Toll样受体4在大鼠炎症牙髓表达的免疫组化研究被引量：3

Immunohistochemical study on dynamic expression of TLR4 in rat pulpitis

在线阅读下载PDF

导出

摘要目的研究内毒素（LPS）诱导大鼠牙髓炎模型中Toll样受体4（TLR4）的表达特点，以探讨TLR4在牙髓炎症中的可能作用，推测它在牙髓炎发生发展中的意义。方法通过对LPS诱导的大鼠磨牙牙髓炎组织切片，同时采用免疫组化方法检测大鼠牙髓炎中TLR4的表达情况。结果1d组：成牙本质细胞呈中度阳性表达，牙髓成纤维细胞为中度至强阳性表达；3～7d组：成牙本质细胞、牙髓成纤维细胞阳性表达减弱；2周组：坏死区扩大呈均质弱阳性表达，成牙本质细胞、牙髓成纤维细胞及内皮细胞减少，呈阳性，修复牙本质呈弱阳性表达；3周组：大部分坏死牙髓组织呈均质弱阳性表达。结论TLR4在大鼠牙髓炎发生、发展呈动态表达，TLR4可能参与调节牙髓炎发生、发展及修复过程。 Objective To study the expression of toll like receptor-4 （TLR4） in rat pulpitis model induced by endotoxin（LPS） so as to evaluate the possible role of TLR4 in rat pulpitis and conjecture its significance in the development of pulpitis. Methods Make the slides of rat molar pulpitis tissue induced by LPS, and examine the expression of TLR4 in rat pulpitis immunohistochemically. Results 1 d group ：TLR4 was moderately positive in odontoblasts and moderately to stongly positive in the pulp fibroblasts. 3-7 d group ： the posi- tive expression reduced in odontoblasts and pulp fibroblasts. 2 weeks group ： necrosis expanded and was homogeneously weakly positive ; odontoblasts ,pulp fibroblasts and endothelial cells reduced and were positve ; reparative dentin was weakly positive. 3 weeks group ： most of the necrosis was homogeneously weakly positive. Conclusions TLR4 is dynamically expressed in the generation and development of rat pulpitis. TLR4 may take part in the regulation of generation,development and repair of pulpitis.

作者兰卫东洪兵

机构地区南京大学附属口腔医院牙体牙髓科

出处《口腔医学》 CAS 2013年第10期672-674,共3页 Stomatology

关键词 TLR4 牙髓炎大鼠 TLR4 pulpitis rat

分类号 R781.31 [医药卫生—口腔医学]

作者简介通信作者：兰卫东 Tel：（025）84683106 E—mail：lwd700123@sina．com

引文网络
相关文献

参考文献14

1Schiaffonati L,Tiberio L. Gene expression in liver after toxic inju- ry: analysis of heat shock response and oxidative stress-induclble genes[ J]. Liver, 1997,17 (4) :183 - 191.
2Medzhitov R,Presto-Hurlburt P,Janeway CA. A human homologue of the drosophila Toll protein signals activation of adaptive immuni- ty[ J]. Nature, 1997,388(3) :394 - 397.
3兰卫东,解保生,王培新,谭葆春,葛久禹.热休克蛋白70在大鼠牙髓炎中的免疫组化研究[J].口腔医学,2004,24(4):202-205. 被引量：10
4Papamichos SI, Kotoula V,Tarlatzis BC, et al. OCT4BI isoform: the novel OCT4 alternative spliced variant as a putative marker of sternness [ J ]. Mol Hum Reprod, 2009,15 ( 5 ) :269 - 270.
5Wang X, Zhao Y, Xiao Z, et al. Alternative translation of OCT4 by an internal ribosome entry site and its novel function in stress response [ J ] . Stem Cells ,2009,27 ( 6 ) : 1265 - 1275.
6Doyle S, Vaidya S, O'Connell R, et al. IRF3 mediates a TLR3/ TLR4-specific antiviral gene program [ J ]. Immunity,2002,17 ( 3 ) : 251 - 263.
7Kawai T, Akira S. The role of pattern-recognition receptors in in- nate immunity :updateon Toll-like receptors[ J ]. Nature Immunolo- gy,2010,11 (5) :373 -384.
8Iwasaki A, Medzhitov R. Toll-like receptor control of the adaptive immune responses[ J]. Nature Immuno1,2004,5 (10) :987 - 995.
9Scheres N, Laine ML, Sipos PM, et al. Periodontal ligament and gingival fibroblasts from periodontitis patients are more active in in- teraction with Porphyromonas gingivalis [ J ]. J Period Res,2011,46 (4) :407 -409.
10Sun Y, Shu R,Zhang MZ. Toll-like receptor4 signaling plays a role in triggering periodontal infection [ J ]. FEMS Immunology and Medical Microbiology, 2008,52 ( 3 ) : 362 - 369.

二级参考文献15

1Barouch W,Prasad K,Greene L,et al.Auxilin-induced interaction of the molecular chaperone Hsc70 with clathrin baskets[J].Biochem,1997,36 (14):4303-4308.
2Rabindran SK,Haroun RI,Clos J,et al.Regulation of heat shock factor trimer formation:role of a conserved leucine zipper[J].Science,1993,259 (5092):230-234.
3Samali A,Holmberg CI,Sistonen L,et al.Thermotolerance and cell death are distinct cellular responses to stress:dependence on heat shock protein[J].FEBS Lett,1999,461 (3):306-310.
4Yokoo T,Kitamura M.IL-1 beta depresses expression of the 70-kilodalton heat shock protein and sensitizes glomerular cells to oxidant initiated apotosis[ J].Immunol,1997,59(6):2886-2892.
5Vanmuylder N,Evrard L,Dourov N.Strong expression of heat shock proteins in growth plate cartilage,an immunohistochemical study of HSP28,HSP70 and HSP110[J].Anat Embryol,1997,195 (4):359-362.
6De Vera ME,Wong JM,Zhou JY,et al.Cytokine-induced nitric oxide synthase gene transcription is blocked by the heat shock response in human liver cells[J].Surgery,1996,120(2):144-149.
7Klosterhalfen B,Hauptmann S,Offner FA,et al.Induction of heat shock protein 70 by zine-bis-( DL-hydrogenaspartate) reduces cytokine liberation,apotosis,and mortality rate in a rate model of LD100 endotoxemia[ J ].Shock,1997,7(4):254-262.
8Yoshikai Y.The role of heat shock proteins in host defense against bacterial infection[J].Rinso Byori,1998,46(6):564-573.
9Iwashina M,Shichiri M,Maramo F,et al.Transfection of inducible nitric oxide synthase gene causes apoptosis in vascular smooth muscle cells[J].Circulation,1998,98(12):1212-1218.
10Miyasaka N,Hirata Y.Nitric oxide and inflammatory arthritides [J].Life Sci,1997,61(21):2073-2081.