较正常对照组升高,但差异均无统计学意义(均P>0.05)。结论:PEDF能够抑制OIR小鼠视网膜新生血管形成,同时下调MCP-1在OIR小鼠视网膜的表达,后者可能是其抑制新生血管形成从而发挥视网膜保护作用的机制之
简介:目的:研究高氧诱导的视网膜新生血管模型鼠中转录因子Islet-1的表达差异。方法:采用高氧诱导的方法制作鼠视网膜新生血管模型,运用荧光造影视网膜铺片及视网膜切片苏木精-伊红染色观察视网膜新生血管的形态。于小鼠出生后第7,12,14,17,26d取视网膜组织,采用Real-timePCR及Westernblot技术测定视网膜组织中Islet-1的表达水平。结果:模型组视网膜铺片及组织切片可见大量视网膜新生血管形成。小鼠出生后第7d,模型组与正常组视网膜组织中Islet-1表达水平无明显差异;小鼠出生后第12~14d,模型组视网膜组织中Islet-1表达水平明显上调;出生后17d,模型组视网膜组织中Islet-1表达水平仍高于正常组;出生后26d,随着视网膜新生血管消退,视网膜组织中Islet-1表达水平降至正常水平。结论:模型鼠视网膜新生血管发生过程中,持续缺氧的视网膜组织通过增加转录因子Islet-1的表达,从而诱导视网膜新生血管的发生。
简介:目的:观察翼状胬肉切除联合自体球结膜瓣移植术后,局部应用1g/L环孢霉素A对胬肉复发的抑制效果。方法:对原发性翼状胬肉患者58例58眼进行前瞻性研究。所有入选眼均采用翼状胬肉切除联合自体球结膜瓣移植术,根据术后是否应用1g/L环孢霉素A滴眼液分为试验组和对照组。术后追踪随访1a,观察患者的胬肉复发率。结果:术后试验组基础泪液分泌试验(SchirmerⅠtest,SⅠt)结果明显优于对照组(9.93±1.59vs8.47±1.53mm/5min);SⅠt结果也显示1g/L环孢霉素A使患眼术后的泪液分泌量较术前有所增加。术后1a试验组与对照组的胬肉复发率分别为10%和39%。对照组并发症的出现率要高于试验组,差异具有统计学意义(P=0.029)。结论:翼状胬肉切除术后局部应用1g/L环孢霉素A滴眼液能够安全有效地降低胬肉的复发率。
简介:目的:研究富含半胱氨酸蛋白61(CCN1/Cyr61)在氧诱导小鼠视网膜新生血管(retinalneovascularization,RNV)中的表达及意义,探讨特异性抑制CCN1对RNV形成的抑制作用。方法:取C57BL/6J小鼠200只,随机分为对照组、高氧组、高氧对照组和CCN1治疗组,每组各50只。高氧对照组和CCN1治疗组分别玻璃体腔内注射空载体质粒和CCN1siRNA表达质粒。ADP酶视网膜铺片观察视网膜血管形态,HE染色计数突破视网膜内界膜的新生血管内皮细胞核数,免疫组织化学、Westernblot和RT-PCR法检测CCN1蛋白及mRNA的表达情况。结果:高氧组和高氧对照组视网膜可见大片无灌注区和大量突破内界膜的新生血管内皮细胞核(25.25±1.26个;23.12±1.16个),CCN1治疗组较高氧组和高氧对照组的无灌注区及新生血管内皮细胞核数(8.47±1.15个)明显减少。高氧组和高氧对照组较对照组相比,CCN1蛋白及mRNA表达显著增高,CCN1治疗组较高氧组和高氧对照组显著减弱,均有统计学意义(均为P〈0.05)。结论:CCN1的异常表达可能与RNV形成密切相关,特异性抑制CCN1能有效抑制RNV的形成,为预防和治疗ROP提供新的思路及对策。
简介:AIM:Toinvestigatewhethertheresponseofacentralhexagonalelementcorrespondingtothemacularareainconventionalmultifocalelectroretinography(mfERG)testswasthesameasthatofexperimentalmfERGusingsinglecentralhexagonalelementstimulation.METHODS:Prospective,observationalstudy.Thirtyhealthysubjectswereincludedinthisstudy.mfERGrecordingswereperformedaccordingtotwoprotocols:stimuluswith37hexagonalelements(protocol1),andstimuluswithasinglecentralelementcreatedbydeactivatingtheother36hexagonalelements(protocol2).Wecompareddifferencesbetweenring1parametersineachprotocol.RESULTS:Inprotocol1,thefirstpositivecomponent(P1)implicittimeandP1amplitudewere37.8±1.8msand6.3±2.7μV.Aftersingleelementstimulation(protocol2),doublepositivewavesappeared.TheimplicittimeandamplitudeofP1were40.7±2.4ms(P<0.001)and9.1±3.3μV(P=0.001),respectively.Theimplicittimeandamplitudeofthesecondpositivecomponent(P2)were68.0±4.5ms(P<0.001,comparedwithP1inprotocol1)and12.3±4.7μV(P<0.001,comparedwithP1inprotocol1),respectively.TheamplitudeofP2inprotocol2wasabouttwotimeshigherthanthatofP1inprotocol1.CONCLUSION:mfERGresponsesofacentralhexagonalelementinasingleelementstimulationprotocolaredifferentfromthoseofmultipleelementstimulation.Thepositivewaveismoreenhancedcomparedtothatoftheconventionalprotocolanditelongatedintotwowavelets.
简介:目的:探讨中老年糖尿病视网膜病变(diabeticretinopathy,DR)患者DR严重程度与血清HbA1c、TNF-α水平的相关性。方法:选取200例糖尿病患者,其中单纯糖尿病患者(DM组)60例,糖尿病伴非增殖期视网膜病变组(NPDR组)80例和糖尿病伴增殖期视网膜病变组(PDR组)60例,并选取80例健康者作为正常对照组(NC组)。观察患者的体检指标,并检测患者的空腹血糖(fastingplasmaglucose,FPG)、餐后2h血糖(2hPG)、血脂、血清糖化血红蛋白(HbA1c)、血清肿瘤坏死因子-α(tumornecrosisfactor,TNF-α)及泪液TNF-α。结果:(1)四组受试者的体质量指数(bodymassindex,BMI)、FPG、2hPG、总胆固醇(totalcholesterol,TC)、甘油三酯(trilycerides,TG)、高密度脂蛋白(highdensitylipoprotein,HDL-C)、低密度脂蛋白(low-densitylipoprotein,LDL-C)等指标比较,差异均具有统计学意义(F=37.211、395.421、42.515、7.385、121.764、121.568、34.567,均P<0.05)。DM、NPDR、PDR三组患者的BMI、FPG、2hPG、TC、TG、HDL-C、LDL-C等指标水平均高于NC组,差异有统计学意义(P<0.05);NPDR组患者的BMI、FPG、2hPG、TC、TG、HDL-C、LDL-C等指标水平均高于PDR组,差异有统计学意义(P<0.05)。(2)四组受试者血清TNF-α、泪液TNF-α及血清HbA1c水平比较,差异均具有统计学意义(F=337.256、215.471、40.522,均P<0.05);DM、NPDR、PDR三组患者的血清TNF-α、泪液TNF-α和血清HbA1c水平均高于NC组,差异有统计学意义(P<0.05);NPDR、PDR两组患者的血清TNF-α、泪液TNF-α和血清HbA1c水平均高于DM组,差异有统计学意义(P<0.05);PDR组患者的血清TNF-α、泪液TNF-α及血清HbA1c水平均高于NPDR组,差异有统计学意义(P<0.05)。(3)泪液TNF-α与血清TNF-α呈正相关(r=0.289,P<0.01);泪液TNF-α与血清HbA1c呈正相关(r=0.375,P<0.01)。结论:中老年DR患者泪液TNF-α水平高于正常人,且随着视网膜病变的加重,泪液TNF-α水平升高。泪液TNF-α与血清TNF-α、HbA1c呈正相关。
简介:目的:研究血管紧张素Ⅱ受体拮抗剂坎地沙坦对糖尿病(DM)大鼠视网膜组织VEGF和MCP-1表达的影响.方法:链脲佐菌素(STZ)制备DM大鼠动物模型36只,随机分为DM模型组和坎地沙坦治疗组,另取18只正常SD大鼠作为正常对照组,每组均随机分为4,8,12wk3个亚组.视网膜铺片联合PAS染色观察视网膜微血管形态学变化,应用SABC免疫组织化学法检测坎地沙坦对大鼠视网膜组织VEGF和MCP-1表达的影响.结果:正常对照组视网膜血管网结构清晰,走行规则;DM模型组血管迂曲阻塞,走行不规则;治疗组见血管网迂曲情况较模型组明显改善,走行较规则.在对照组和模型4wk组中大鼠视网膜组织无VEGF和MCP-1阳性表达或只呈弱阳性表达;模型8wk和12wk组两者阳性表达明显增强,且随着病程延长呈递增趋势.治疗组两者的表达则均较同时期模型组明显减弱,差异有统计学意义(P〈0.05).结论:研究血管紧张素Ⅱ受体拮抗剂坎地沙坦可降低DM大鼠视网膜VEGF和MCP-1的表达.
简介:目的探讨前房注入1%利多卡因作为表面麻醉的一种辅助麻醉在眼前段内眼手术中的麻醉效果.方法对29例42眼患者眼前段内眼手术,在手术进入前房前,通过1mm前房穿刺或侧切口注入1%利多卡因,观察麻醉效果及术中术后并发症.结果Ⅰ级手术中完全无疼痛,手术配合良好;Ⅱ级术中疼痛轻微,可以耐受配合手术完成;Ⅲ级术中疼痛较剧,难以忍受.Ⅰ级者40眼,Ⅱ级者2眼,Ⅲ级者0眼,术中、术后无出现并发症.结论表面麻醉联合前房注入1%利多卡因是一种安全、有效、并发症少的麻醉方法.
简介:AIM:Toinvestigatetheexpressionofdendriticcell-associatedC-typelectin-1(dectin-1)attheearlyperiodofAspergillusfumigatusinfectioninrat’scornealepithelium.·METHODS:Atotalof72Wistarratswererandomlydividedintothreegroups:A,BandC.Therighteyeswerechosenasexperimentaleyes.GroupAwascontrolgroup.RatsingroupBwerenotinoculatedwithAspergillusfumigatus.GroupCwastakenasAspergillusfumigatuskeratitismodel.RatsingroupBandC(sixfromeachgroup)wereexecutedrandomlyat4,8,16and24hoursafterexperimentalmodelbeingestablishedtoassesstheexpressionofdectin-1mRNAthroughreal-timePCR.AnothersixratsingroupBandCwereexecutedrandomlyat24hourstoassesstheexpressionofdectin-1proteinthroughimmunohistochemistry.·RESULTS:Theresultsofreal-timePCRindicatedthatdectin-1mRNAexpressionwaslowincornealepitheliumofnormalrats’.Therewasnosignificantlydifferenceofdectin-1mRNAexpressioningroupAandB(P>0.05).TheexpressionofAspergillusfumigatusinfectedcornealepitheliumincreasedgraduallyafter8hoursingroupC.ThesynchronousexpressionofgroupAandChadsignificantdifference(P<0.01).Immunohistochemistydiscoveredthatdectin-1receptorexistedinnormalrat’scornealepithelium.Dectin-1proteinincreasedafter24hoursingroupC.TherewasasignificantdifferenceofsynchronousexpressioningroupBandC(P<0.01).·CONCLUSION:Dectin-1existsinrat’scornealepitheliumanditsexpressionsignificantlyincreasesattheearlyperiodofAspergillusfumigatusinfection.Dectin-1isapatternrecognitionreceptorthatexpressesincornealepitheliumandinvolvesinimmuneresponsetoAspergillusfungalkeratitis.
简介:AIM:Toinvestigatewhether15-Lipoxygenase-1(15-LOX-1)playsanimportantroleintheregulationofangiogenesis,inhibitinghypoxia-inducedproliferationofretinalmicrovascularendothelialcells(RMVECs)andtheunderlyingmechanism.METHODS:PrimaryRMVECswereisolatedfromtheretinasofC57/BL6JmiceandidentifiedbyanevaluationforFITC-markedCD31.ThehypoxiamodelswereestablishedwiththeBio-bagandevaluatedwithablood-gasanalyzer.ExperimentswereperformedusingRMVECstreatedwithandwithouttransferAd-15-LOX-1orAd-vectorbothunderhypoxiaandnormoxiaconditionat12,24,48,72hours.Theefficacyofthegenetransferwasassessedbyimmunofluorescencestaining.CellsproliferationwasevaluatedbytheCCK-8method.RNAandproteinexpressionsof15-LOX-1,VEGF-A,VEGFR-2,eNOsandPPAR-rwereanalyzedbyreal-timereversetranscriptionpolymerasechainreaction(RT-PCR)andWesternblot.RESULTS:RoutineevaluationforFITC-markedCD31showedthatcellswerepure.Theresultsofblood-gasanalysisshowedthatwhenthecultureswereexposedtohypoxiaformorethan2hours,thePo2was4.5to5.4Kpa.WeverifiedRMVECscouldbeinfectedwithAd-15-LOX-1orAd-vectorviaFluorescencemicroscopy.CCK-8analysisrevealedthattheproliferativecapacitiesofRMVECsinhypoxicgroupweresignificantlyhigherateachtimepointthantheywereinnormoxicgroup(P<0.05).Inahypoxiccondition,theproliferativecapacitiesofRMVECsin15-LOX-1groupweresignificantlyinhibited(P<0.05).Real-timeRT-PCRanalysisrevealedthattheexpressionsofVEGF-A,VEGF-R2andeNOsmRNAincreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).However,theexpressionsof15-LOX-1,PPAR-rmRNAdecreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).Italsoshowedthatinahypoxiccondition,theexpressionsofVEGF-A,VEGF-R2andeNOsmRNAdecreasedsignificantlyin15-LOX-1groupcomparedwithhypoxiagroup(P<0.01).However,15-LOX-1andPPAR-rmRNAincreasedsigni
简介:AIM:Toevaluatetheeffectofbrinzolamide-timololfixedcombinationonintraocularpressure(IOP)aftercataractsurgery.METHODS:Thestudyincluded92eyesof87patientswhounderwentcataractsurgeryandintraocularlensimplantation.Patientsscheduledforphacoemulsificationwereassignedto1of2groups.Thetreatmentgroupreceived1dropofbrinzolamide-timololfixedcombinationimmediatelyaftersurgery,andthecontrolgroupreceivednotreatment.TheIOPwasmeasuredpreoperativelyandat2hand24hpostoperatively.RESULTS:ThemeanIOPchangewaslowerinthetreatmentgroupthaninthecontrolgroupat2hpostoperatively.ThedifferencebetweenthemeanIOPvaluesofthetwogroupsat2hpostoperativelywasfoundtobestatisticallysignificant.Twenty-fourhoursafterthesurgery,themeanIOPchangewasstillhigherinthecontrolgroupwhencomparedtothetreatmentgroup.CONCLUSION:ThefixedcombinationbrinzolamidetimololcaneffectivelyreduceIOPaftercataractsurgery.
简介:目的本研究针对初发性翼状胬肉局部使用丝裂霉素C(MMC)一次性注射治疗,用免疫组织化学方法对经MMC治疗的翼状胬肉标本中血管内皮生长因子(VEGF)和转化生长因子(TGF-β_1)的表达进行分析研究,并与未使用MMC治疗者的翼状胬肉标本作对比。观察局部注射MMC对翼状胬肉组织中VEGF和TGF-β_1的表达的影响。方法需手术者共19例20眼,随机分为二组:A组直接切除胬肉,留标本作免疫组织化学检查;B组于翼状胬肉颈部进针,向胬肉组织内局部注射MMC,0.1~0.2ml(0.4mg/ml),3周至10周后手术切除胬肉,留标本作免疫组织化学检查。分别对A、B二组标本中VEGF和TGF-β_1的表达进行分析研究。结果A组VEGF、TGF-β_1的表达较B组高,差异有统计学意义(P〈0.05)。结论丝裂霉素C翼状胬肉局部注射可以抑制静止期翼状胬肉中VEGF、TGF-β_1因子的表达。MMC在低浓度、低剂量下使用未出现眼部严重并发症。
简介:目的:构建表达小鼠CD4+T细胞钙支架蛋白AHNAK1的短发夹RNA(shorthairpinRNA,shRNA)慢病毒载体,并研究其对小鼠甲状腺相关性眼病(thyroid-associatedophthalmopathy,TAO)的抑制效应。方法:设计并筛选对AHNAK1具有良好干扰效力的shRNA序列,慢病毒载体包装干扰序列,感染小鼠CD4+T细胞,检测AHNAK1静默对T细胞功能的抑制作用,采用实验动物模型观察AHNAK1体内抑制甲状腺相关性眼病的效果。结果:成功筛选出具有良好干扰效力的shRNA,并包装入慢病毒。病毒滴度为1.0伊106TU/mL,转染慢病毒的CD4+T细胞展现出失能倾向,抑制炎症免疫反应;在动物模型中抑制T细胞中AHNAK1表达可以有效控制甲状腺眼病的发生发展,显著降低治疗组T细胞中IL-2、IL-1茁和IFN-酌的表达。结论:成功构建了表达小鼠AHNAK1shRNA的慢病毒,具有抑制T细胞分泌IL-2、IL-1茁和IFN-酌的表达效应,能够有效抑制甲状腺眼病的发生发展。
简介:AIM:ToinvestigatetheinterferingeffectofY-27632,aROCK-Iselectiveinhibitor,onthesignaltransductionpathwayoftransforminggrowthfactor-β1(TGF-β1)inocularTenoncapsulefibroblasts(OTFS)invitro.METHODS:AfterOTFSfrompassages4to6invitrowereinducedbyTGF-β1andthentreatedbyY-27632,thechangesoftheOTFScellcycleswereanalyzedviaflowcytometry,andtheproteinsexpressionoftheα-smoothmuscularactin(α-SMA),connectivetissuegrowthfactor(CTGF),collagenIwerecalculatedbyWesternblot.AfterOTFStreatedbythedifferentconcentrationsofY-27632,theexpressionlevelsoftheα-SMA,CTGFandcollagenImRNAwereassayedbyRT-PCR.RESULTS:Y-27632hadnomarkedlyeffectontheOTFScellcycles.AftertreatedbyTGF-β1,OTFSinG1periodsignificantlyincreased.ThecellcyclesdistributionbybothTGF-β1andY-27632hadnoremarkabledifferencefromthatincontrolgroup.Y-27632significantlyinhibitedtheproteinsexpressionsofbothα-SMAandCTGF,whiletosomeextentinhibitedthatofcollagenI.TGF-β1significantlypromotedtheproteinsexpressionsofα-SMA,CTGFandcollagenI.AfterOTFStreatedbybothTGF-β1andY-27632,ofα-SMA,theproteinexpressionwassimilarwiththatincontrolgroup(P=0.066>0.05),buttheproteinexpressionofCTGForcollagenI,respectively,wassignificantlydifferentfromthatincontrolgroup(P=0.000<0.01).Thedifferencesofexpressionsoftheα-SMA,CTGFandcollagenImRNAin30,150,750μmol/LY-27632groupwerestatisticallysignificant,comparedwiththoseincontrolgroup,respectively(α-SMA,P=0.002,0.000,0.000;CTGF,P=0.014,0.002,0.001;collagenI,P=0.003,0.002,0.000).CONCLUSION:BlockingtheRho/ROCKsignalingpathwaybyusingofY-27632couldinhibitthecellularproliferationandtheexpressionofbothCTGFandα-SMAwhateverOTFSinducedbyTGF-β1ornot.Y-27632suppressedtheexpressionofcollagenImRNAwithoutinduction.