欢迎您！东篱公司
退出
-
申报数据库
-
立项数据库
-
成果数据库
-
项目获奖数据库
中文摘要：
目的主要研究丝裂原激活蛋白激酶（MAPK）信号途径在内毒素脂多糖（LPS）诱导大鼠施万细胞（Scs）诱导型一氧化氮合酶（iNOS）基因表达和一氧化氮（NO）产生中的作用。方法先用3种MAPK的特异性抑制剂PD98059（ERK1／2）、SB202190（P38MAPK）和SP600125（JNK）以不同浓度预处理细胞1h，再用LPS作用施万细胞4h后，用RT-PCR检测细胞中iNOS mRNA、IL-6 mRNA和TNF-αmRNA的表达；Western blotting观察iNOS蛋白水平的表达变化；通过测定细胞培养液中亚硝酸盐含量来观察NO的水平。结果LPS可显著激活施万细胞中MAPK信号通路诱导iNOS表达。MAPK的抑制剂预处理细胞后，可显著抑制细胞iNOS mRNA和NO的合成及IL-6mRNA和，TNF-α mRNA的表达。结论MAPK信号通路参与了LPS介导的大鼠施万细胞iNOS基因表达和NO产生，通过阻断细胞内信号转导通路来减少iNOS及其他细胞因子的产生，为抑制周围神经损伤后的炎症以及免疫反应发生提供了一条新思路。
英文摘要：
Objective To explore the role of mitogen-activated protein kinase （MAPK）in lipopolysaccharide （LPS）- induced iNOS expression and NO production in rat Schwann cells by the use of inhibitors PD98059 selective for extracellular signalregulated kinase 1/2（EPK1/2）, SB202190 for P38 MAPK and SP600125 for the c-Jun NH2-terminal kinase （JNK）. Methods Schwann cells were pretreated with PD98059 （30, 50, 70μmol/L）, SB202190 （10, 20, 40μmol/L） and SP600125 （10, 30, 50μmol/L） at the indicated concentrations for 1 hour before the stimulation with LPS （10mg/L） for 4 hour. The estimation of iNOS mRNA, IL-6 mRNA and TNF-α mRNA was performed by RT-PCR; the changes of iNOS protein expression were investigated by Western blotting. The NO level was observed with measurement of nitrite in the cell culture medium. Results LPS could significantly activate MAPK signal pathway and lead to the expression of iNOS and NO production. The iNOS expression and NO production induced by LPS stimulation were significantly inhibited by the three highly specific inhibitors of MAPK. In addition, the inhibitors decreased LPS-induced the expression of IL-6 mRNA and TNF-α mRNA. Conclusion Activation of MAPK pathway is involved in iNOS expression and NO production in rat Schwann cells, and the inhibition of the signal transduction pathway can be effective to reduce the production of iNOS and NO, which may be a useful strategy against inflammatory and immune reaction after peripheral nerve injury.
同期刊论文项目
同项目期刊论文
Altered beta-1,4-galactosyltransferase I expression during early inflammation after spinal cord cont
Elevated beta 1,4-galactosyltransferase-I induced by the intraspinal injection of lipopolysaccharide
SSeCKS promote beta-amyloid-induced PC12 cells neurotoxicity by up-regulating tau phosphorylation in
Cyclin D3/CDK11(p58) Complex Involved in Schwann Cells Proliferation Repression Caused by Lipopolysa
A Critical Role of Src-Suppressed C Kinase Substrate in Rat Astrocytes After Chronic Constriction In
Lipopolysaccharide-evoked HSPA12B expression by activation of MAPK cascade in microglial cells of th
The expression patterns of beta 1,4 galactosyltransferase I and V mRNAs, and Gal beta 1-4GlcNAc grou
期刊信息
位置：