|
- 2016
NLRP3/Caspase-1炎性体通路在大鼠根尖周炎中表达的研究
|
Abstract:
摘要 目的:研究大鼠实验性根尖周炎中NLRP3/Caspase-1炎性体通路的表达。方法:30只大鼠双侧下颌第一磨牙开髓后封入PBS缓冲液棉球,玻璃离子封闭髓腔,分别于开髓后0、7、14、21d和28d处死大鼠,分离双侧下颌骨。组织学处理后HE染色观察根尖周组织炎症状况,免疫组织化学染色和实时荧光定量PCR分别检测NLRP3、Caspase-1和IL-1β的表达情况。结果:NLRP3、Caspase-1和IL-1β在炎性根尖周组织中均有表达;与对照组相比,三者表达水平均明显增高,差异有统计学意义(P<0.05);其中Caspase-1和IL-1β阳性细胞数与NLRP3阳性细胞数呈显著正相关(P<0.01)。结论:根尖周组织中存在着NLRP3/Caspase-1炎性体通路,提示该通路在根尖周组织固有免疫中可发挥重要作用。 [关键词]炎性体NLRP3Caspase-1根尖周
[1] | Lamkanfi M, Dixit VM, BE Schekman R, et al. Inflammasomes and their roles in health and disease [J]. Annu Rev Cell Dev Biol, 2012, 28∶137-161 |
[2] | Allen IC, Scull MA, Moore CB, et al. The NLRP3 inflammasome mediates in vivo innate immunity to influenza A virus through recognition of viral RNA [J]. Immunity, 2009, 30∶556-565 |
[3] | Franchi L, Eigenbrod T, Muoz-Planillo R, et al. The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis [J]. Nat Immunol, 2009, 10∶241-247 |
[4] | Song Z, Lin Z, He F, et al. NLRP3 is expressed in human dental pulp cells and tissues [J]. J Endod, 2012, 38(12)∶1592-1597 |
[5] | Guarda G, Zenger M, Yazdi AS, et al. Differential expression of NLRP3 among hematopoietic Cells [J]. J Immunol, 2011, 186∶2529-2534 |
[6] | Thirumala-Devi K. Central roles of NLRs and inflammasomes in viral infection [J]. Nat Rev Immunol, 2010, 10(10)∶688-698 |
[7] | 刘生波,刘元元. NLRP3在大鼠实验性根尖周炎中的表达[J].口腔医学研究,2013, 29(11)∶1002-1004 |
[8] | Schroder K, Tschopp J. The inflammasomes [J]. Cell, 2010, 140(6)∶821-832 |
[9] | Jiang wk, Lv Hp, Wang HJ, et al. Activation of the NLRP3/caspase-1 inflammasome in human dental pulp tissue and human dental pulp fibroblasts [J]. Cell Tissue Res, 2015, 2∶2118-2132 |
[10] | Anand PK, Malireddi RK, Kanneganti TD. Role of the nlrp3 inflammasome in microbial Infection [J]. Front Microbiol, 2011, 2∶12 |
[11] | Sutterwala FS, Ogura Y, Szczepanik M, et al. Critical role for NALP3/CIAS1/Cryopyrin in innate and adaptive immunity through its regulation of caspase-1 [J]. Immunity, 2006, 24∶317-327 |
[12] | Yilmaz O, Sater AA, Yao LY, et al. ATP-dependent activation of an inflammasome in primary gingival epithelial cells infected by Porphyromonas gingivalis [J]. Cell Microbiol, 2010, 12∶188-198 |
[13] | Feldmeyer L, Keller M, Niklaus G, et al. The inflammasome mediates UVB-induced activation and secretion of interleukin-1beta by keratinocytes [J]. Curr Biol, 2007, 17∶1140-1145 |
[14] | Goldbach-Mansky R, Kastner DL. Autoinflammation: the prominent role of IL-1 in monogenic autoinflammatory diseases and implications for common illnesses [J]. J Allergy Clin Immunol, 2009, 124∶1141-1149 |
[15] | Okada Y, Tsuzuki Y, Hokari R, et al. Anti-inflammatory effects of the genus Bifidobacterium on macrophages by modification of phospho-I kappaB and SOCS gene expression [J]. Int J Exp Pathol, 2009, 90∶131-140 |