OBJECTIVE: To investigate changes of autophagy after traumatic brain injury (TBI) and its possible role. METHODS: Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structure was detected by transmission electronic microscope. Microtubule-associated protein 1 light chain 3 (LC3) and Beclin 1 were also used to investigate the activation of autophagy post-TBI. Double labeling with LC3 and caspase-3, or Beclin 1 and Fluoro-Jade to show the relationship between autophagy and apoptosis or neuron degeneration after TBI. RESULTS: An increase of autophagic double membrane structure was observed in early stage (1 h), and the increase lasted for at least 32 d post-TBI. LC3 and Beclin 1 proteins also began to elevate at 1 h time point post-TBI in neurons, 3 d later in astrocytes, and peaked at about 8 d post-TBI. In both cell types, LC3 and Beclin 1 maintained at a high level until 32 d post-TBI. Most LC3 and Beclin 1 positive cells were near the side (including hippocampus), but not in the core of the injury. In addition, in the periphery of the injury site, not all caspase-3 positive (+) cells merged with LC3 (+) cells post-TBI; In hippocampal area, almost all Beclin 1 (+) neurons did not merge with Fluoro-Jade (+) neurons from 1 h to 48 h post-TBI. CONCLUSION: Autophagy is activated and might protect neurons from degeneration at early stage post-TBI and play a continuous role afterwards in eliminating aberrant cell components.
OBJECTIVE: To investigate changes of autophagy after traumatic brain injury (TBI) and its possible role. METHODS:Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structure was detected by transmission electronic microscope. Microtubule-associated protein 1 light chain 3 (LC3) and Beclin 1 were also used to investigate the activation of autophagy post-TBI. Double labeling with LC3 and caspase-3, or Beclin 1 and Fluoro-Jade to show the relationship between autophagy and apoptosis or neuron degeneration after TBI. RESULTS: An increase of autophagic double membrane structure was observed in early stage (1 h), and the increase lasted for at least 32 d post-TBI. LC3 and Beclin 1 proteins also began to elevate at 1 h time point post-TBI in neurons, 3 d later in astrocytes, and peaked at about 8 d post-TBI. In both cell types, LC3 and Beclin 1 maintained at a high level until 32 d post-TBI. Most LC3 and Beclin 1 positive cells were near the side (including hippocampus), but not in the core of the injury. In addition, in the periphery of the injury site, not all caspase-3 positive (+) cells merged with LC3 (+) cells post-TBI; In hippocampal area, almost all Beclin 1 (+) neurons did not merge with Fluoro-Jade (+) neurons from 1 h to 48 h post-TBI. CONCLUSION: Autophagy is activated and might protect neurons from degeneration at early stage post-TBI and play a continuous role afterwards in eliminating aberrant cell components.
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