β防御素在肺气虚证大鼠发病中的作用(3)
发布时间:2021-06-06
发布时间:2021-06-06
安徽中医学院学报第29卷第5期2010年10月JOURNAL
OFANI-nflITCMOOLLEGEVoL29No.5
Oct.2010
49
胞外基质的早期尚可发挥其增强宿主防御功能,但很快出现细胞毒性和趋化现象,造成机体损伤[2]。防御素可诱导上皮细胞释放中性粒细胞趋化因子IL~8和中性粒细胞活化蛋白78,它们又间接地提高中性粒细胞在炎症位点的募集和活化[3],Zhang症和呼吸功能不全。
肺功能恶化时伴随人B:防御素的减少,严重的疾病可导致口防御素减少,并继发宿主防御缺陷[5]。
本实验结果和文献报道一致。感染3d时,模型组大鼠在铜绿假单胞菌的诱生下肺黏膜上皮细胞过量产生p。防御素,从而募集和趋化炎症细胞,发挥细胞毒作用,导致急性炎症的出现。肺组织B:防御素释放入血使得血清8防御素同时增高。30d和
100
H
利则气道涩。”《素问 评热病论篇》谓:“邪之所凑,其气必虚。”由于肺功能减退导致肺气虚证大鼠气短、气促、易乏力,这和肺气虚证的表现是相符的,也为揭示肺气虚的本质提供了科学的理论根据和实验依据。
参考文献:
F1]程惠娟,汪长中,王艳,等.呼吸道生物被膜菌致肺气虚
大鼠模型的研制[J].上海中医药大学学报,2009,23
(3):38-41.
等n1在小鼠的气管内给予防御素可导致急性气道炎
[23
Hiem
tory
stra
PS.Defensinsandcathelieidinsininflamma—
lungdisease:Beyondantimierobialactivity[J].Bio—
ehemSocTrans,2006,34(2):276-278.
a1.Neu—
[33
Van
t
WS,MannesseLSPG,WanSMAGA,et
rophildefensinsstimulatethereleaseofeytokinesby
cells:Modulationbydexamethasone
airwayepithelial
d时。模型组大鼠感染进入慢性期,随着肺组织[J].1nflamm[4]Zhang
fensins
Res,2002,51:8-15.
损伤和肺功能逐渐减退,肺黏膜上皮细胞产生的B防御素也随之减少。因此,感染30d和100d时模型组大鼠血清p防御素,气管冲洗液、肺匀浆8:防御素显著低于阴性对照组。6防御素的降低,使得慢性感染期肺气虚大鼠呼吸道失去了化学屏障,不能抵抗外来病原体的侵入,表现为易患呼吸道感染,血清8防御素的降低提示机体整体抗感染能力也是降低的。《诸病源候论 卷之十三 气病诸候》认为:“肺主于气,邪乘于肺则肺胀,胀则肺管不利,不
H。PorroG,OrzeehN,eta1.Neutrophilde—
mediate
acute
inflammatory
response
and
lung
dysfunctionindose-relatedLung(;ell
fashion[J].AmJ
Physilo
MolPhysiol,2001,280(5):I.947一I.954.
a1.Beta-de—
pa
[5]Chen
CI,Schailer-BalsS,PaulKP,et
fensinsandLI。37inbronchoalveolarlavagefluidoftientswithcystic45’50.
fibrosis[J].JCystFibros,2004,3:
(收稿日期:2010—03—17)
RoleofBeta-defensininPathogenesisofLung-q/DeficiencySyndromeinRatsCHENGHui-juan,W.ANGChang-zhong,GUANYah,WANG
(DepartmentofIntegratedTraditionalChineseandWesternMedicine,Anhui
ChineseMedicine,AnhuiHefei
230038,China)
contents
Yan,ⅢLi—hua
CollegeofTraditional
I-Abstract]ObjectiveToobservethechangesofserum
of
p-defensin,andthe
levels
on
of&-defensin
lung—qidefi—
inbronchiallavagefluidandlunghomogenates,andinvestigatetheeffectsof13-defensinciencysyndromeinrats.Methodswithcold
stress
Nasaldripofbiofilmbacteria(Pseudomonasaeruginosa)combined
to
andexhaustiveswimmingwasemployed
developlung—qideficiencysyndrome.His—
topathologicalchangesoflungwereobserved3,30,100daysafterinfection,respectively.Enzymelinkedimmunosorbentassaywasused
to
assaytheserumcontentsofp—defensin,andthelevelsof[3z-defensinin
bronchiallavagefluidandlunghomogenates.Resultsservedinmodel
rats
Anobviously
contents
acute
pulmonaryinfectionwasob—andthelevelsof
3daysafterinfection,theserum
of
ft-defensin
62-defensin
in
lunghomogenatesweresignificantlyincreased.Chronicpulmonaryinfectionwasdeveloped30,100daysafterinfection,respectively;theserumly
contents
of
p-defensin
andthelevelsof
62-defensin
weresignificant—
decreased.Conclusion/3-defensins
wereinvolvedinpathogenesisoflung—qideficiencysyndrome;itpar—
acute
ticipatesininflammatoryreactionduringdromeduringchronicphase.
phase,andinducesandaggravateslung—qideficiencysyn—
[Keywords]Lung—qideficiencysyndrome;13-defensin;Biofilm;Pseudomonasaeruginosa
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