Objective To investigate the protective effect of astrocyte-derived mitochondria on propofol-induced neuronal injury. Methods Primary cortical neurons and astrocytes were isolated and cultured from newborn Sprague Dawley rats, and extracellular mitochondria were isolated from astrocytes. Neurons were randomly divided into a control group (group C), propofol group (group P), propofol+healthy mitochondria group (group PM), and propofol+damaged mitochondria group (group PMD). Group C was left untreated, while the other three groups were treated with 100 μmol/L propofol and incubated for 6 hours. On this basis, group PM was incubated with concentrated astrocyte-derived mitochondria for 24 hours, and group PMD was incubated with damaged astrocyte-derived mitochondria for 24 hours. Mitochondrial transfer was observed by confocal microscopy. The neuronal mitochondrial membrane potential, adenosine triphosphate (ATP) content, reactive oxygen species levels, mitochondrial superoxide (mSox), cell viability, apoptosis rate, mortality rate, as well as the relative expression levels of B‑cell lymphoma‑2‑associated X protein (Bax), B‑cell lymphoma‑2 (Bcl‑2), peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α), phosphorylated dynamin‑related protein 1 at serine 616 (pDRP1 [S616]), brain‑derived neurotrophic factor (BDNF), and cleaved cysteinyl aspartate specific proteinase-3 (Cleaved-Caspase‑3) were compared among the four groups. Results Under confocal microscopy, red fluorescent signals were observed in the soma and axons of neurons, indicating successful mitochondrial transfer into neurons. In group C and group PM, the neuronal mitochondrial networks were well‑fused, with mitochondria presenting a long tubular morphology and a distinct network structure. In group P and group PMD, the mitochondrial networks were thick, short, and spherical, with a disordered and tangled arrangement. Compared with group C, the other three groups exhibited decreased neuronal mitochondrial membrane potential and neuronal viability, as well as increased reactive oxygen species levels, apoptosis rate, and neuronal mortality rate (P<0.05). Compared with group P, group PM showed increased neuronal mitochondrial membrane potential and cell viability, as well as decreased reactive oxygen species levels, apoptosis rate and neuronal mortality rate (P<0.05). Compared with group PM, group PMD exhibited decreased neuronal mitochondrial membrane potential and neuronal viability, as well as increased reactive oxygen species levels, apoptosis rate, and mortality rate (P<0.05). Compared with group C, groups P and PMD showed decreased ATP content and increased mSox content in neurons (P<0.05). Compared with group P, group PM exhibited increased ATP content and decreased mSox content in neurons (P<0.05). Compared with group PM, group PMD had increased mSox content in neurons (P<0.05). Compared with group C, the relative protein expression levels of Bax, Cleaved‑Caspase‑3, and pDRP1(S616) were up‑regulated, while those of Bcl‑2 and BDNF were down‑regulated in groups P and PMD (P<0.05). Compared with group P, the relative protein expression levels of Bax, pDRP1(S616) and Cleaved‑Caspase‑3 in the neurons of group PM were down‑regulated, while those of Bcl‑2 and BDNF were up‑regulated (P<0.05). Compared with group PM, the relative protein expression levels of Bax, pDRP1(S616) and Cleaved‑Caspase‑3 were up‑regulated, while those of Bcl‑2 and BDNF were down‑regulated in group PMD (P<0.05). Conclusion Healthy astrocyte‑derived mitochondria can effectively alleviate propofol‑induced neuronal injury through intercellular transfer. They may exert neuroprotective effects by supplementing energy metabolic substrates, restoring mitochondrial membrane potential, promoting ATP production, attenuating oxidative stress injury, inhibiting excessive mitochondrial fission, maintaining the expression balance of apoptosis‑related proteins, and upregulating endogenous protective factors including Bcl‑2 and BDNF.

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