Transfer of massive mitochondria from astrocytes reduce propofol neurotoxicity

Studies have shown that propofol-induced neurotoxicity is mediated by disruption of mitochondrial fission and fusion, leading to an imbalance in energy supply for developing neurons. Healthy mitochondria released from astrocytes migrate to compromised neurons to mitigate propofolinduced neurotoxicity, yet the precise mechanisms involved require further clarification. In our investigation, primary neurons were incubated with pro-pofol, which decreased ATP synthesis and mitochondrial membrane potential, increased ROS generation and neuronal apoptosis. Notably, astrocytes did not respond to the deleterious effects of propofol. The culture me-dium of neurons or astrocytes incubated with propofol was collected. It was found that mitochondrial ratio was decreased and mitochondrial function was impaired. Non-contact co-culture of neuro-astrocytes facilitated transcellular mitochondrial transfer in both physiological and propofol interventions, but failed to reverse propofol-induced neurotoxicity. The more pronounced damage to neuronal mitochondria induced by propofol compared to that in astrocytes alludes to secondary injury. Damaged neurons incubated with large, functional extracellular mitochondria derived from astrocytes demonstrates transfer of mitochondria to neurons, effectively reversing propofol-induced neurotoxicity. This discovery presents a novel mitochondrial transfer of neuroastrocytes crosstalk that contributes to neuroprotection and neurological recovery in neurotoxicity.

Automated summary

Studies have shown that propofol-induced neurotoxicity is caused by disruption of mitochondrial fission and fusion, leading to an energy supply imbalance for developing neurons. Healthy mitochondria released by astrocytes can migrate to compromised neurons to mitigate propofol-induced neurotoxicity, but the exact mechanisms involved still need further clarification.