摘要
目的研究PI3K/Akt信号通路中相关蛋白Akt、pAkt在磷脂壁酸(lipoteichoic acid,LTA)和脂多糖(lipopolysaccharide,LPS)诱导引起的人牙髓细胞(human dental pulp cells,HDPCs)损伤中的表达情况及PI3K/Akt激活剂胰岛素样生长因子(IGF)-1对人牙髓细胞损伤的保护作用。方法甲基噻唑基四唑(MTT)法检测LTA、LPS作用24、48、72 h后对HDPCs增殖的影响以及IGF-1对LTA、LPS引起的HDPCs增殖抑制的保护作用,蛋白免疫印迹法检测LTA、LPS刺激HDPCs 24 h后及使用IGF-1和脂磷壁酸、脂多糖共同处理HDPCs相关蛋白Akt、pAkt表达水平的变化。结果 LTA和LPS抑制HDPCs增殖具有浓度依赖性。IGF-1可降低LTA、LPS引起的HDPCs增殖抑制程度。使用IGF-1和脂磷壁酸、脂多糖共同处理HDPCs后pAkt(Ser473)蛋白表达上调,这种作用可被LY294002取消。结论 IGF-1对脂磷壁酸、脂多糖引起的hHDPCs增殖抑制有保护作用,这种保护作用可能通过激活PI3K/Akt信号通路发挥作用。
Objective To explore the protein expression of Akt,pAkt,in the human dental pulp cells stimulated by LTA and LPS,and to investigate the protection function of IGF-1 to the human dental pulp cell. Methods MTT chromatometry was used to determine cell inhibition rate of HPDCs stimulated by different concentrations LTA and LPS,and to determine cell inhibition rate of HPDCs costimulated by IGF-1 and LTA or LPS. The protein expression of Akt,pAkt,in HPDCs were then evaluated by western bloting. Results LTA and LPS inhibited HPDCs viability in a dose-dependent fashion. IGF-1 had a protection function of HPDCs inhibition caused by LTA and LPS. The protein expression of pAkt（ Ser473） in HPDCs co-stimulated by IGF-1 and LTA or LPS was higher than other groups. Conclusions IGF-1 had a protection function to HPDCs inhibition caused by LTA and LPS,and this function might have a relationship with PI3 K /Aktpathway.
出处
《口腔医学》
CAS
2014年第9期674-678,共5页
Stomatology
作者简介
通信作者：彭志翔Tel：（020）83822804 E-mail：pengzhixiang@gmail．com
