The abilities of AP1 and AP2 to reduce the secretion of pro-inflammatory cytokines Interleukin (IL)-1, IL-6, and Tumor necrosis factor (TNF)-¦Á from stimulated astrocytes were tested. In addition, the abilities of AP1 and AP2 to reduce oxidative stress in astrocytes were tested using an oxidative-sensitive fluorescent dye. The reduction of chondroitin sulfate proteoglycan (CSPG) in stimulated astrocytes was tested using the dot blot method. Reduction of H2O2-induced death was tested in PC12 cells. Astrocyte-conditioned medium (ACM) and TNF-¦Á-stimulated astrocyte-conditioned medium (SACM) were used to assess the effects of AP2 on PC12 cells treated with H2O2.
AP1 and AP2 reduced pro-inflammatory cytokines, reactive oxygen species (ROS), and CSPG in TNF-¦Á stimulated astrocytes. AP1 protected H2O2-treated PC12 cells cultured in ACM. Co-incubation of PC12 cells in H2O2, and ACM collected from AP1 treated astrocytes did not prevent cell death.
AP1 and AP2 effectively ameliorated astrocytic pro-inflammatory reactions and prevented PC12 cell death with different efficacies. These compounds may be candidates for treatment of spinal-cord injury and neurodegeneration.