ABSTRACT
Objective To investigate the effects of lipoxin A4 on store-operated calcium channel (SOC) and production of reactive oxygen species in macrophages induced by hpopolysaccharide (LPS).Method Macrophages were randomly assigned Io one of the following six groups:control group,LPS group,Thapsigargin group,lipoxin A4+LPS group,lipoxin A4+Thapsigargin group,2-Aminoethoxydiphenylborate+Thapsigargin group.The intracellular[Ca2+]iwas analyzed by eonfoeal laser microscopy.The production of reactive oxygen specips(ROS) was assayed by flow cytometry.Results LPS increased intracellular[Ca2+]i and reactive oxygen species in a dose-dependent manner.Lipoxin A4 suppressed approximately 75% of the Ca2+ ertry signal induced by thapsigargin and suppressed approximately 93% of the Ca2+ entry signal induced by LPS.The increase in intracellular[Ca2+]i was associated with increased ROS production which was abolished in the presence of lipoxin A4.Conclusions These findings indicate that the LPS-indueed intracellular[Ca2*]i increase depends on the Ca2+entry through SOC channel,and lipoxin A4 inhibits Ca2+ influx and ROS production through SOC channel in ratine maerophages induced by LPS.
ABSTRACT
A three-dimensional finite element model of the maxillary canine was developed including periodontal ligament, pulp and alveolar bone. And the stress distributions in the periodontal tissue were obtained under different orthodontic force. The specific aims were to make the model by means of the more advanced and accurate twin CT, to provide more accurate data for clinical use, and to build a more accurate model for the simulation of maxillary canine movement under orthodontic forces.