目的：探讨人脐血间充质干细胞(hUCB-MSC)在博莱霉素诱导大鼠肺纤维化的治疗效果及可能治疗的作用机制。方法：HUCB-MSC传代培养至P4代。60只健康雄性SD大鼠（清洁级），随机分为4组：博莱霉素组，干细胞治疗组，地塞米松治疗组和阴性对照组。博莱霉素组的建立：由博莱霉素在气管内滴入建立肺纤维化模型。干细胞治疗组的建立：当肺间质纤维化的模型成立后，立即从尾静脉注射用5-溴-2-脱氧尿苷（BrdU）标记的干细胞。地塞米松治疗组：肺间质模型建立后第二天，腹腔注射地塞米松7天。阴性对照组：气管内滴注等量的生理盐水。在第7、14和28天，每组处死5只大鼠。通过HE和Masson染色，免疫组化法观察转化生长因子β1（TGF-β1）和BrdU标记的干细胞的表达。肺羟脯氨酸含量通过酸水解来确定。结果：干细胞治疗组第7日、14日和28日在肺组织中看到了BrdU标记的干细胞。与阴性对照组相比，博莱霉素组、干细胞治疗组和地塞米松治疗组显著增加肺泡炎和肺纤维化的分数（P0.05）。在7日、14日和28日，肺泡炎在干细胞治疗组和地塞米松治疗组的得分均较博莱霉素组显著降低（P0.05）；在第28天，肺间质纤维化的干细胞治疗组和地塞米松治疗组的得分均较博莱霉素组显著降低（P0.05）。地塞米松治疗组和干细胞治疗组比较肺泡炎、肺纤维化评分无显著差异（P0.05）。与博来霉素组相比，干细胞治疗组和地塞米松治疗组中TGF-β1阳性细胞的数目和肺组织中的羟脯氨酸的含量在所有时间点均有显著下降（P0.05）。干细胞治疗组和地塞米松治疗组肺组织中TGF-β1阳性细胞数量和羟脯氨酸含量没有显著差异（P0.05）。结论：脐血间充质干可移植到受损的肺组织，并有效地减少肺纤维化的早期肺泡炎和肺纤维化。脐血间充质干细胞的作用机制可能涉及抑制TGF-β1的表达和减少胶原蛋白的形成。
附原文
OBJECTIVE:Toinvestigatethetherapeuticeffectandpossibleactionmechanismofhumanumbilicalcordbloodmesenchymalstemcells(hUCB-MSCs)inthetreatmentofbleomycin-inducedpulmonaryfibrosisinrats.METHODS:ThesecondgenerationofhUCB-MSCswasculturedtothefourthgeneration.SixtyhealthymaleSprague-Dawleyrats(cleangrade)wererandomlyandequallydividedinto4groups:bleomycingroup,stemcelltreatmentgroup,dexamethasonetreatmentgroup,andnegativecontrolgroup.Apulmonaryfibrosismodelwasestablishedbyintratrachealinstillationofbleomycininthebleomycingroup,stemcelltreatmentgroup,anddexamethasonetreatmentgroup.Thestemcelltreatmentgroupwasinjectedwithstemcellslabeledwith5-bromo-2-deoxyuridine(Brdu)viathecaudalveinimmediatelyafterthemodelwasestablished.Thedexamethasonetreatmentgroupwasintraperitoneallyinjectedwithdexamethasonefor7dfromthenextdayafterthemodelwasestablished.Thenegativecontrolgroupwasgivenanequalvolumeofnormalsalinebyintra-trachealinstillation.Ineachgroup,5ratsweresacrificedinthe7th,14th,and28thdays.Theexpressionoftransforminggrowthfactorβ1(TGF-β1)andBrdu-labeledstemcellswereobservedbyHEandMassonstainingandimmunohistochemistry.Lunghydroxyprolinecontentwasdeterminedbyacidhydrolysis.RESULTS:ThestemcelltreatmentgroupshadBrdu-labeledstemcellsseeninlungtissueinthe7th,14th,and28thdays.Comparedwiththenegativecontrolgroup,thebleomycingroup,stemcelltreatmentgroup,anddexamethasonetreatmentgrouphadsignificantlyincreasedscoresofalveolitisandpulmonaryfibrosis(P0.05).Inthe7th,14th,and28thdays,thescoresofalveolitisinstemcelltreatmentgroupanddexamethasonetreatmentgroupweresignificantlylowerthanthoseinbleomycingroup(P0.05);inthe28thday,thescoresofpulmonaryfibrosisinstemcelltreatmentgroupanddexamethasonetreatmentgroupweresignificantlylowerthanthatinbleomycingroup(P0.05).Therewerenosignificantdifferencesinscoresofalveolitisandpulmonaryfibrosisbetweenthedexamethasonetreatmentgroupandstemcelltreatmentgroup(P0.05).Comparedwiththebleomycingroup,thestemcelltreatmentgroupanddexamethasonetreatmentgrouphadsignificantlydecreasednumberofTGF-β1-positivecellsandhydroxyprolinecontentinlungtissueatalltimepoints(P0.05).TherewerenosignificantdifferencesinnumberofTGF-β1-positivecellsandhydroxyprolinecontentinlungtissuebetweenthestemcelltreatmentgroupanddexamethasonetreatmentgroup(P0.05).CONCLUSION:hUCB-MSCscanbetransplantedintodamagedlungtissueandeffectivelyreducealveolitisandpulmonaryfibrosisintheearlystageofpulmonaryfibrosis.TheactionmechanismofhUCB-MSCsmayinvolveinhibitingtheexpressionofTGF-β1andreducingtheformationofcollagen.
引自：WangHY,LiuC,WangY,etal.Experimentaltreatmentofpulmonaryinterstitialfibrosiswithhumanumbilicalcordbloodmesenchymalstemcells.ZhonghuaLaoDongWeiShengZhiYeBingZaZhi.Sep;31(9):-.
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