The role and expression mechanism of an inflammatory mediator in human denial pulp cell

人牙髓细胞炎症介质的作用及表达机制

• 批准号: 15592034
• 负责人: HASHIZUME Hideki
• 金额: $ 2.11万
• 依托单位: Nihon University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2003
• 资助国家: 日本
• 起止时间: 2003 至 2004
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15592034/
• 关键词: human dental pulp cell; Plasminogen activator; IL-1β; protein tyrosin kinase; Plasminogen Activator; チロシンリン酸化; NFκB; Plasminogen activator; IL-1

1.IL-1β(50pg/ml) activated t-PA in the lysate and medium in a time-dependent (0〜12hrs) manner.2.IL-1β activated t-PA in the lysate and medium in a concentration -dependent(50〜100pg) manner.3.Pyrrolidine dithocarbamate, a NFκB inhibitor inhibited the IL-1β-induced tPA activation.4.Genistein and herbimycin, protein tyrosine kinase inhibitors, inhibited the IL-1β-induced tPA activation.5.On the contrary, orthovanadate, a protein tyrosine phosphatase inhibitor, augmented the effect of IL-1β.These observations suggest that regulation of tyrosine phosphorylation is necessary for IL-1β induced t-PA activation, and the synthesis of t-PA via NFκB is involved in the effect of IL-1β in HDP.6.Phorbol 12-myrisatate 13-acetate, protein kinase C activator t PA augmented the effect if IL-1β induced tPA activation.7.Ionomycine, Ca^<2+> mobilizing reagent did not augment the IL-1β induced tPA activation

1。IL-1β（50pg/mL）在裂解物中激活的T-PA，以时间依赖性（0至12小时）的方式激活了T-PA。2。 IL-1β激活的裂解物中的T-PA和浓度依赖性（50至100pg）的方式3。 NFκB抑制剂吡咯烷二甲甲酸酯抑制了IL-1β诱导的TPA激活。4。染料木黄酮和草食霉素，蛋白酪氨酸激酶抑制剂抑制了IL-1β诱导的TPA激活。5。相反，蛋白质酪氨酸磷酸酶抑制剂正叉酸扩大了IL-1β的作用。这些观察结果表明，对IL-1β诱导的T-PA激活是必要的，并且通过NFκB合成T-PA的合成参与IL-1β在HDP.6.6.phorbol 12-丙二醇酯13-乙酸盐13-乙酸盐中的效果，蛋白质激酶C活化剂T PA增强效应IL-1 <iil-lim-1 <iil-caivination caivination> limenty t pa sivation> tpa sivation> t pa sivation。动员试剂不会增加IL-1β诱导的TPA激活