Fig. 6

Schematic diagram summarizing the protective effects of TFDM against H₂O₂-induced astrocyte apoptosis through a mitochondria-dependent pathway. Proposed protective mechanisms of TFDM against H₂O₂ injury via CaMKII-dependent mitochondria-mediated apoptosis and PI3K/AKT/mTOR signaling pathways in astrocytes. H₂O₂ induces an increase in [Ca2+], and H₂O₂ exposure induces an increase in ROS levels, which might contribute to an elevation of the resting [Ca2+], possibly leading to neurotoxicity in the hippocampus. TFDM relieves CaMKII-dependent mitochondria-mediated apoptosis, including the expression of Bax, Bcl-2, and caspase-3/9 and the activation of p38MAPK and ERK1/2, following cellular H₂O₂ injury